Jashin J. Wu

Early clinical studies suggested that the anti–interleukin-17 receptor A monoclonal antibody brodalumab has efficacy in the treatment of psoriasis.

Psoriasis is a chronic, immune-mediated disorder with cutaneous and systemic manifestations and substantial negative effects on patient quality of life. Psoriasis has a strong, albeit polygenic, genetic basis. Whereas approximately half of the accountable genetic effect of psoriasis maps to the major histocompatibility complex, >70 other loci have been identified, many of which implicate nuclear factor-κB, interferon signalling and the IL-23–IL-23 receptor axis. Psoriasis pathophysiology is characterized by abnormal keratinocyte proliferation and immune cell infiltration in the dermis and epidermis involving the innate and adaptive immune systems, with important roles for dendritic cells and T cells, among other cells. Frequent comorbidities are rheumatological and cardiovascular in nature, in particular, psoriatic arthritis. Current treatments for psoriasis include topical agents, photo-based therapies, traditional systemic drugs and biologic agents. Treatments can be used in combination or as monotherapy. Biologic therapies that target specific disease mediators have become a mainstay in the treatment of moderate-to-severe disease, whereas advances in the treatment of mild-to-moderate disease have been limited. Psoriasis is a chronic, immune-mediated disease that can severely affect patient quality of life. Various kinds of skin manifestations are possible; psoriatic arthritis is a common but underdiagnosed comorbidity. Treatments for psoriasis include topical agents, phototherapy and systemic and biologic agents.

Psoriasis is a chronic, inflammatory multisystem disease that affects up to 3.2% of the US population. This guideline addresses important clinical questions that arise in psoriasis management and care, providing recommendations based on the available evidence. The treatment of psoriasis with biologic agents will be reviewed, emphasizing treatment recommendations and the role of the dermatologist in monitoring and educating patients regarding benefits as well as associated risks. Psoriasis is a chronic, inflammatory multisystem disease that affects up to 3.2% of the US population. This guideline addresses important clinical questions that arise in psoriasis management and care, providing recommendations based on the available evidence. The treatment of psoriasis with biologic agents will be reviewed, emphasizing treatment recommendations and the role of the dermatologist in monitoring and educating patients regarding benefits as well as associated risks. The information presented here represents the authors disclosed relationship with industry during guideline development. Authors (listed alphabetically) with relevant conflicts with respect to this guideline are noted with an asterisk. In accordance with American Academy of Dermatology (AAD) policy, a minimum 51% of work group (WG) members did not have any relevant conflicts of interest. Participation in 1 or more of the activities listed here constitute a relevant conflict:•Service as a member of a speaker bureau, consultant, or advisory board, for pharmaceutical companies on psoriasis disease state or psoriasis drugs that are in development or US Food and Drug Administration (FDA)-approved.•Sponsored research funding or investigator-initiated studies (with partial or full funding from pharmaceutical companies) on psoriasis disease state or psoriasis drugs that are in development or FDA-approved. If a potential conflict was noted, the WG member recused himself or herself from discussion and drafting of recommendations pertinent to the topic area of interest. Complete group consensus was obtained for draft recommendations. Areas in which complete consensus was not achieved, are shown transparently in the guideline. April W. Armstrong, MD, MPH,* served as a consultant for AbbVie, Bristol-Myers Squibb, Celgene Corporation, Genzyme Corporation, GlaxoSmithKline, Janssen-Ortho Inc, Janssen Pharmaceuticals, Inc, Leo Pharma, Inc, Menlo Therapeutics, Modernizing Medicine, Ortho Dermatologics, Pfizer, Inc, Regeneron, Sanofi, and Science 37, Inc, receiving honoraria; as a speaker for AbbVie, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Regeneron Pharmaceuticals, Inc, and Sanofi receiving honoraria; as a speaker and/or faculty educator for AbbVie, Eli Lilly and Company, and Janssen Pharmaceuticals, Inc, receiving honoraria; as a principal investigator and/or investigator for Amgen, Celgene, Dermira, Eli Lilly and Company, Janssen-Ortho, Inc, Leo Pharma, Inc, National Institutes of Health, Novartis, Regeneron, and UCB receiving grants and/or research funding; as an investigator for Regeneron and Sanofi receiving no compensation; as an advisory board member for AbbVie, Amgen, Janssen-Ortho Inc, Merck & Co, Inc, Novartis, Pfizer, Inc, and UCB receiving honoraria; and as a data safety member for Boehringer Ingelheim receiving honoraria. Cody Connor, MD has no conflicts of interest to disclose. Kelly M. Cordoro, MD,* served as a consultant for Valeant receiving honoraria; as a consultant for Pfizer, Inc, receiving fees; as an advisory board member for Anacor Pharmaceuticals, Inc, receiving honoraria; and in another position as a member of the Scientific Steering Committee for Celgene receiving fees. Dawn M.R. Davis, MD, served as an investigator for Regeneron receiving no compensation. Boni E. Elewski, MD,* served as a consultant for Boehringer Ingelheim, Celgene Corporation, IntendisGmBH, Lilly ICOS LLC, Merz Pharmaceuticals LLC, Novan, Novartis Pharmaceuticals Corp, Pfizer, Inc, Sun Pharmaceutical Industries, Ltd, and Valeant Pharmaceuticals International receiving honoraria; as a principal investigator for AbbVie, Amgen, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Incyte Corporation, Janssen-Ortho Inc, LEO Pharma, Merck & Co, Inc, Novan, Novartis Pharmaceuticals Corp, Pfizer, Inc, Sun Pharmaceuticals, Ltd, Valeant Pharmaceuticals International, and Vioment receiving grants and/or research funding; as an advisory board member for LEO Pharma receiving honoraria; and in another role for Hoffman-La Roche, Ltd, receiving fees. Craig A. Elmets, MD, served as a consultant for Ferndale Laboratories, Inc, receiving honoraria; as a consultant for Vaxin receiving stock and/or stock options; as a consultant/advisory board member for Vertex Pharmaceuticals receiving fees/honoraria; as a principal investigator for the California Association of Winegrape Growers, Kyowa Hakko USA, and Solgenix LLC receiving grants and/or research funding; as an investigator for Elorac, Inc, Idera Pharmaceuticals, Inc, Kyowa Hakko USA, and Solgenix LLC receiving grants and/or research funding; as a data safety monitoring board member for Astellas Pharma US, Inc, and LEO Laboratories, Ltd, receiving fees; as a stockholder for Medgenics, Inc, receiving no fees; and as a stockholder for Aevi Genomic Medicine (receiving stock) and Immunogen (paid to spouse). Joel M. Gelfand, MD, MSCE,* served as a consultant for AbbVie, Boehringer Ingelheim, Dermira, Dr Reddy, GlaxoSmithKline, Janssen Pharmaceuticals, Inc, Menlo Therapeutics, Novartis Pharmaceuticals Corp, Pfizer, Inc, Regeneron, Sanofi US Services, and Valeant Pharmaceuticals North America LLC receiving honoraria; as a consultant for BMS receiving fees; as a speaker for the American Academy of Dermatology receiving honoraria; as a speaker and/or faculty educator for CME supported by Eli Lilly and Company receiving fees; as a principal investigator for AbbVie, Celgene, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Novartis Pharmaceuticals Corp, Ortho Dermatologics, Pfizer, Inc, Regeneron, and Sanofi/Sanofi US Services receiving grants and/or research funding; as an investigator for Sanofi receiving grants and/or research funding; as an advisory board member for Sanofi US Services receiving honoraria; as a data safety monitoring board member for Coherus Biosciences and Merck & Co, Inc, receiving honoraria; in another role for the Society for Investigative Dermatology receiving honoraria; in another role for Elsevier, Inc, and SID receiving no compensation; and in another role for Eli Lilly and Company and UCB receiving fees. Kenneth B. Gordon, MD,* served as a consultant for AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Demira, Dermavant Sciences, Kyowa Hakko Kirin Pharma, Inc, Leo Pharma, Ortho Dermatologics, Sun Pharmaceuticals, Ltd, and UCB receiving honoraria; as a consultant for Genzyme receiving fees; as a principal investigator for AbbVie, Amgen, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Merck & Co, Inc, and Novartis Pharmaceuticals Corp receiving grants and/or research funding; and as an advisory board member for Celgene Corporation, Janssen Pharmaceuticals Inc, Lilly ICOS LLC, Novartis Pharmaceuticals Corp, and Pfizer, Inc, receiving honoraria. Alice B. Gottlieb, MD, PhD,* served as a consultant for Abbott Laboratories, AbbVie, Akros Pharma, Inc, Allergan, Amgen, Amicus Therapeutics, Baxalta Incorporated, Bristol-Myers Squibb, Canfite, Celgene Corporation, CSL Behring, Dermira, Dr Reddy, DUSA Pharmaceuticals, Inc, GlaxoSmithKline, Incyte Corporation, KPI Therapeutics, Lilly ICOS LLC, Meiji Seika Pharma Co, Ltd, Merck & Co, Inc, Mitsubishi Pharma, Novartis Pharmaceuticals Corp, Sanofi-Aventis, Sienna Biopharmaceuticals, Sun Pharmaceutical Industries, Takeda Pharmaceuticals USA, Inc, Teva, UCB, Valeant Pharmaceuticals International, Valeant Pharmaceuticals North America LLC, XBiotech, and Xenoport, Inc, receiving honoraria; as a consultant for Aclaris Therapeutics, Inc, Merck & Co Inc, and XBiotech receiving no compensation; as a speaker for AbbVie, Eli Lilly and Company, and Janssen Biotech receiving honoraria; as a principal investigator for Abbott Laboratories, AbbVie, Allergan, Amgen, Celgene Corporation, Coronado Biosciences, Immune Control, Incyte Corporation, Janssen-Ortho, Inc, LEO Pharma, Lerner Medical Devices, Inc, Lilly ICOS LLC, Merck & Co, Inc, Novartis Pharmaceuticals Corp, Novo Nordisk A/S, Pfizer Inc, UCB, Xbiotech, and Xenoport, Inc, receiving grants and/or research funding; as a principal investigator for Janssen-Ortho, Inc, receiving honoraria; as an advisory board member for Abbott Laboratories, Actelion, Amgen, Astellas Pharma US, Inc, Beiersdorf, Inc., BMS, Celgene Corporation, Coronado Biosciences, Dermira, Genentech, Janssen-Ortho, Inc, Leo Pharma US, Lilly ICOS LLC, Novartis Pharmaceuticals Corp, Novo Nordisk A/S, Pfizer, Inc, and UCB receiving honoraria; in another role for Amgen receiving grants and/or research funding; in another role for Crescendo Bioscience and Karyopharm Therapeutics receiving no compensation; in another role (data safety) for Catabasis Pharmaceuticals, Inc, receiving honoraria; and in another role for DermiPsor receiving honoraria. Daniel H. Kaplan, MD, PhD, served as a consultant for Eli Lilly and Company receiving no compensation and as a member of the data safety monitoring board for Hapten Pharma receiving fees. Arthur Kavanaugh, MD,* served as a principal investigator for AbbVie, Amgen, BMS, Celgene Corporation, Eli Lilly and Company, Janssen Biotech, Novartis, Pfizer, Inc, and UCB receiving grants and/or research funding. Dario Kivelevitch, MD has a first-degree relative employed by GlaxoSmithKline and Boehringer Ingelheim. Matthew Kiselica has no conflicts of interest to disclose. Neil J. Korman*, MD, PhD,* served as a consultant for Novartis Pharmaceuticals Corp receiving honoraria; as a consultant for Dr Reddy's Laboratory receiving fees; as a speaker for AbbVie, Eli Lilly and Company, Janssen, Novartis and Regeneron receiving honoraria; as a principal investigator for AbbVie, Amgen, Celgene Corporation, Dermira, Eli Lilly and Company, Kyowa Hakko Kirin Pharma, Inc, LEO Pharma, Menlo Therapeutics, Pfizer, Prothena, Regeneron, Rhizen, Inc, Syntimmune, and UCB receiving grants and/or research funding; as an advisory board member for Amgen, Celgene Corporation, Eli Lilly and Company, Genentech, GlaxoSmithKline, Janssen Pharmaceuticals, Inc, Novartis Pharmaceuticals Corp, Pfizer, Inc, and Principia Biopharma receiving honoraria; as an advisory board member for Immune, Regeneron, Sun Pharma, and Valeant receiving fees; as an advisory board member/consultant for AbbVie, Eli Lilly, GlaxoSmithKline, Pfizer Inc., and Principa receiving honoraria/fees; and in another role for Janssen Pharmaceuticals, Inc, receiving grants and/or research funding. Daniela Kroshinsky, MD, MPH, FAAD has no conflicts of interest to disclose. Mark Lebwohl, MD,* served as a consultant for Allergan, Aqua, Arcutis, Inc, Boehringer Ingelheim, Bristol-Myers Squibb, Leo Pharma, Menlo Therapeutics, Mitsubishi Pharma/Neuroderm LTD, Promious/Dr. Reddy, Theravance Biopharma, and Verrica Pharmaceuticals Inc receiving honoraria; as a principal investigator for AbbVie, Amgen, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Incyte Corporation, Janssen Research and Development LLC/Johnson & Johnson, Kadmon Corporation LLC, Leo Pharma, MedImmune/Astra Zeneca, Novartis Pharmaceuticals Corp, Ortho-Dermatologics, Pfizer, Inc, SCIDerm, UCB, and ViDac Pharma receiving grants and/or research funding; and in another role for Corrona, Inc, Facilitation of International Dermatology Education, and the Foundation for Research and Education in Dermatology receiving honoraria. Craig L. Leonardi, MD,* served as a consultant for Celgene Corporation and Dermira receiving honoraria; as a speaker for AbbVie, Amgen, Celgene Corporation, Eli Lilly and Company, Novartis, and Sun Pharmaceuticals, Ltd, receiving honoraria; as a principal investigator for Actavis, Amgen, Boehringer Ingelheim, Celgene Corporation, Cellceutix, Coherus Biosciences, Corrona, Dermira, Eli Lilly and Company, Galderma Laboratories, LP, Glenmark Generics, Inc, Janssen Pharmaceuticals, Inc, Leo Pharma, Inc, Novartis, Novella, Pfizer, Inc, Sandoz (a Novartis company), Sienna Biopharmaceuticals, Stiefel a GSK company, UCB, and Warner Chillcott receiving other financial benefits; and as an advisory board member for AbbVie, Amgen, Boehringer Ingelheim, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Leo Pharma A/S, Ortho Dermatologics, Pfizer, Inc, Sandoz (a Novartis company), and UCB receiving honoraria. Jason Lichten, MD has no conflicts of interest to disclose. Henry W. Lim, MD, served as a principal or coinvestigator for Estee Lauder, Ferndale Laboratories, Inc, Incyte, and Unigen receiving grants and/or research funding; and as a speaker and/or faculty educator for Pierre Fabre Dermatologie receiving honoraria. Nehal N. Mehta, MD, MSCE,* is a full-time US government employee and has served as a consultant for Amgen, Eli Lilly, and Leo Pharma receiving grants/other payments; as a principal investigator and/or investigator for AbbVie, Celgene, Janssen Pharmaceuticals, Inc, and Novartis receiving grants and/or research funding; and as a principal investigator for the National Institute of Health receiving grants and/or research funding. Alan Menter, MD,* served as a consultant for Abbott Labs, AbbVie, Amgen, Eli Lilly and Company, Galderma USA, Janssen Pharmaceuticals Inc, LEO Pharma US, Menlo Therapeutics, Novartis, Sienna Biopharmaceuticals, and Wyeth Labs receiving honoraria; as a consultant for New Enterprise Associates, Promius Pharma LLC, Spherix Global Insights US, UCB, and Valeant Pharmaceuticals North America receiving fees; as a consultant for Afecta Pharmaceuticals receiving no compensation; as a speaker for Abbott Labs, AbbVie, Amgen, Janssen Biotech, LEO Pharma, US, Pfizer, Inc, Promius Pharma LLC, Sienna Pharmaceuticals, UCB, and Wyeth Labs receiving honoraria; as a principal investigator for AbbVie, Amgen, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Medimetriks Pharmaceuticals, Inc, Merck & Co, Inc, Novartis Pharmaceutical Corp, and Pfizer, Inc, receiving grant and/or research funding; as an investigator for Eli Lilly and Company and UCB receiving honoraria; investigator for Abbott Labs, Leo Pharma US, and Sienna Biopharmaceutical receiving grants; as an advisory board member for Abbott Labs, AbbVie, Boehringer Ingelheim, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, LEO Pharma US, Medscape, Pfizer, Inc, and Sienna Biopharmaceuticals, receiving honoraria; as an advisory board member for Amgen receiving grant and/or research funding; as an advisory board member for Afecta Pharmaceuticals receiving no compensation; and as an independent contractor for Prime Education receiving fees. Amy Paller, MD,* served as a consultant for Amgen, Amicus Therapeutics, Anacor Pharmaceuticals, Inc, Aqua Pharmaceuticals, BridgeBio Pharma, Castle Creek Pharma, Celgene Corporation, Dermira, Eli Lilly and Company, Galderma Laboratories, LP, Genentech, Menlo Therapeutics, Novartis Pharmaceuticals Corp, Pfizer Inc, Pierre Fabre Dermatologie, Proctor and Gamble, Regeneron, Sanofi, Scioderm, Shire, Sol-Gel Technologies, Stiefel (a GSK company), UCB, and Valeant Pharmaceuticals North America LLC receiving honoraria; as a speaker/educator for Expanscience receiving honoraria; as a principal investigator for AbbVie, Amgen, Anacor Pharmaceuticals, Inc., AnaptysBio, Celgene Corporation, Eli Lilly, Galderma, Janssen Pharmaceuticals, Inc., Leo Pharma, Regeneron and Scioderm receiving no compensation. Sylvia L. Parra, MD, FAAD has no conflicts of interest to disclose. Arun L. Pathy, MD, FAAD has no conflicts of interest to disclose. Elizabeth Farley Prater, MD, FAAD has no conflicts of interest to disclose. Reena Rupani, MD, served as speaker for Nutrafol receiving no compensation. Michael Siegel, PhD has no conflicts of interest to disclose. Benjamin Stoff, MD, MA, served as an investigator for Celtaxsys, Inc, receiving fees. Bruce E. Strober, MD, PhD,* served as a consultant for AbbVie, Almirall, Amgen, Boehringer Ingelheim, Celgene Corporation, Dermira, Eli Lilly and Company, GlaxoSmithKline, Janssen-Ortho, Inc, Leo Pharma, Inc, Maruho Co, Ltd, Medac Pharma, Inc, Menlo Therapeutics, Novartis Pharmaceuticals Corp, Ortho Dermatologics, Pfizer, Inc, Sanofi-Regeneron, Sun Pharmaceuticals Industries, and UCB receiving honoraria; as a consultant for Affibody, Bristol-Myers Squibb, Meiji Seika Pharma Co, Ltd, and UCB receiving fees; as a principal investigator for AbbVie, Amgen, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Janssen-Ortho, Inc, Merck & Co, Pfizer, Inc, and Sun Pharmaceutical Industries receiving no compensation; as a principal investigator for Galderma Research & Development, LLC receiving grants and/or research funding; as an advisory board member for AbbVie, Amgen, Bristol-Myers Squibb, Celgene Corporation, Dermira, Eli Lilly and Company, Janssen-Ortho, Inc, Novartis Pharmaceuticals Corp, Pfizer, Inc, Sanofi-Regeneron, Sun Pharmaceuticals Industries, and UCB receiving honoraria; as a consultant/advisory board for AstraZeneca Pharmaceuticals LP receiving fees/honoraria; and in another role for AbbVie and Janssen-Ortho, Inc, receiving no compensation. Emily B. Wong, MD, FAAD has no conflicts of interest to disclose. Jashin J. Wu,* MD, served as a consultant for Abbvie, Almirall, Allergan, Amgen, Bristol-Myers Squibb, Celgene, Dermira, Dr Reddy's Laboratories, Eli Lilly and Company, Janssen Biotech, LEO Pharma, Novartis, Ortho Dermatologics, Pfizer, Inc, Promius Pharma, Regeneron, Sun Pharmaceutical Industries, Ltd, UCB, and Valeant Pharmaceuticals North America, LLC receiving fees and and/or or honoraria; as a speaker for AbbVie, Celgene, Novartis, Regeneron, Sun Pharmaceutical Industries Ltd, UCB, and Valeant Pharmaceuticals North America LLC receiving honoraria; and as a principal and/or investigator for AbbVie, AstraZeneca, Boehringer Ingelheim, Coherus Biosciences, Dermira, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Merck & Co, Inc, Novartis, Pfizer, Inc, Regeneron, Sandoz (a Novartis company), and Sun Pharmaceutical Industries, Ltd, receiving research and/or grant funding. Vidhya Hariharan, PhD, has no conflicts of interest to disclose. Adherence to these guidelines will not ensure successful treatment in every situation. Furthermore, these guidelines should not be interpreted as setting a standard of care, nor should they be deemed either inclusive of all proper methods of care or exclusive of other methods of care reasonably directed toward obtaining the same results. The ultimate judgment regarding the propriety of any specific therapy must be made by the physician and the patient in light of all the circumstances presented by the individual patient and the known variability and biologic behavior of the disease. Furthermore, the treatment dosages used in clinical trials may not be effective in certain cases, and some patients may require shorter intervals between doses and/or higher treatment doses of a particular biologic agent. This guideline reflects the best available data at the time the guideline was prepared. The results of future studies will likely require revisions to the recommendations in this guideline to reflect new data. This guideline will cover the use of biologic agents in the treatment of psoriasis in adults; psoriasis in the pediatric population will be covered in the “Guidelines of care for the management and treatment of pediatric psoriasis” guideline. This guideline will not cover the treatment of psoriatic arthritis (PsA) in detail, its management is reviewed in detail by the American College of Rheumatology and National Psoriasis Foundation treatment guidelines.7Kimball A.B. Gladman D. Gelfand J.M. et al.National Psoriasis Foundation clinical consensus on psoriasis comorbidities and recommendations for screening.J Am Acad Dermatol. 2008; 58: 1031-1042Abstract Full Text Full Text PDF PubMed Scopus (315) Google Scholar, 7Kimball A.B. Gladman D. Gelfand J.M. et al.National Psoriasis Foundation clinical consensus on psoriasis comorbidities and recommendations for screening.J Am Acad Dermatol. 2008; 58: 1031-1042Abstract Full Text Full Text PDF PubMed Scopus (315) Google Scholar A multidisciplinary WG of psoriasis experts consisting of dermatologists (including private practitioners), a rheumatologist, a cardiologist, and representatives from a patient advocacy organization was convened to update and expand on the previously published 2008 AAD psoriasis guideline.1Menter A. Gottlieb A. Feldman S.R. et al.Guidelines of care for the management of psoriasis and psoriatic arthritis: section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics.J Am Acad Dermatol. 2008; 58: 826-850Abstract Full Text Full Text PDF PubMed Scopus (882) Google Scholar The WG determined the scope of the guideline and identified important clinical questions with regard to biologic treatment of psoriasis (Table I). WG members completed a disclosure of interests that was periodically updated and reviewed for potential relevant conflicts of interests throughout the guideline development process.Table IClinical questionsWhat are the efficacy, effectiveness, effect of switching, and adverse effects of the following biologic drugs used as monotherapy or in combination with other psoriasis therapies to treat moderate-to-severe psoriasis in adults?•Etanercept (FDA approval on April 30, 2004)•Infliximab (FDA approval on September 27, 2006)•Adalimumab (FDA approval on January 22, 2008)•Certolizumab (FDA approval on May 27, 2018)•Ustekinumab (FDA approval on September 25, 2009)•Secukinumab (FDA approval on January 21, 2015)•Ixekizumab (FDA approval on March 22, 2016)•Brodalumab (FDA approval on February 15, 2017)•Guselkumab (FDA approval on July 13, 2017)•Tildrakizumab (FDA approval on March 21, 2018)•Risankizumab (FDA approval pending)FDA, US Food and Drug Administration. Open table in a new tab FDA, US Food and Drug Administration. An evidence-based model was used, and evidence was obtained by using a search of the PubMed and MEDLINE databases from January 1, 2008, to December 31, 2017, for clinical questions addressed in the previous version of this guideline published in 2008-2011, and for all newly identified clinical questions. Searches were limited to publications in the English language. Medical Subject Heading (MeSH) terms used in various combinations in the literature search included psoriasis (vulgaris, plaque, guttate, erythrodermic, pustular, palmoplantar, inverse, nail), biologic therapy (adalimumab, etanercept, infliximab, secukinumab, ustekinumab, brodalumab, tildrakizumab, guselkumab, risankizumab, tofacitinib), biosimilar, cessation, interruption, failure (primary, secondary), combination therapy, anti–TNF-α inhibitors, interleukin inhibitors, therapy switch/alternate, and superior. After removal of duplicate data, 354 articles were retained for final review based on relevancy and the highest level of available evidence for the outlined clinical questions. Evidence tables were generated for these studies and utilized by the WG in developing recommendations. The Academy's prior published guidelines on psoriasis were evaluated, as were other current published guidelines on psoriasis. The available evidence was evaluated by using a unified system called the Strength of Recommendation Taxonomy, which was developed by editors of the US family medicine and primary care journals (ie, American Family Physician, Family Medicine, Journal of Family Practice, and BMJ USA). Evidence was graded by using a 3-point scale based on the quality of methodology (eg, randomized controlled trial [RCT], case-control study, prospective or retrospective cohort study, case series) and the overall focus of the study (ie, diagnosis; treatment, prevention, and/or screening; or prognosis) as follows:I.Good-quality patient-oriented evidence (ie, evidence measuring outcomes that matter to patients: morbidity, mortality, symptom improvement, cost reduction, and quality of life [QOL]).II.Limited-quality patient-oriented evidence.III.Other evidence including consensus guidelines, opinion, case studies, or disease-oriented evidence (ie, evidence measuring intermediate, physiologic, or surrogate end points that may or may not reflect improvements in patient outcomes). Clinical recommendations were developed on the basis of best available evidence, as summarized in the tables in the guideline. These are ranked as follows:A.Recommendation based on consistent and good-quality patient-oriented evidence.B.Recommendation based on inconsistent or limited-quality patient-oriented evidence.C.Recommendation based on consensus, opinion, case studies, or disease-oriented evidence. In those situations in which documented evidence-based data are not available, we have utilized expert opinion to generate our clinical recommendations or opted not to issue a recommendation. This guideline has been developed in accordance with the American Academy of Dermatology/AAD Association Administrative Regulations for Evidence-Based Clinical Practice Guidelines (May 2014),2American Academy of Dermatology. Evidence-based clinical practice guidelines. Available at: https://www.aad.org/forms/policies/uploads/ar/ar%20evidence-based%20clinical%20practice%20%20guidelines.pdf. Accessed March 1, 2018.Google Scholar which includes the opportunity for review and comment by the entire AAD membership and final review and comment by the AAD Board of Directors. Additionally, this guideline has been developed in collaboration with the National Psoriasis Foundation, and as part of the review process, the National Psoriasis Foundation medical board members provided their feedback. This guideline will be considered current for a period of 5 years from the date of publication unless reaffirmed, updated, or retired before that time. Psoriasis vulgaris is a chronic inflammatory skin disease that classically presents with well-demarcated, red plaques with silvery scale, commonly involving the scalp, elbows, knees, and presacral region, though any area of the skin may be involved, including the palms, soles, nails, and genitalia. Although the severity of psoriasis is defined in part by the total body surface area (BSA) involved, with involvement of less than 3% of BSA considered mild, involvement of 3% to 10% of BSA considered moderate, and involvement of greater than 10% considered severe disease, psoriasis can be severe irrespective of BSA when it has serious emotional consequences or when it occurs in select locations, including but not restricted to, the hands, feet, scalp, face, or genital area, or when it causes intractable pruritus. The Psoriasis Area Severity Index (PASI) is a more specific means of quantifying the extent and severity of psoriasis, as it takes into account not only BSA but also the intensity of redness, scaling, and plaque thickness, ultimately producing a score from 0 (no disease) to 72 (maximal disease severity). The PASI is used for monitoring response to treatments in clinical trials and as a research tool to judge the severity of psoriasis. It is rarely utilized by dermatologists in clinical practice to guide management. Psoriasis is an inflammatory, immune-mediated condition involving cutaneous T cells, dendritic cells, and keratinocytes, with subsequent release of a variety of cytokines and other soluble mediators. These chemical signals are responsible for keratinocyte hyperproliferation manifesting as characteristic scaly plaques, and they also contribute to the augmented inflammation underlying a number of systemic disease associations, including metabolic syndrome, cardiovascular disease, and PsA. To inhibit the inflammation underpinning this condition, a number of topical and systemic medications have been created with varying success. The term biologic agents refers to engineered monoclonal antibodies and fusion proteins that exert their therapeutic actions by blocking specific cytokines or cytokine receptors critical to psoriatic inflammation.

Background Wide-ranging prevalence estimates of psoriatic arthritis (PsA) in patients with psoriasis have been reported. Objectives To assess the prevalence and incidence of PsA in patients with psoriasis. Methods Two authors independently searched 3 databases for studies reporting on the prevalence or incidence of PsA in patients with psoriasis. A proportion meta-analysis was performed to calculate the pooled proportion estimates of PsA in patients with psoriasis. Results A total of 266 studies examining 976,408 patients with psoriasis were included. Overall, the pooled proportion (95% confidence interval [CI]) of PsA among patients with psoriasis was 19.7% (95% CI, 18.5%-20.9%). In children and adolescents (<18 years of age), the pooled prevalence was 3.3% (95% CI, 2.1%-4.9%). The PsA prevalence was 22.7% (95% CI, 20.6%-25.0%) in European patients with psoriasis, 21.5% (95% CI, 15.4%-28.2%) in South American patients with psoriasis, 19.5% (95% CI, 17.1%-22.1%) in North American patients with psoriasis, 15.5% (95% CI, 0.009%-51.5%) in African patients with psoriasis, and 14.0% (95% CI, 95% CI, 11.7%-16.3%) in Asian patients with psoriasis. The prevalence of PsA was 23.8% (95% CI, 20.1%-27.6%) in studies in which the Classification Criteria for Psoriatic Arthritis were applied. The incidence of PsA among patients with psoriasis ranged from 0.27 to 2.7 per 100 person-years. Limitations Between-study heterogeneity may have affected the estimates. Conclusions We found that 1 in 4 patients with psoriasis have PsA. With the growing recognition of the Classification Criteria for Psoriatic Arthritis, more homogenous and comparable prevalence estimates are expected to be reported. Wide-ranging prevalence estimates of psoriatic arthritis (PsA) in patients with psoriasis have been reported. To assess the prevalence and incidence of PsA in patients with psoriasis. Two authors independently searched 3 databases for studies reporting on the prevalence or incidence of PsA in patients with psoriasis. A proportion meta-analysis was performed to calculate the pooled proportion estimates of PsA in patients with psoriasis. A total of 266 studies examining 976,408 patients with psoriasis were included. Overall, the pooled proportion (95% confidence interval [CI]) of PsA among patients with psoriasis was 19.7% (95% CI, 18.5%-20.9%). In children and adolescents (<18 years of age), the pooled prevalence was 3.3% (95% CI, 2.1%-4.9%). The PsA prevalence was 22.7% (95% CI, 20.6%-25.0%) in European patients with psoriasis, 21.5% (95% CI, 15.4%-28.2%) in South American patients with psoriasis, 19.5% (95% CI, 17.1%-22.1%) in North American patients with psoriasis, 15.5% (95% CI, 0.009%-51.5%) in African patients with psoriasis, and 14.0% (95% CI, 95% CI, 11.7%-16.3%) in Asian patients with psoriasis. The prevalence of PsA was 23.8% (95% CI, 20.1%-27.6%) in studies in which the Classification Criteria for Psoriatic Arthritis were applied. The incidence of PsA among patients with psoriasis ranged from 0.27 to 2.7 per 100 person-years. Between-study heterogeneity may have affected the estimates. We found that 1 in 4 patients with psoriasis have PsA. With the growing recognition of the Classification Criteria for Psoriatic Arthritis, more homogenous and comparable prevalence estimates are expected to be reported.

Psoriasis is a chronic, inflammatory, multisystem disease that affects up to 3.2% of the US population. This guideline addresses important clinical questions that arise in psoriasis management and care, providing recommendations on the basis of available evidence.

OBJECTIVE To assess whether patients with psoriasis treated with tumor necrosis factor (TNF) inhibitors have a decreased risk of myocardial infarction (MI) compared with those not treated with TNF inhibitors. DESIGN Retrospective cohort study. SETTING Kaiser Permanente Southern California health plan. PATIENTS Patients with at least 3 International Classification of Diseases, Ninth Revision, Clinical Modification, codes for psoriasis (696.1) or psoriatic arthritis (696.0) (without antecedent MI) between January 1, 2004, and November 30, 2010. MAIN OUTCOME MEASURE Incident MI. RESULTS Of 8845 patients included, 1673 received a TNF inhibitor for at least 2 months (TNF inhibitor cohort), 2097 were TNF inhibitor naive and received other systemic agents or phototherapy (oral/phototherapy cohort), and 5075 were not treated with TNF inhibitors, other systemic therapies, or phototherapy (topical cohort). The median duration of follow-up was 4.3 years (interquartile range, 2.9, 5.5 years), and the median duration of TNF inhibitor therapy was 685 days (interquartile range, 215, 1312 days). After adjusting for MI risk factors, the TNF inhibitor cohort had a significantly lower hazard of MI compared with the topical cohort (adjusted hazard ratio, 0.50; 95% CI, 0.32-0.79). The incidence of MI in the TNF inhibitor, oral/phototherapy, and topical cohorts were 3.05, 3.85, and 6.73 per 1000 patient-years, respectively. CONCLUSIONS Use of TNF inhibitors for psoriasis was associated with a significant reduction in MI risk and incident rate compared with treatment with topical agents. Use of TNF inhibitors for psoriasis was associated with a non-statistically significant lower MI incident rate compared with treatment with oral agents/phototherapy.

Psoriasis is a chronic inflammatory disease involving multiple organ systems and affecting approximately 2% of the world's population. In this guideline, we focus the discussion on systemic, nonbiologic medications for the treatment of this disease. We provide detailed discussion of efficacy and safety for the most commonly used medications, including methotrexate, cyclosporine, and acitretin, and provide recommendations to assist prescribers in initiating and managing patients on these treatments. Additionally, we discuss newer therapies, including tofacitinib and apremilast, and briefly touch on a number of other medications, including fumaric acid esters (used outside the United States) and therapies that are no longer widely used for the treatment of psoriasis (ie, hydroxyurea, leflunomide, mycophenolate mofetil, thioguanine, and tacrolimus). Psoriasis is a chronic inflammatory disease involving multiple organ systems and affecting approximately 2% of the world's population. In this guideline, we focus the discussion on systemic, nonbiologic medications for the treatment of this disease. We provide detailed discussion of efficacy and safety for the most commonly used medications, including methotrexate, cyclosporine, and acitretin, and provide recommendations to assist prescribers in initiating and managing patients on these treatments. Additionally, we discuss newer therapies, including tofacitinib and apremilast, and briefly touch on a number of other medications, including fumaric acid esters (used outside the United States) and therapies that are no longer widely used for the treatment of psoriasis (ie, hydroxyurea, leflunomide, mycophenolate mofetil, thioguanine, and tacrolimus). The American Academy of Dermatology (AAD) strives to produce clinical guidelines that reflect the best available evidence supplemented with the judgment of expert clinicians. Significant efforts are taken to minimize the potential for conflicts of interest to influence guideline content. The management of conflict of interest for this guideline complies with the Council of Medical Specialty Societies’ “Code of Interactions with Companies.” Funding of guideline production by medical or pharmaceutical entities is prohibited, full disclosure is obtained and evaluated for all guideline contributors throughout the guideline development process, and recusal is used to manage identified relationships. The AAD conflict of interest policy summary may be viewed at www.aad.org. The information below represents the author's disclosed relationship with industry during guideline development. Authors (listed alphabetically) with relevant conflicts with respect to this guideline are noted with an asterisk (∗). In accordance with AAD policy, a minimum 51% of workgroup members did not have any relevant conflicts of interest. Participation in one or more of the below-listed activities constitutes a relevant conflict:•Service as a member of a speaker bureau, consultant, advisory board, for pharmaceutical companies on psoriasis disease state or psoriasis drugs in development or United States Food and Drug Administration (FDA) approved•Sponsored research funding or investigator-initiated studies with partial/full funding from pharmaceutical companies on psoriasis disease state or psoriasis drugs in development or FDA approved If a potential conflict was noted, the work group member recused themselves from discussion and drafting of recommendations pertinent to the topic area of interest. Complete group consensus was obtained for draft recommendations. Areas where complete consensus was not achieved are shown transparently in the guideline. Adherence to this guideline will not ensure successful treatment in every situation. Furthermore, these guidelines should not be interpreted as setting a standard of care, nor should they be deemed either inclusive of all proper methods of care, or exclusive of other methods of care reasonably directed toward obtaining the same results. The ultimate judgment regarding the propriety of any specific therapy must be made by the physician and the patient in light of circumstances presented by the individual patient and the known variability and biologic behavior of the disease. Furthermore, the treatment dosages used in clinical trials may not be effective in certain cases, and some patients may require shorter intervals between doses and/or higher treatment doses of a particular treatment methodology. This guideline reflects the best available data at the time the guideline was prepared. The results of future studies may require revisions to the recommendations in this guideline to reflect new data. This guideline will cover the use of oral-systemic, nonbiologic medication in the treatment of psoriasis. For a full description of the methodology used herein, please refer to Appendix 1. See section below for full definition statement (Table I).Table IClinical questionsWhat are the efficacy, effectiveness, adverse effects, contraindications, and recommended monitoring for oral systemic therapies used to treat psoriasis in adults?1.Methotrexate—FDA approval 19722.Apremilast—FDA approval 20143.Cyclosporine—FDA approval 19974.Acitretin—FDA approval 19975.Tofacitinib—Not FDA approved for psoriasis6.Fumaric acid esters—Not FDA approved for psoriasis7.Hydroxyurea—Not FDA approved for psoriasis8.Mycophenolate mofetil—Not FDA approved for psoriasis9.Azathioprine— Not FDA approved for psoriasis10.Leflunomide—Not FDA approved for psoriasis11.Tacrolimus—Not FDA approved for psoriasis12.Thioguanine—Not FDA approved for psoriasisFDA, Food and Drug Administration. Open table in a new tab FDA, Food and Drug Administration.

Psoriasis can be a socially isolating disease due to debilitating physical symptoms and the stigma patients feel because of the appearance of their skin. Mental health comorbidities such as anxiety, depression and suicidal ideation and behaviour (SIB) are prevalent in patients with psoriasis. Patients with mild psoriasis can experience psychiatric comorbidities; however, disorders such as depression and SIB are more common in patients with severe psoriasis or psoriatic arthritis. Psychiatric disorders can both result from and contribute to progression of psoriasis, suggesting that psoriasis and psychiatric conditions, such as depression, may have overlapping biological mechanisms. Proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are elevated in both psoriasis and depression, indicating that the inflammatory process may be involved in the progression of both diseases. Elevated cytokine levels in the central nervous system cause physiologic and biochemical changes that may contribute to the development of depression. In this review of the literature, we discuss the evidence that supports the association of psoriasis with mental health disorders and the tools used to detect the presence of these comorbidities. Additionally, we review the most prominent hypotheses on the mechanisms by which the inflammatory response and elevated cytokines can cause depression. These results highlight the role that systemic inflammation plays in the various mental health comorbidities associated with psoriasis, including depression and SIB.

Psoriasis is a chronic, inflammatory, multisystem disease that affects up to 3.2% of the United States population. This guideline addresses important clinical questions that arise in psoriasis management and care and provides recommendations based on the available evidence. The treatment of psoriasis with topical agents and with alternative medicine will be reviewed, emphasizing treatment recommendations and the role of dermatologists in monitoring and educating patients regarding benefits as well as risks that may be associated. This guideline will also address the severity assessment methods of psoriasis in adults. Psoriasis is a chronic, inflammatory, multisystem disease that affects up to 3.2% of the United States population. This guideline addresses important clinical questions that arise in psoriasis management and care and provides recommendations based on the available evidence. The treatment of psoriasis with topical agents and with alternative medicine will be reviewed, emphasizing treatment recommendations and the role of dermatologists in monitoring and educating patients regarding benefits as well as risks that may be associated. This guideline will also address the severity assessment methods of psoriasis in adults. DisclaimerAdherence to these guidelines will not ensure successful treatment in every situation. Furthermore, these guidelines should not be interpreted as setting a standard of care, nor should they be deemed either inclusive of all proper methods of care, or exclusive of other methods of care reasonably directed toward obtaining the same results. The ultimate judgment regarding the propriety of any specific therapy must be made by the physician and the patient in light of circumstances presented by the individual patient and the known variability and biological behavior of the disease. Furthermore, the treatment dosages used in clinical trials may not be effective in certain cases, and some patients may require shorter intervals between doses and/or higher treatment doses of a particular treatment methodology. This guideline reflects the best available data at the time the guideline was prepared. The results of future studies may require revisions to the recommendations in this guideline to reflect new data.Conflict of interest statementThe American Academy of Dermatology (AAD) strives to produce clinical guidelines that reflect the best available evidence supplemented with the judgment of expert clinicians. Significant efforts are taken to minimize the potential for conflicts of interest to influence guideline content. The management of conflict of interest for this guideline complies with the Council of Medical Specialty Societies Code of Interactions with Companies. Funding of guideline production by medical or pharmaceutical entities is prohibited, full disclosure is obtained and evaluated for all guideline contributors throughout the guideline development process, and recusal is used to manage identified relationships. The AAD conflict of interest policy summary may be viewed at www.aad.org.The information below represents the authors who disclosed a relationship with industry during guideline development. Authors (listed alphabetically) with relevant conflicts with respect to this guideline are noted with an asterisk (∗). In accordance with the AAD policy, fewer than 51% of workgroup members had any relevant conflicts of interest.Participation in one or more of the below-listed activities constitutes a relevant conflict:•service as a member of a speaker bureau, consultant, advisory board, for pharmaceutical companies on the psoriasis disease state or psoriasis drugs in development or United States (US) Food and Drug Administration (FDA) approved;•sponsored research funding or investigator-initiated studies with partial/full funding from pharmaceutical companies on the psoriasis disease state or psoriasis drugs in development or FDA approved.Draft guideline recommendations were developed through a collaborative approach between conflicted and nonconflicted section leaders. Initial recommendations were presented to the full workgroup for finalization.ScopeThis guideline will cover the use of topical agents and alternative medicine (AM) in the treatment of psoriasis in adults as well as the assessment of disease severity; psoriasis in the pediatric population will be covered in a separate guideline section, “Joint American Academy of Dermatology-National Psoriasis Foundation (NPF) guidelines of care for the management and treatment of psoriasis in pediatric patients.”1Menter A. Cordoro K.M. Davis D.M.R. et al.Joint American Academy of Dermatology-National Psoriasis Foundation guidelines of care for the management and treatment of psoriasis in pediatric patients [published correction appears in J Am Acad Dermatol. 2020;82(3):574].J Am Acad Dermatol. 2020; 82: 161-201Abstract Full Text Full Text PDF PubMed Scopus (0) Google ScholarMethodFor a full description of the methodology used herein, please refer to the Appendix section.Definition of reviewSee the Appendix for full definition statement.IntroductionPsoriasis is a common inflammatory disease, affecting approximately 3.2% of the population.2Rachakonda T.D. Schupp C.W. Armstrong A.W. Psoriasis prevalence among adults in the United States.J Am Acad Dermatol. 2014; 70: 512-516Abstract Full Text Full Text PDF PubMed Scopus (415) Google Scholar While skin involvement is the most prominent manifestation of this disease, recognition of psoriasis as a chronic, multisystem inflammatory disorder is imperative to optimize management and reduce comorbidities.Topical medications are the most common agents used to treat patients with mild to moderate psoriasis. They are frequently used as adjunctive therapies for patients on phototherapy, systemic, or biologic therapy. Alternative medicine (AM) is not typically part of conventional medical care. It may have origins outside of usual Western practice and may be desired by and benefit a subset of patients.3National Center for Complementary and Integrative HealthComplementary, Alternative, or Integrative Health: What's In a Name? NCCIH Clearinghouse.https://nccih.nih.gov/health/integrative-healthDate: 2019Date accessed: October 1, 2019Google Scholar,4van de Kerkhof P.C. Cambazard F. Hutchinson P.E. et al.The effect of addition of calcipotriol ointment (50 micrograms/g) to acitretin therapy in psoriasis.Br J Dermatol. 1998; 138: 84-89Crossref PubMed Scopus (0) Google ScholarThis section will review the assessment of psoriasis severity and the management and treatment of psoriasis with topical therapy and AM modalities in adult psoriasis patients (Table I).Table IClinical questions1.What are the efficacy, effectiveness, and adverse events of the following therapies used as monotherapy and/or combination therapy to treat psoriasis in adults?a.Topical corticosteroidsb.Calcineurin inhibitors (Topical tacrolimus and pimecrolimus)c.Vitamin D analoguesd.Tazarotenee.Moisturizersf.Salicylic acidg.Anthralinh.Coal tari.Biologic agent combinationj.Nonbiologic combinationi.Methotrexateii.Cyclosporineiii.Acitretin2.What are the efficacy, effectiveness, and adverse events of the following alternative medicines used for adult psoriasis?a.Traditional Chinese medicineb.Herbal therapiesi.Aloe veraii.St John's wortc.Diet/dietary supplementsi.Fish oilii.Vitamin Diii.Curcumin (Turmeric)iv.Zincv.Gluten-free dietd.Mind/bodyi.Hypnosisii.Stress reduction/meditation3.What is the accuracy, clinical utility, and treatment parameters for using the following severity measures to measure psoriasis severity and response to treatment?a.Body surface area (BSA)b.Psoriasis Area and Severity Index (PASI)c.Physician Global Assessment (PGA)d.PGA × BSAe.Psoriasis Symptom Inventory (PSI)f.Dermatology of Life Quality Index (DLQI)g.Pruritus assessment Open table in a new tab I. Topical agentsTopical corticosteroidsEfficacyTopical corticosteroids, which provide high efficacy and good safety, play a key role in the treatment of psoriasis, especially for localized disease. Topical corticosteroids have anti-inflammatory, antiproliferative, immunosuppressive, and vasoconstrictive effects. These effects are exerted via intracellular corticosteroid receptors, which regulate gene transcription, including several that code for proinflammatory mediators. Topical corticosteroids are classified into 7 categories based on their skin vasoconstrictive activity, ranging in strength from ultra-high (class 1) to low (class 6 and 7; Table II).5Cornell R.C. Stoughton R.B. Correlation of the vasoconstriction assay and clinical activity in psoriasis.Arch Dermatol. 1985; 121: 63-67Crossref PubMed Scopus (157) Google Scholar, 6Bolognia J. Schaffer J.V. Cerroni L. Dermatology.4th ed. Elsevier, Philadelphia2018Google Scholar, 7Gabros S. Zito P.M. Topical corticosteroids.StatPearls. Treasure Island (FL), 2019Google Scholar, 8Jacob S.E. Steele T. Corticosteroid classes: a quick reference guide including patch test substances and cross-reactivity.J Am Acad Dermatol. 2006; 54: 723-727Abstract Full Text Full Text PDF PubMed Scopus (61) Google ScholarTable IIClassification of topical corticosteroid6Bolognia J. Schaffer J.V. Cerroni L. Dermatology.4th ed. Elsevier, Philadelphia2018Google Scholar, 7Gabros S. Zito P.M. Topical corticosteroids.StatPearls. Treasure Island (FL), 2019Google Scholar, 8Jacob S.E. Steele T. Corticosteroid classes: a quick reference guide including patch test substances and cross-reactivity.J Am Acad Dermatol. 2006; 54: 723-727Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar∗Reprinted from Dermatology: 2-Volume Set, 4th Edition, Jean Bolognia, Julie Schafer, and Lorenzo Cerroni, Glucocorticosteroids, Page No. 2190, Copyright 2018, with permission from Elsevier.WHO potency groupClassificationTopical corticosteroidSuper-potentUltrahighClass 11.Augmented betamethasone dipropionate 0.05%aOintment.,bGel.2.Clobetasol propionate 0.05%aOintment.,bGel.,cCream.,dLotion.,eFoam.,fSolution.,gScalp solution application, in some classifications class 2.,hSpray.,iShampoo 0.05%.3.Desoximetasone 0.25%hSpray.4.Augmented diflorasone diacetate 0.05%aOintment.5.Fluocinonide 0.1%cCream.6.Flurandrenolide 4 μg/cm2jTape.7.Halobetasol propionate 0.05%aOintment.,cCream.HighClass 21.Amcinonide 0.1%aOintment.2.Betamethasone dipropionate 0.05%aOintment.3.Augmented betamethasone dipropionate 0.05%cCream.,dLotion.4.Desoximetasone 0.25%aOintment.,cCream.5.Desoximetasone 0.05%bGel.6.Augmented diflorasone diacetate 0.05%cCream.7.Diflorasone diacetate 0.05%aOintment.8.Fluocinonide 0.05%aOintment.,bGel.,cCream.,fSolution.9.Halcinonide 0.1%aOintment.,cCream.10.Mometasone furoate 0.1%aOintment.11.Triamcinolone acetonide 0.5%aOintment.Class 31.Amcinonide 0.1%cCream.,dLotion.2.Betamethasone dipropionate 0.05%cCream.,kLotion, depending upon classification, class 3 or 5.3.Betamethasone valerate 0.1%aOintment.4.Betamethasone valerate 0.12%lFoam, depending upon classification, class 3 or 4.5.Diflorasone diacetate 0.05%cCream.6.Fluticasone propionate 0.005%aOintment.7.Triamcinolone acetonide 0.1%aOintment.8.Triamcinolone acetonide 0.5%cCream.Moderate (medium)Class 41.Betamethasone valerate 0.12%lFoam, depending upon classification, class 3 or 4.2.Desoximetasone 0.05%cCream.3.Fluocinolone acetonide 0.025%aOintment.4.Flurandrenolide 0.05%aOintment.5.Hydrocortisone valerate 0.2%aOintment.6.Mometasone furoate 0.1%cCream.,dLotion.7.Triamcinolone acetonide 0.1%cCream.,mKenalog ointment (manufactured by APOTHECON, a Bristol-Myers Squibb Company; Princeton, NJ).8.Triamcinolone acetonide 0.2%hSpray.Class 51.Betamethasone dipropionate 0.05%kLotion, depending upon classification, class 3 or 5.2.Betamethasone valerate 0.1%cCream.,dLotion.3.Clocortolone pivalate 0.1%cCream.4.Fluocinolone acetonide 0.025%cCream.5.Fluocinolone acetonide 0.01%nOil.,oShampoo.6.Fluticasone propionate 0.05%cCream.,dLotion.7.Flurandrenolide 0.05%cCream.,dLotion.8.Hydrocortisone butyrate 0.1%aOintment.,cCream.,dLotion.,fSolution.9.Hydrocortisone probutate 0.1%cCream.10.Hydrocortisone valerate 0.2%cCream.11.Prednicarbate 0.1%aOintment.,cCream.12.Triamcinolone acetonide 0.025%aOintment.13.Triamcinolone acetonide 0.01%dLotion.LowClass 61.Alclometasone dipropionate 0.05%aOintment.,cCream.2.Betamethasone valerate 0.05%dLotion.3.Desonide 0.05%aOintment.,bGel.,cCream.,dLotion.,eFoam.4.Fluocinolone acetonide 0.01%cCream.,fSolution.5.Triamcinolone acetonide 0.025%cCream.,dLotion.Class 71.Dexamethasone sodium phosphate 0.1%cCream.2.Hydrocortisone 0.5%-2.5%aOintment.,bGel.,cCream.,dLotion.,fSolution.3.Methylprednisolone acetate 0.25%cCream.WHO, World Health Organization.∗ Reprinted from Dermatology: 2-Volume Set, 4th Edition, Jean Bolognia, Julie Schafer, and Lorenzo Cerroni, Glucocorticosteroids, Page No. 2190, Copyright 2018, with permission from Elsevier.a Ointment.b Gel.c Cream.d Lotion.e Foam.f Solution.g Scalp solution application, in some classifications class 2.h Spray.i Shampoo 0.05%.j Tape.k Lotion, depending upon classification, class 3 or 5.l Foam, depending upon classification, class 3 or 4.m Kenalog ointment (manufactured by APOTHECON, a Bristol-Myers Squibb Company; Princeton, NJ).n Oil.o Shampoo. Open table in a new tab Choosing a corticosteroid with appropriate potency plus the appropriate vehicle should be based on the disease severity, disease location, patient preference, and the age of the patient. Lower potency corticosteroids should be used on the face, intertriginous areas, and areas that are susceptible to steroid atrophy (eg, forearms) and other adverse effects. In adults, corticosteroids in classes 2 through 5 (moderate to high potency; Table II) are generally recommended as initial therapy. Areas with thick, chronic plaques often require treatment with class 1 (ultrahigh-potency) corticosteroids. In numerous randomized controlled trials (RCTs), different potency topical corticosteroids were effective and safe at 2 to 4 weeks in the treatment of mild to severe plaque psoriasis.9Bernhard J. Whitmore C. Guzzo C. et al.Evaluation of halobetasol propionate ointment in the treatment of plaque psoriasis: report on two double-blind, vehicle-controlled studies.J Am Acad Dermatol. 1991; 25: 1170-1174Abstract Full Text PDF PubMed Scopus (30) Google Scholar, 10Gottlieb A.B. Ford R.O. Spellman M.C. The efficacy and tolerability of clobetasol propionate foam 0.05% in the treatment of mild to moderate plaque-type psoriasis of nonscalp regions.J Cutan Med Surg. 2003; 7: 185-192Crossref PubMed Google Scholar, 11Lebwohl M. Sherer D. Washenik K. et al.A randomized, double-blind, placebo-controlled study of clobetasol propionate 0.05% foam in the treatment of nonscalp psoriasis.Int J Dermatol. 2002; 41: 269-274Crossref PubMed Scopus (48) Google Scholar Evidence on the efficacy of topical corticosteroids from RCTs varies due to the differences in study designs, patient populations, and end points, making it difficult to do an accurate statistical comparison of the majority of published studies.For ultrahigh-potency (class 1) corticosteroids, the efficacy rates in several RCTs vary from 58% to 92%.9Bernhard J. Whitmore C. Guzzo C. et al.Evaluation of halobetasol propionate ointment in the treatment of plaque psoriasis: report on two double-blind, vehicle-controlled studies.J Am Acad Dermatol. 1991; 25: 1170-1174Abstract Full Text PDF PubMed Scopus (30) Google Scholar,10Gottlieb A.B. Ford R.O. Spellman M.C. The efficacy and tolerability of clobetasol propionate foam 0.05% in the treatment of mild to moderate plaque-type psoriasis of nonscalp regions.J Cutan Med Surg. 2003; 7: 185-192Crossref PubMed Google Scholar,12Camarasa J.M. Ortonne J.P. Dubertret L. Calcitriol shows greater persistence of treatment effect than betamethasone dipropionate in topical psoriasis therapy.J Dermatolog Treat. 2003; 14: 8-13Crossref PubMed Scopus (41) Google Scholar,13Keegan B.R. Desoximetasone 0.25% spray for the relief of scaling in adults with plaque psoriasis.J Drugs Dermatol. 2015; 14: 835-840PubMed Google Scholar In a double-blind, vehicle-controlled trial of 204 patients with moderate to severe psoriasis, after 2 weeks of treatment, the halobetasol propionate ointment (class 1) group improved the Physician's Global Assessment (PGA) scores by 92% compared with 39% in vehicle-treated patients (P < .0003).9Bernhard J. Whitmore C. Guzzo C. et al.Evaluation of halobetasol propionate ointment in the treatment of plaque psoriasis: report on two double-blind, vehicle-controlled studies.J Am Acad Dermatol. 1991; 25: 1170-1174Abstract Full Text PDF PubMed Scopus (30) Google Scholar An RCT of 279 patients with mild to moderate psoriasis found that after 2 weeks of treatment with clobetasol foam (class 1), 68% of patients achieved a Physician's Static Global Assessment (PSGA) score of 0 or 1 compared with 21% of patients treated with vehicle (P < .0001).10Gottlieb A.B. Ford R.O. Spellman M.C. The efficacy and tolerability of clobetasol propionate foam 0.05% in the treatment of mild to moderate plaque-type psoriasis of nonscalp regions.J Cutan Med Surg. 2003; 7: 185-192Crossref PubMed Google Scholar Another double-blind RCT of 81 patients used the Investigator Global Assessment scale to assess patients with mild to moderate psoriasis and demonstrated that after 2 weeks of treatment with clobetasol foam (class 1), 58% of patients achieved moderate or marked improvement, or almost or completely clear psoriasis compared with 15% in vehicle-treated patients (P < .0005).11Lebwohl M. Sherer D. Washenik K. et al.A randomized, double-blind, placebo-controlled study of clobetasol propionate 0.05% foam in the treatment of nonscalp psoriasis.Int J Dermatol. 2002; 41: 269-274Crossref PubMed Scopus (48) Google ScholarFor high-potency (class 2 and 3) corticosteroids, the efficacy rates in several RCTs vary from 68% to 74%. In a double blind-RCT of 35 patients with psoriasis treated with 0.25% desoximetasone cream (class 2) for 3 weeks, 68% of the desoximetasone group compared with 23% of the vehicle group achieved improvement in their mean overall evaluation scores (P < .001).14Savin R.C. Desoximetasone—a new topical corticosteroid: short-and long-term experiences.Cutis. 1978; 21: 403-407PubMed Google Scholar Two RCTs with fluticasone propionate 0.005%, a class 3 corticosteroid, showed 68% to 69% of patients with moderate to severe psoriasis in the treatment group achieved, good, excellent, or clear skin after 4 weeks compared with 29% to 30% in the vehicle group (P = .00001).15Olsen E.A. Efficacy and safety of fluticasone propionate 0.005% ointment in the treatment of psoriasis.Cutis. 1996; 57: 57-61PubMed Google ScholarFor moderate-potency (class 4 and 5) corticosteroids, the efficacy rates in several RCTs vary from 70% to 83%.16Pauporte M. Maibach H. Lowe N. et al.Fluocinolone acetonide topical oil for scalp psoriasis.J Dermatolog Treat. 2004; 15: 360-364Crossref PubMed Scopus (33) Google Scholar,17Stein L.F. Sherr A. Solodkina G. Gottlieb A.B. Chaudhari U. Betamethasone valerate foam for treatment of nonscalp psoriasis.J Cutan Med Surg. 2001; 5: 303-307Crossref PubMed Google Scholar An RCT of 40 patients with nonscalp psoriasis revealed that 70% of patients treated with betamethasone valerate foam 0.12% (class 4) achieved greater than 50% improvement compared with 24% of patients in the placebo group after 12 weeks of treatment (P < .001).17Stein L.F. Sherr A. Solodkina G. Gottlieb A.B. Chaudhari U. Betamethasone valerate foam for treatment of nonscalp psoriasis.J Cutan Med Surg. 2001; 5: 303-307Crossref PubMed Google Scholar In an RCT of patients with moderate to severe scalp psoriasis, the group treated with fluocinolone acetonide 0.01% oil (class 5 corticosteroid) had a higher proportion of patients achieving good or better improvement from baseline compared with the vehicle-treated group after 3 weeks of treatment (83% vs 36%; P < .001).16Pauporte M. Maibach H. Lowe N. et al.Fluocinolone acetonide topical oil for scalp psoriasis.J Dermatolog Treat. 2004; 15: 360-364Crossref PubMed Scopus (33) Google Scholar Additionally, an RCT showed that fluticasone propionate 0.05% cream (class 5) was superior to hydrocortisone butyrate 0.1% cream (class 7) in achieving clearance, excellent, or good treatment response after 3 weeks of treatment (79% vs 68%; P < .05).18James M. A randomized, double-blind, multicenter trial comparing fluticasone propionate cream, 0.05%, and hydrocortisone-17-butyrate cream, 0.1%, applied twice daily for 4 weeks in the treatment of psoriasis.Cutis. 2001; 67: 2-9PubMed Google ScholarOwing to the inconsistent criteria in RCT design, comparisons between different corticosteroids and classes are complex. Nevertheless, a systematic review of topical corticosteroids for the treatment of psoriasis revealed that potent and super-potent topical corticosteroids were more efficacious than mild or moderately potent corticosteroids.19Mason J. Mason A.R. Cork M.J. Topical preparations for the treatment of psoriasis: a systematic review.Br J Dermatol. 2002; 146: 351-364Crossref PubMed Scopus (141) Google ScholarTreatment of psoriasis in intertriginous areas, such as the groin, or hair-bearing skin, such as the scalp, can be challenging due to the difficulty of applying a topical product to these areas based on the vehicle selection. Therefore, appropriate selection of the vehicle depending on hair density and individual hairstyles and preferences is essential for the efficacy of the treatment. Several RCTs and systematic reviews of scalp psoriasis treatment demonstrate the safety and efficacy of various potency topical corticosteroids used for 3 to 12 weeks.16Pauporte M. Maibach H. Lowe N. et al.Fluocinolone acetonide topical oil for scalp psoriasis.J Dermatolog Treat. 2004; 15: 360-364Crossref PubMed Scopus (33) Google Scholar,17Stein L.F. Sherr A. Solodkina G. Gottlieb A.B. Chaudhari U. Betamethasone valerate foam for treatment of nonscalp psoriasis.J Cutan Med Surg. 2001; 5: 303-307Crossref PubMed Google Scholar,20Mason A.R. Mason J.M. Cork M.J. Hancock H. Dooley G. Topical treatments for chronic plaque psoriasis of the scalp: a systematic review.Br J Dermatol. 2013; 169: 519-527Crossref PubMed Scopus (22) Google Scholar The duration of the therapy depends on factors such as the strength of topical corticosteroids, the severity of the disease, anatomic location, and age of the patient. Similarly, a steroid-sparing agent can be considered to avoid adverse effects.Additionally, intralesional corticosteroids can be used for localized nonresponding or very thick lesions on glabrous skin, scalp, nails, palms, and soles. Several studies and reports have shown that intralesional corticosteroids can be effective for the treatment of psoriasis.21Richards R.N. Update on intralesional steroid: focus on dermatoses.J Cutan Med Surg. 2010; 14: 19-23Crossref PubMed Scopus (20) Google Scholar, 22Chan C.S. Van Voorhees A.S. Lebwohl M.G. et al.Treatment of severe scalp psoriasis: from the Medical Board of the National Psoriasis Foundation.J Am Acad Dermatol. 2009; 60: 962-971Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar, 23Handa S. Newer trends in the management of psoriasis at difficult to treat locations: scalp, palmoplantar disease and nails.Indian J Dermatol Venereol Leprol. 2010; 76: 634-644Crossref PubMed Scopus (16) Google Scholar Triamcinolone acetonide in a dose up to 20 mg/mL can be used every 3 to 4 weeks.24Kenalog®-10 Injection (triamcinolone acetonide injectable suspension, USP) [package insert]. Bristol-Myers Squibb Company, Princeton, NJ2018https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/012041s045lbl.pdfDate accessed: April 23, 2020Google Scholar The injection volume varies pending lesional size and the area affected.Risks/harms and benefitsThe most common local skin adverse effects of topical corticosteroid use include skin atrophy, striae, folliculitis, telangiectasia, and purpura.25Abraham A. Roga G. Topical steroid-damaged skin.Indian J Dermatol. 2014; 59: 456-459Crossref PubMed Scopus (31) Google Scholar Face and intertriginous areas, as well as chronically treated areas, especially forearms, are at greatest risk to develop these adverse effects. Topical corticosteroids may exacerbate acne, rosacea, perioral dermatitis, and tinea infections and may occasionally cause contact dermatitis. Rebound (ie, when the disease recurs and is more severe than before treatment) can occur from abrupt withdrawal of topical corticosteroids, although the frequency and severity of this phenomenon are unknown. The daily use of ultrahigh- and high-potency (class 1-3) corticosteroids for up to 4 weeks is generally safe with minimal risk of skin atrophy.26Castela E. Archier E. Devaux S. et al.Topical corticosteroids in plaque psoriasis: a systematic review of risk of adrenal axis suppression and skin atrophy.J Eur Acad Dermatol Venereol. 2012; 26: 47-51Crossref PubMed Scopus (0) Google ScholarRisk of hypothalamic pituitary adrenal axis suppression from the use of topical corticosteroids for extensive plaque or scalp psoriasis has been reported to be low.26Castela E. Archier E. Devaux S. et al.Topical corticosteroids in plaque psoriasis: a systematic review of risk of adrenal axis suppression and skin atrophy.J Eur Acad Dermatol Venereol. 2012; 26: 47-51Crossref PubMed Scopus (0) Google Scholar In a systematic review of 13 randomized studies, studies performed for up to 4 weeks found the percentage of patients with a reduction in the morning cortisol level was 0% with halobetasol or fluocinonide, 0% to 48% with clobetasol propionate, and 0% to 18% with betamethasone dipropionate. Nevertheless, results of adrenocorticotropic hormone stimulation tests, the gold standard for assessing hypothalamic-pituitary-adrenal axis suppression, were always within normal reference ranges, even when assessed after 6 to 12 months of topical corticosteroid use.26Castela E. Archier E. Devaux S. et al.Topical corticosteroids in plaque psoriasis: a systematic review of risk of adrenal axis suppression and skin atrophy.J Eur Acad Dermatol Venereol. 2012; 26: 47-51Crossref PubMed Scopus (0) Google Scholar Rare systemic adverse effects include Cushing syndrome and osteonecrosis of the femoral head.27Takahashi H. Tsuji H. Honma M. Ishida-Yamamoto A. Iizuka H. Femoral head osteonecrosis after long-term topical corticosteroid treatment in a psoriasis patient.J Dermatol. 2012; 39: 887-888Crossref PubMed Scopus (0) Google Scholar,28el Maghraoui A. Tabache F. Bezza A. Ghafir D. Ohayon V. Archane M.I. Femoral head osteonecrosis after topical corticosteroid therapy.Clin Exp Rheumatol. 2001; 19: 233PubMed Google Scholar Topical products that contain corticosteroid should not be used for more than 12 weeks for nail disease, because there are isolated reports of bone atrophy with persistent use.29Malec-Milewska M. Sekowska A. Koleda I. Horosz B. Guc M. Jastrzebski J. Sympathetic nerve blocks for the management of postherpetic neuralgia-19 years of pain clinic experience.Anaesthesiol Intensive Ther. 2014; 46: 255-261Crossref PubMed Scopus (3) Google Scholar,30Rigopoulos D. Gregoriou S. Daniel Iii, C.R. et al.Treatment of nail psoriasis with a two-compound formulation of calcipotriol plus betamethasone dipropionate ointment.Dermatology. 2009; 218: 338-341Crossref PubMed Scopus (36) Google Scholar Increased intraocular pressure, glaucoma, and cataracts have been rarely reported with the use of topical corticosteroids around the eye.31Garrott H.M. Walland M.J. Glaucoma from topical corticosteroids to the eyelids.Clin Exp Ophthalmol. 2004; 32: 224-226Crossref PubMed Scopus (38) Google Scholar,32Day A. Abramson A.K. Patel M. Warren R.B. Menter M.A. The spectrum of oculocutaneous disease: part II. Neoplastic and drug-related causes of oculocutaneous disease.J Am Acad Dermatol. 2014; 70: 821.e-821.e19Abstract Full Text Full Text PDF Scopus (3) Google Scholar In rare cases, type 2 diabetes has been reported with topical corticosteroid use.33Andersen Y.M.F. Egeberg A. Ban L. et al.Association between topical corticosteroid use and type 2 diabetes in two European population-based adult cohorts.Diabetes Care. 2019; 42: 1095-1103Crossref PubMed Scopus (11) Google ScholarDespite the safety data,26Castela E. Archier E. Devaux S. et al.Topical corticosteroids in plaque psoriasis: a systematic review of risk of adrenal axis suppression and skin atrophy.J Eur Acad Dermatol Venereol. 2012; 26: 47-51Crossref PubMed Scopus (0) Google Scholar caution is advised, because the greatest risk for systemic adverse effects occurs when ultrahigh- or high-potency corticosteroids are used over a large surface (>20% body surface area [BSA]) or under occlusion for a prolonged period (>4 weeks) . Clinicians should consider limiting the use of class 1 corticosteroids to no more than twice daily for up to 4 weeks, when possible.34Clobex® [package insert]. Galderma Laboratories, L.P., Fort Worth, TX2012https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021535Orig1s003,%20021644Orig1s003lbl.pdfDate accessed: October 17, 2019Google Scholar In the event of a flare, repeated courses of a class 1 corticosteroid can be administered. Longer durations of class 1 corticosteroid therapy for psoriasis of the palms and soles are acceptable with close attention to the development of potential adverse effects. Gradual reduction in the frequency of use after clinical improvement is recommended, but the exact details of this tapering are not well established. Topical corticosteroids can be tapered off by reducing use to every other day, then eventually 2 times a week, and finally discontinuation if psoriasis is well controlled and stable during the whole process. T

Psoriasis is a chronic, multisystem, inflammatory disease that affects approximately 1% of children, with onset most common during adolescence. This guideline addresses important clinical questions that arise in psoriasis management and provides evidence-based recommendations. Attention will be given to pediatric patients with psoriasis, recognizing the unique physiology, pharmacokinetics, and patient-parent-provider interactions of patients younger than 18 years old. The topics reviewed here mirror those discussed in the adult guideline sections, excluding those topics that are irrelevant to, or lack sufficient information for, pediatric patients.

Background Individuals with psoriasis are at increased risk for psychiatric comorbidities, including suicidal ideation and behavior (SIB). Objective To distinguish between the underlying risk and potential for treatment-induced psychiatric adverse events in patients with psoriasis being treated with brodalumab, a fully human anti–interleukin 17 receptor A monoclonal antibody. Methods Data were evaluated from a placebo-controlled, phase 2 clinical trial; the open-label, long-term extension of the phase 2 clinical trial; and three phase 3, randomized, double-blind, controlled clinical trials (AMAGINE-1, AMAGINE-2, and AMAGINE-3) and their open-label, long-term extensions of patients with moderate-to-severe psoriasis. Results The analysis included 4464 patients with 9161.8 patient-years of brodalumab exposure. The follow-up time–adjusted incidence rates of SIB events were comparable between the brodalumab and ustekinumab groups throughout the 52-week controlled phases (0.20 vs 0.60 per 100 patient-years). In the brodalumab group, 4 completed suicides were reported, 1 of which was later adjudicated as indeterminate; all patients had underlying psychiatric disorders or stressors. Limitations There was no comparator arm past week 52. Controlled study periods were not powered to detect differences in rare events such as suicide. Conclusions Comparison with controls and the timing of events do not indicate a causal relationship between SIB and brodalumab treatment. Individuals with psoriasis are at increased risk for psychiatric comorbidities, including suicidal ideation and behavior (SIB). To distinguish between the underlying risk and potential for treatment-induced psychiatric adverse events in patients with psoriasis being treated with brodalumab, a fully human anti–interleukin 17 receptor A monoclonal antibody. Data were evaluated from a placebo-controlled, phase 2 clinical trial; the open-label, long-term extension of the phase 2 clinical trial; and three phase 3, randomized, double-blind, controlled clinical trials (AMAGINE-1, AMAGINE-2, and AMAGINE-3) and their open-label, long-term extensions of patients with moderate-to-severe psoriasis. The analysis included 4464 patients with 9161.8 patient-years of brodalumab exposure. The follow-up time–adjusted incidence rates of SIB events were comparable between the brodalumab and ustekinumab groups throughout the 52-week controlled phases (0.20 vs 0.60 per 100 patient-years). In the brodalumab group, 4 completed suicides were reported, 1 of which was later adjudicated as indeterminate; all patients had underlying psychiatric disorders or stressors. There was no comparator arm past week 52. Controlled study periods were not powered to detect differences in rare events such as suicide. Comparison with controls and the timing of events do not indicate a causal relationship between SIB and brodalumab treatment.

<h3>Importance</h3> Risankizumab selectively inhibits interleukin 23, a cytokine that contributes to psoriatic inflammation. <h3>Objective</h3> To evaluate the efficacy and safety of risankizumab vs placebo and continuous treatment vs withdrawal in adults with moderate to severe plaque psoriasis. <h3>Design, Setting, and Participants</h3> Multinational, phase 3, randomized, double-blind, placebo-controlled trial conducted from March 6, 2016, to July 26, 2018. A total of 507 eligible patients had stable moderate to severe chronic plaque psoriasis for 6 months or longer, body surface area involvement greater than or equal to 10%, Psoriasis Area and Severity Index (PASI) greater than or equal to 12, and a static Physician’s Global Assessment (sPGA) score greater than or equal to 3. Intention-to-treat analysis was conducted. <h3>Interventions</h3> Patients were randomized (4:1, interactive response technology) to risankizumab, 150 mg, subcutaneously, or placebo at weeks 0 and 4 (part A1). All patients received risankizumab at week 16. At week 28, patients randomized to risankizumab who achieved an sPGA score of 0/1 were rerandomized 1:2 to risankizumab or placebo every 12 weeks (part B). <h3>Main Outcomes and Measures</h3> Co-primary end points for the part A1 phase included proportions of patients achieving greater than or equal to 90% improvement in PASI (PASI 90) and sPGA score of 0/1 at week 16. The PASI measures severity of erythema, infiltration, and desquamation weighted by area of skin involvement over the head, trunk, upper extremities, and lower extremities; scores range from 0 (no disease) to 72 (maximal disease activity). The sPGA assesses average thickness, erythema, and scaling of all psoriatic lesions; scores range from 0 (clear) to 4 (severe), with 0/1 indicating clear or almost clear. Primary and secondary end points in part B included proportion of rerandomized patients achieving an sPGA score of 0/1 at week 52 (primary) and week 104 (secondary). <h3>Results</h3> Of 563 patients screened, 507 were randomized to risankizumab (n = 407) or placebo (n = 100). Most patients were men (356 [70.2%]); median age was 51 years (interquartile range, 38-60 years). At week 16, 298 patients (73.2%) in the treatment group vs 2 patients (2.0%) receiving placebo achieved a PASI 90 response, and 340 patients (83.5%) receiving risankizumab vs 7 patients (7.0%) receiving placebo achieved sPGA 0/1 scores (placebo-adjusted differences: PASI 90: 70.8%; 95% CI, 65.7%-76.0%; sPGA 0/1: 76.5%; 95% CI, 70.4%-82.5%;<i>P</i> &lt; .001 for both). At week 28, 336 responders were rerandomized to risankizumab (n = 111) or treatment withdrawal (n = 225). At week 52, the sPGA 0/1 score was achieved by 97 patients (87.4%) receiving risankizumab vs 138 patients (61.3%) receiving placebo. At week 104, the sPGA 0/1 score was achieved by 90 patients (81.1%) receiving risankizumab vs 16 patients (7.1%) receiving placebo (placebo-adjusted differences: week 52: 25.9%; 95% CI, 17.3%-34.6%; week 104: 73.9%; 95% CI, 66.0%-81.9%;<i>P</i> &lt; .001 for both). Rates of treatment-emergent adverse events were similar between risankizumab (186 [45.7%]) and placebo (49 [49.0%]) in part A1 and remained stable over time. <h3>Conclusions and Relevance</h3> Risankizumab showed superior efficacy compared with placebo through 16 weeks and treatment withdrawal through 2 years. Risankizumab was well tolerated, with no unexpected safety findings during the 2-year trial. <h3>Trial Registration</h3> ClinicalTrials.gov Identifier:NCT02672852

Psoriasis severity categories have been important tools for clinicians to use in treatment decisions as well as to determine eligibility criteria for clinical studies. However, owing to the heterogeneity of severity classifications and their lack of consideration for the impact of psoriasis involvement of special areas or past treatment history, patients may be miscategorized, which can lead to undertreatment of psoriasis.To develop a consensus statement on the classification of psoriasis severity.A modified Delphi approach was developed by the International Psoriasis Council to define psoriasis severity.After completion of the exercise, 7 severity definitions were preferentially ranked. This most preferred statement rejects the mild, moderate, and severe categories in favor of a dichotomous definition: Psoriasis patients should be classified as either candidates for topical therapy or candidates for systemic therapy; the latter are patients who meet at least one of the following criteria: (1) body surface area >10%, (2) disease involving special areas, and (3) failure of topical therapy.This effort might have suffered from a lack of representation by all relevant stakeholders, including patients.The consensus statement describes 2 categories of psoriasis severity, while accounting for special circumstances where patients may require systemic therapy.

Thalidomide was first introduced in the 1950s as a sedative but was quickly removed from the market after it was linked to cases of severe birth defects. However, it has since made a remarkable comeback for the U.S. Food and Drug Administration-approved use in the treatment of erythema nodosum leprosum. Further, it has shown its effectiveness in unresponsive dermatological conditions such as actinic prurigo, adult Langerhans cell histiocytosis, aphthous stomatitis, Behçet's syndrome, graft-versus-host disease, cutaneous sarcoidosis, erythema multiforme, Jessner-Kanof lymphocytic infiltration of the skin, Kaposi sarcoma, lichen planus, lupus erythematosus, melanoma, prurigo nodularis, pyoderma gangrenosum and uraemic pruritus. This article reviews the history, pharmacology, mechanism of action, clinical uses and adverse effects of thalidomide.

Background Previous studies provide evidence that there is a greater frequency of autoimmune diseases among patients with psoriasis than in the general population. Objective This study examined the association between psoriasis and 21 common autoimmune diseases, specified a priori. Methods A retrospective cohort study was conducted among persons who were members of Kaiser Permanente Southern California from 2004 to 2011. A total of 25,341 patients with 2 or more diagnosis codes for any psoriatic disease were evaluated. Five persons not meeting this case definition were matched to each psoriatic patient based on age, sex, and length of enrollment. Results Patients with psoriasis were more likely to have at least 1 other autoimmune disease (odds ratio [OR] 1.6; 95% confidence interval [CI] 1.5-1.7) and to have at least 2 other autoimmune diseases (1.9; 95% CI 1.6-2.4). Of the 17 conditions evaluated, associations with 14 were found to be statistically significant. The strongest association was with rheumatoid arthritis (3.6; 95% CI 3.4-3.9). Limitations Patients with autoimmune conditions are likely to have a greater number of health care encounters, which may result in overascertainment and misascertainment of immune-mediated conditions, although the patients included in the study averaged 5.2 years of observation and the comparison subjects were matched on length of enrollment. Conclusions The study suggests a genetic or environmental cause common across autoimmune diseases. Further investigation of individuals with multiple autoimmune diseases may yield important clues about the origin and pathogenesis of the disease. Previous studies provide evidence that there is a greater frequency of autoimmune diseases among patients with psoriasis than in the general population. This study examined the association between psoriasis and 21 common autoimmune diseases, specified a priori. A retrospective cohort study was conducted among persons who were members of Kaiser Permanente Southern California from 2004 to 2011. A total of 25,341 patients with 2 or more diagnosis codes for any psoriatic disease were evaluated. Five persons not meeting this case definition were matched to each psoriatic patient based on age, sex, and length of enrollment. Patients with psoriasis were more likely to have at least 1 other autoimmune disease (odds ratio [OR] 1.6; 95% confidence interval [CI] 1.5-1.7) and to have at least 2 other autoimmune diseases (1.9; 95% CI 1.6-2.4). Of the 17 conditions evaluated, associations with 14 were found to be statistically significant. The strongest association was with rheumatoid arthritis (3.6; 95% CI 3.4-3.9). Patients with autoimmune conditions are likely to have a greater number of health care encounters, which may result in overascertainment and misascertainment of immune-mediated conditions, although the patients included in the study averaged 5.2 years of observation and the comparison subjects were matched on length of enrollment. The study suggests a genetic or environmental cause common across autoimmune diseases. Further investigation of individuals with multiple autoimmune diseases may yield important clues about the origin and pathogenesis of the disease.

Fungal infections are very common in tropical countries and can have an important impact in terms of public health. Lobomycosis is the most common fungal infection in the tropical rain forest of South America, and paracoccidioidomycosis (South American blastomycosis) is a widespread and sometimes severe illness. Chromoblastomycosis and mycetomoas are causes of morbidity around the world and rhinosporidiosis a common cause of infection in some areas. Sporotrichosis is a worldwide subcutaneous mycosis with a very high incidence in tropical countries and also an important illness in immunocompromised patients. In the past, most of these mycoses were restricted to very specific geographic areas and natural reservoirs. There are, however, some situations where people from other regions come in contact with the pathogens. A common situation involves accidental contamination of a traveler, tourist, or worker who has contact with a tropical mycosis. Even minor trauma to the skin surface or the inhalation of fungal spores can infect the patient. Thus, recognizing the clinical symptoms and dermatological findings of the diseases, as well as the geographical distribution of the pathogens, can be critical in diagnosing the tropical mycoses.

An urgent need exists in the United States to establish treatment goals in psoriasis.We aim to establish defined treatment targets toward which clinicians and patients with psoriasis can strive to inform treatment decisions, reduce disease burden, and improve outcomes in practice.The National Psoriasis Foundation conducted a consensus-building study among psoriasis experts using the Delphi method. The process consisted of: (1) literature review, (2) pre-Delphi question selection and input from general dermatologists and patients, and (3) 4 Delphi rounds.A total of 25 psoriasis experts participated in the Delphi process. The most preferred instrument was body surface area (BSA). The most preferred time for evaluating patient response after starting new therapies was at 3 months. The acceptable response at 3 months postinitiation was either BSA 3% or less or BSA improvement 75% or more from baseline. The target response at 3 months postinitiation was BSA 1% or less. During the maintenance period, evaluation every 6 months was most preferred. The target response at every 6 months maintenance evaluation is BSA 1% or less.Although BSA is feasible in practice, it does not encompass health-related quality of life, costs, and risks of side effects.With defined treatment targets, clinicians and patients can regularly evaluate treatment responses and perform benefit-risk assessments of therapeutic options individualized to the patient.

Atopic dermatitis (AD) has been linked with psychiatric disease in adults. However, the exact relationship and its consequences have been insufficiently studied. Our aim of this study was to assess the association between depression, anxiety, and AD in adults and examine the risk of hospitalization and suicide.We utilized questionnaire data from a large general population study with data on social habits and psychiatric symptoms to compare prevalences of depression, anxiety, suicidal ideation, and anxiety attacks, in adults with and without a history of AD. Additionally, we used nationwide hospital/clinic registry and prescription data to examine the risk of anxiety and depression in Danish adults with mild and moderate-severe AD, as well as the risk of hospitalization and suicide.In the general population study, those with AD reported clinician-diagnosed depression and anxiety more often than non-AD subjects, and had an increased prevalence of suicidal ideation and depressive symptoms. In the health registry study, moderate-severe AD patients had increased risk of antidepressant and anxiolytic medication use, while patients with mild AD only had increased risk of anxiolytic medication use. There was no increased risk of hospitalization or outpatient contacts due to depression or anxiety, or risk of suicide in AD patients.Depression, anxiety, and suicidal ideation are more common among AD individuals, but do not lead to psychiatric consultations, hospitalization, or suicide.

Psoriasis, a chronic inflammatory disease associated with an accelerated risk of myocardial infarction, provides an ideal human model to study inflammatory atherogenesis in vivo. We hypothesized that the increased cardiovascular risk observed in psoriasis would be partially attributable to an elevated subclinical coronary artery disease burden composed of noncalcified plaques with high-risk features. However, inadequate efforts have been made to directly measure coronary artery disease in this vulnerable population. As such, we sought to compare total coronary plaque burden and noncalcified coronary plaque burden (NCB) and high-risk plaque (HRP) prevalence between patients with psoriasis (n=105), patients with hyperlipidemia eligible for statin therapy under National Cholesterol Education Program-Adult Treatment Panel III guidelines (n=100) who were ≈10 years older, and healthy volunteers without psoriasis (n=25).Patients underwent coronary computed-tomography angiography for total coronary plaque burden and NCB quantification and HRP identification, defined as low attenuation (<30 hounsfield units), positive remodeling (>1.10), and spotty calcification. A consecutive sample of the first 50 patients with psoriasis was scanned again 1 year after therapy.Despite being younger and at lower traditional risk than patients with hyperlipidemia, patients with psoriasis had increased NCB (mean±SD: 1.18±0.33 versus 1.11±0.32, P=0.02) and similar HRP prevalence (P=0.58). Furthermore, compared to healthy volunteers, patients with psoriasis had increased total coronary plaque burden (1.22±0.31 versus 1.04±0.22, P=0.001), NCB (1.18±0.33 versus 1.03±0.21, P=0.004), and HRP prevalence beyond traditional risk (odds ratio, 6.0; 95% confidence interval, 1.1-31.7; P=0.03). Last, among patients with psoriasis followed for 1 year, improvement in psoriasis severity was associated with improvement in total coronary plaque burden (β=0.45, 0.23-0.67; P<0.001) and NCB (β=0.53, 0.32-0.74; P<0.001) beyond traditional risk factors.Patients with psoriasis had greater NCB and increased HRP prevalence than healthy volunteers. In addition, patients with psoriasis had elevated NCB and equivalent HRP prevalence as older patients with hyperlipidemia. Last, modulation of target organ inflammation (eg, skin) was associated with an improvement in NCB at 1 year, suggesting that control of remote sites of inflammation may translate into reduced coronary artery disease risk.

Psoriasis is a chronic, inflammatory skin disease and has significant associated morbidity and effect on quality of life. It is important to determine whether dietary interventions help reduce disease severity in patients with psoriatic diseases.To make evidence-based dietary recommendations for adults with psoriasis and/or psoriatic arthritis from the Medical Board of the National Psoriasis Foundation.We used literature from prior systematic reviews as well as additional primary literature from the MEDLINE database from January 1, 2014, to August 31, 2017, that evaluated the impact of diet on psoriasis. We included observational and interventional studies of patients with psoriasis or psoriatic arthritis. The quality of included studies was assessed using the Newcastle-Ottawa scale for observational studies and the Cochrane Risk of Bias Tool for interventional studies. We made evidence-based dietary recommendations, which were voted on by the National Psoriasis Foundation Medical Board.We identified 55 studies meeting the inclusion criteria for this review. These studies represent 77 557 unique participants of which 4534 have psoriasis. Based on the literature, we strongly recommend dietary weight reduction with a hypocaloric diet in overweight and obese patients with psoriasis. We weakly recommend a gluten-free diet only in patients who test positive for serologic markers of gluten sensitivity. Based on low-quality data, select foods, nutrients, and dietary patterns may affect psoriasis. For patients with psoriatic arthritis, we weakly recommend vitamin D supplementation and dietary weight reduction with a hypocaloric diet in overweight and obese patients. Dietary interventions should always be used in conjunction with standard medical therapies for psoriasis and psoriatic arthritis.Adults with psoriasis and/or psoriatic arthritis can supplement their standard medical therapies with dietary interventions to reduce disease severity. These dietary recommendations from the National Psoriasis Foundation Medical Board will help guide clinicians regarding the utility of dietary interventions in adults with psoriatic diseases.

Psoriasis is a chronic inflammatory disease involving multiple organ systems and affecting approximately 3.2% of the world's population. In this section of the guidelines of care for psoriasis, we will focus the discussion on ultraviolet (UV) light–based therapies, which include narrowband and broadband UVB, UVA in conjunction with photosensitizing agents, targeted UVB treatments such as with an excimer laser, and several other modalities and variations of these core phototherapies, including newer applications of pulsed dye lasers, intense pulse light, and light-emitting electrodes. We will provide an in-depth, evidence-based discussion of efficacy and safety for each treatment modality and provide recommendations and guidance for the use of these therapies alone or in conjunction with other topical and/or systemic psoriasis treatments. Psoriasis is a chronic inflammatory disease involving multiple organ systems and affecting approximately 3.2% of the world's population. In this section of the guidelines of care for psoriasis, we will focus the discussion on ultraviolet (UV) light–based therapies, which include narrowband and broadband UVB, UVA in conjunction with photosensitizing agents, targeted UVB treatments such as with an excimer laser, and several other modalities and variations of these core phototherapies, including newer applications of pulsed dye lasers, intense pulse light, and light-emitting electrodes. We will provide an in-depth, evidence-based discussion of efficacy and safety for each treatment modality and provide recommendations and guidance for the use of these therapies alone or in conjunction with other topical and/or systemic psoriasis treatments. The American Academy of Dermatology (AAD) strives to produce clinical guidelines that reflect the best available evidence supplemented with the judgment of expert clinicians. Significant efforts are taken to minimize the potential for conflicts of interest to influence guideline content. The management of conflict of interest for this guideline complies with the Council of Medical Specialty Societies' Code of Interactions with Companies. Funding of guideline production by medical or pharmaceutical entities is prohibited, full disclosure is obtained and evaluated for all guideline contributors throughout the guideline development process, and recusal is used to manage identified relationships. The AAD conflict of interest policy summary may be viewed at www.aad.org. The authors' disclosed relationship with industry during guideline development appear at the end of this guideline. In accordance with AAD policy, a minimum 51% of workgroup members did not have any relevant conflicts of interest. Participation in 1 or more of the following activities constitutes a relevant conflict:•Service as a member of a speaker bureau, consultant, or advisory board member for pharmaceutical companies on the psoriasis disease state or psoriasis drugs in development or US Food and Drug Administration–approved.•Sponsored research funding or investigator-initiated studies with partial/full funding from pharmaceutical companies on the psoriasis disease state or psoriasis drugs in development or US Food and Drug Administration–approved. If a potential conflict was noted, the workgroup member recused himself or herself from discussion and drafting of recommendations pertinent to the topic area of interest. Complete group consensus was obtained for draft recommendations. Areas in which complete consensus was not achieved are shown transparently in the guideline. Authors (listed alphabetically) with relevant conflicts with respect to this guideline are noted with an asterisk*. April W. Armstrong,* MD, MPH, served as an investigator for AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Dermira, Eli Lilly and Company, Janssen-Ortho Inc, Leo Pharma Inc, National Institutes of Health, Novartis, Regeneron, and UCB, receiving grants and/or research funding; as an investigator for Regeneron and Sanofi, receiving no compensation; as an advisory board member for AbbVie, Amgen, Janssen-Ortho Inc, Merck & Co, Inc, Novartis, Pfizer, Inc, and UCB, receiving honoraria; as a consultant for AbbVie, Bristol-Myers Squibb, Celgene, Dermavant, Eli Lilly and Company, Genentech, Sanofi Genzyme, GlaxoSmithKline, Janssen-Ortho Inc, Janssen Pharmaceuticals, Inc, Leo Pharma, Inc, Menlo Therapeutics, Modernizing Medicine, Novartis Pharmaceuticals Corp, Ortho Dermatologics, Pfizer, Inc, Regeneron, Science 37, Inc, and Valeant, receiving honoraria; as a speaker for AbbVie, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Regeneron Pharmaceuticals, Inc, and Sanofi, receiving honoraria; and as a data safety member for Boehringer Ingelheim, and Merck & Co, Inc, receiving honoraria. Cody Connor, MD, has no relationships to disclose. Kelly M. Cordoro,* MD, served as a consultant for Valeant, receiving honoraria; as a consultant for Pfizer, Inc, receiving fees; as an advisory board member for Anacor Pharmaceuticals, Inc, receiving honoraria; and in another position as a member of the scientific steering committee for Celgene, receiving fees. Dawn M.R. Davis, MD, served as an investigator for Regeneron, receiving no compensation. Boni E. Elewski,* MD, served as a consultant for Boehringer Ingelheim, Celgene Corporation, Leo Pharma, Lilly ICOS LLC, Menlo Therapeutics, Novan (receiving no fees), Novartis Pharmaceuticals Corp, Pfizer, Inc, Sun Pharmaceutical Industries, Ltd, Valeant Pharmaceuticals International, and Verrica Pharmaceuticals, receiving honoraria; as a principal investigator for AbbVie, Amgen, AnaptysBio, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene Corporation, Eli Lilly and Company, Incyte Corporation, InflaRX GmbH, Janssen-Ortho Inc, LEO Pharma, Menlo Therapeutics, Merck & Co, Inc, Novartis Pharmaceuticals Corp, Pfizer, Inc, Regeneron, Sun Pharmaceuticals,Ltd, Valeant Pharmaceuticals International, Vanda Pharmaceuticals, and Vioment, receiving grants/research funding; as an advisory board member for Foundation for Research & Education of Dermatology, LEO Pharma, and Verrica Pharmaceuticals, Inc, receiving honoraria; and in another role for Hoffman-La Roche Ltd, receiving fees. Craig A. Elmets, MD, served as a consultant for Ferndale Laboratories, Inc, receiving honoraria; as a consultant/advisory board member for Vertex Pharmaceuticals, receiving fees and/or honoraria; as a principal investigator for the California Association of Winegrape Growers, receiving grants and/or research funding; as an investigator for Elorac,Inc, Idera Pharmaceuticals,Inc, Kyowa Hakko USA, and Solgenix LLC, receiving grants/research funding; as a data safety monitoring board member for Astellas Pharma US, Inc, and LEO Laboratories Ltd, receiving fees; as a stockholder for Medgenics, Inc, receiving no fees; and as a stockholder for Aevi Genomic Medicine (receiving stock) and Immunogen (paid to spouse). Joel M. Gelfand,* MD, MSCE, served as a consultant for AbbVie, BMS, Boehringer Ingelheim, Dermira, Dr Reddy, GlaxoSmithKline, Janssen Pharmaceuticals, Inc, Menlo Therapeutics, Novartis Pharmaceuticals Corp, Pfizer, Inc, Regeneron, Sanofi US Services, UCB (DSMB), and Valeant Pharmaceuticals North America LLC, receiving honoraria; as a consultant for BMS, receiving fees; as a speaker and/or faculty educator for CME supported by Eli Lilly and Company, receiving fees; as a principal investigator for AbbVie, Boehringer Ingelheim, Celgene, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Novartis Pharmaceuticals Corp, Ortho Dermatologics, Pfizer, Inc, Regeneron, and Sanofi/Sanofi US Services, receiving grants/research funding; as an investigator for Sanofi, receiving grants and/or research funding; as an advisory board member for Sanofi US Services, receiving honoraria; as a data safety monitoring board member for Coherus Biosciences and Merck & Co, Inc, receiving honoraria. In addition, Dr Gelfand has received payment for CME work related to psoriasis that was supported indirectly by Lilly and Company, Ortho Dermatologics, and Novartis; served in another role for Elsevier, Inc, receiving no compensation; served in another role for Eli Lilly and Company and UCB, receiving fees; and served in another role for Resiquimod, receiving patent royalties or other compensation for intellectual rights. Kenneth B. Gordon,* MD, served as a consultant for AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Demira, Dermavant Sciences, Kyowa Hakko Kirin Pharma, Inc, Leo Pharma, Ortho Dermatologics, Sun Pharmaceuticals Ltd, and UCB, receiving honoraria; as a consultant for Genzyme, receiving fees; as a principal investigator for AbbVie, Amgen, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Merck & Co, Inc, and Novartis Pharmaceuticals Corp, receiving grants and/or research funding; and as an advisory board member for Celgene Corporation, Janssen Pharmaceuticals Inc, Lilly ICOS LLC, Novartis Pharmaceuticals Corp, and Pfizer, Inc, receiving honoraria. Alice B. Gottlieb,* MD, PhD, served as a consultant for Abbott Laboratories, AbbVie, Akros Pharma, Inc, Allergan, Amgen, Amicus Therapeutics, Baxalta Incorporated, Bristol-Myers Squibb, Canfite, Celgene Corporation, CSL Behring, Dermira, Dr Reddy, DUSA Pharmaceuticals, Inc, GlaxoSmithKline, Incyte Corporation, KPI Therapeutics, Lilly ICOS LLC, Meiji Seika Pharma Co, Ltd, Merck & Co, Inc, Mitsubishi Pharma, Novartis Pharmaceuticals Corp, Sanofi-Aventis, Sienna Biopharmaceuticals, Sun Pharmaceutical Industries, Takeda Pharmaceuticals USA, Inc, Teva, UCB, Valeant Pharmaceuticals International, Valeant Pharmaceuticals North America LLC, XBiotech, and Xenoport, Inc, receiving honoraria; as a consultant for Aclaris Therapeutics, Inc, Avotres Inc, Merck & Co Inc, and XBiotech, receiving no compensation; as a speaker for AbbVie, Eli Lilly and Company, and Janssen Biotech, receiving honoraria; as a principal investigator for Abbott Laboratories, AbbVie, Allergan, Amgen, Celgene Corporation, Coronado Biosciences, Immune Control, Incyte Corporation, Janssen-Ortho Inc, LEO Pharma, Lerner Medical Devices,Inc, Lilly ICOS LLC, Merck & Co, Inc, Novartis Pharmaceuticals Corp, Novo Nordisk A/S, Pfizer Inc, UCB, Xbiotech, and Xenoport,Inc, receiving grants/research funding; as a principal investigator for Janssen-Ortho Inc, receiving honoraria; as an advisory board member for Abbott Laboratories, Actelion, Allergan, Amgen, Astellas Pharma US, Inc, Beiersdorf, Inc, BMS, Celgene Corporation, Coronado Biosciences, Dermira, Dr Reddy, Genentech, Janssen-Ortho Inc, Janssen Biotech, Leo Pharma US, Lilly ICOS LLC, Novartis Pharmaceuticals Corp, Novo Nordisk A/S, Pfizer, Inc, UCB, and Valeant, receiving honoraria; in another role for Amgen, receiving grants and/or research funding; in another role for Crescendo Bioscience and Karyopharm Therapeutics, receiving no compensation; in another role (data safety) for Catabasis Pharmaceuticals, Inc, receiving honoraria; and in another role for DermiPsor, receiving honoraria. Daniel H. Kaplan, MD, PhD, served as a consultant for Eli Lilly and Company, receiving no compensation and as a member of the data safety monitoring board for Hapten Sciences, receiving fees. Arthur Kavanaugh,* MD, served as a principal investigator for AbbVie, Amgen, BMS, Celgene Corporation, Eli Lilly and Company, Janssen Biotech, Novartis, Pfizer, Inc, and UCB, receiving grants/research funding. Matthew Kiselica, BA/BS, has no relationships to disclose. Dario Kivelevitch, MD, has a first-degree relative employed by Boehringer Ingelheim. Neil J. Korman,* MD, PhD, served as a consultant for Novartis Pharmaceuticals Corp, receiving honoraria; as a consultant for Dr Reddy's Laboratory, receiving fees; as a speaker for AbbVie, Celgene, Eli Lilly and Company, Genentech, Janssen, Novartis, Regeneron, and Sanofi, receiving honoraria; as a principal investigator for AbbVie, Amgen, Celgene Corporation, Chugai, Dermira, Eli Lilly and Company, Kyowa Hakko Kirin Pharma, Inc, LEO Pharma, Menlo Therapeutics, Merck, Pfizer, Prothena, Regeneron, Rhizen,Inc, Syntimmune, Trevi, and UCB, receiving grants and/or research funding; as an advisory board member for Amgen, Celgene Corporation, Eli Lilly and Company, Genentech, GlaxoSmithKline, Janssen Pharmaceuticals, Inc, Novartis Pharmaceuticals Corp, Pfizer, Inc, and Principia Biopharma, receiving honoraria; as an advisory board member for Dr Reddy's Laboratory, Immune Pharmaceuticals, Regeneron, Sanofi, Sun Pharma, and Valeant, receiving fees; as an advisory board member/consultant for AbbVie, Eli Lilly and Company, GlaxoSmithKline, Pfizer Inc, and Principa, receiving honoraria/fees; and in another role for Janssen Pharmaceuticals, Inc, receiving grants and/or research funding. Daniela Kroshinsky, MD, MPH, has no relationships to disclose. Mark Lebwohl,* MD, served as a consultant for Allergan, Almirall, Arcutis, Inc, Boehringer Ingelheim, Bristol-Myers Squibb, Castle Biosciences, Inc, Leo Pharma, Menlo Therapeutics, Mitsubishi Pharma, Neuroderm LTD, Pfizer, Inc, Promius/Dr Reddy, Theravance Biopharma, and Verrica Pharmaceuticals, Inc, receiving honoraria; as a principal investigator or investigator for AbbVie, Amgen, Inc, AstraZeneca, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Incyte Corporation, Janssen Research and Development LLC/Johnson & Johnson, Leo Pharma, Medimmune, Novartis Pharmaceuticals Corp, Ortho-Dermatologics, Pfizer, Inc, SCIDerm, UCB, and ViDac Pharma receiving grants and/or research funding; and in another role for Corrona, Inc, Facilitation of International Dermatology Education, and the Foundation for Research and Education in Dermatology, receiving honoraria. Craig L. Leonardi,* MD, served as a consultant/advisory board member for AbbVie, Amgen, Boehringer Ingelheim, Celgene Dermira, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Leo Pharma A/S, Ortho Dermatologics, Pfizer, Inc, Sandoz (a Novartis Company), UCB, and Vitae, receiving honoraria; as a speaker for AbbVie, Amgen, Celgene Corporation, Eli Lilly and Company, Novartis, Sun Pharmaceuticals, Ltd, and UCB, receiving honoraria; and as a principal investigator for Actavis, Amgen, Boehringer Ingelheim, Celgene Corporation, Cellceutix, Coherus Biosciences, Corrona, Dermira, Eli Lilly and Company, Galderma Laboratories, LP, Glenmark Generics, Inc, Janssen Pharmaceuticals, Inc, Leo Pharma, Inc, Merck, Novartis, Novella, Pfizer, Inc, Sandoz (a Novartis Company), Sienna Biopharmaceuticals, Stiefel a GsK company, UCB, and Warner Chillcott, receiving other financial benefits (fee for service). Jason Lichten, MD, has no relationships to disclose. Henry W. Lim, MD, served as a principal or coinvestigator for Estee Lauder, Ferndale Laboratories,Inc, Incyte, and Unigen, receiving grants and/or research funding; and as a speaker and/or faculty education for Pierre Fabre Dermatologie, receiving honoraria. Nehal N. Mehta,* MD, MSCE, is a full-time US government employee and has served as a consultant for Amgen, Eli Lilly and Company, and Leo Pharma, receiving grants/other payments; as principal investigator and/or investigator for AbbVie, Celgene, Janssen Pharmaceuticals, Inc, and Novartis, receiving grants and/or research funding; and as a principal investigator for the National Institute of Health, receiving grants and/or research funding. Alan Menter,* MD, served as a consultant for Abbott Labs, AbbVie, Amgen, Eli Lilly and Company, Galderma USA, Janssen Pharmaceuticals Inc, LEO Pharma US, Menlo Therapeutics, Novartis, Sienna Biopharmaceuticals, and Wyeth Labs, receiving honoraria; as a consultant for New Enterprise Associates, Promius Pharma LLC, Spherix Global Insights US, UCB, and Valeant Pharmaceuticals North America, receiving fees; as a consultant for Afecta Pharmaceuticals, receiving no compensation; as a speaker for Abbott Labs, AbbVie, Amgen, Janssen Biotech, LEO Pharma, US, Pfizer, Inc, Promius Pharma LLC, Sienna Pharmaceuticals, UCB, and Wyeth Labs, receiving honoraria; as a principal investigator for AbbVie, Amgen, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Medimetriks Pharmaceuticals,Inc, Merck & Co, Inc, Novartis Pharmaceutical Corp, and Pfizer, Inc, receiving grant and/or research funding; as an investigator for Eli Lilly and Company, and UCB, receiving honoraria; as an investigator for Abbott Labs, Leo Pharma US, and Sienna Biopharmaceuticals, receiving grants; as an advisory board member for Abbott Labs, AbbVie, Boehringer Ingelheim, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, LEO Pharma US, Medscape, Pfizer, Inc, and Sienna Biopharmaceuticals, receiving honoraria; as an advisory board member for Amgen, receiving grant and/or research funding; as an advisory board member for Afecta Pharmaceuticals, receiving no compensation; and as an independent contractor for Prime Education, receiving fees. Amy S. Paller,* MD, served as a consultant for Amgen, Amicus Therapeutics, Anacor Pharmaceuticals, Inc, Aqua Pharmaceuticals, Boehringer Ingelheim International GmbH, BridgeBio Pharma, Castle Creek Pharma, Celgene Corporation, Dermavant Sciences, Dermira, Eli Lilly and Company, Galderma Laboratories, LP, Leo Pharma Inc, Genentech, Menlo Therapeutics, MorphoSys AG, Novartis Pharmaceuticals Corp, Pfizer Inc, Pierre Fabre Dermatologie, Proctor and Gamble, Regeneron, Sanofi, Scioderm, Shire, Sol-Gel Technologies, Stiefel a GSK company, Theravance Biopharma, UCB, Union Therapeuthic, Valeant Pharmaceuticals North America LLC, Vitae Pharmaceuticals, and Verrica, receiving honoraria; as a speaker/educator for Expanscience, receiving honoraria; as a principal investigator for AbbVie, Amgen, Anacor Pharmaceuticals, Inc, AnaptysBio, Celgene Corporation, Eli Lilly and Company, Galderma, Janssen Pharmaceuticals, Inc, Leo Pharma, Regeneron, and Scioderm, receiving no compensation. Sylvia L. Parra, MD, has no relationships to disclose. Arun L. Pathy, MD, has no relationships to disclose. Elizabeth A. Farley Prater, MD, has no relationships to disclose. Reena N. Rupani, MD, served as speaker for Nutrafol, receiving honoraria. Michael Siegel, PhD has no relationships to disclose. Benjamin Stoff, MD, MA, served as an investigator for Celtaxsys, Inc, receiving fees. Bruce E. Strober,* MD, PhD, served as a consultant for AbbVie, Almirall, Amgen, Boehringer Ingelheim, Celgene Corporation, Dermira, Eli Lilly and Company, GlaxoSmithKline, Janssen-Ortho Inc, Leo Pharma, Inc, Maruho Co, Ltd, Medac Pharma, Inc, Menlo Therapeutics, Novartis Pharmaceuticals Corp, Ortho Dermatologics, Pfizer, Inc, Sanofi-Regeneron, Sun Pharmaceuticals Industries, and UCB, receiving honoraria; as a consultant for Affibody, Arena, Bristol-Myers Squibb, Dermavant, Meiji Seika Pharma Co, Ltd, Sebela Pharmaceuticals, Sirtris, and UCB, receiving fees; as a principal investigator for AbbVie, Boehringer Ingelheim, Celgene Corporation, Eli Lilly and Company, Galderma, Janssen-Ortho Inc, Merck & Co, Pfizer, Inc, Sienna, and Sun Pharmaceutical Industries, receiving no compensation; as an advisory board member for AbbVie, Amgen, Bristol-Myers Squibb, Celgene Corporation, Dermira, Eli Lilly and Company, Janssen-Ortho Inc, Novartis Pharmaceuticals Corp, Pfizer, Inc, Sanofi-Regeneron, Sun Pharmaceuticals Industries, and UCB, receiving honoraria; as consultant/advisory board for AstraZeneca Pharmaceuticals LP, receiving fees/honoraria; and in another role for AbbVie and Janssen-Ortho Inc, receiving no compensation. Emily B. Wong, MD, has no relationships to disclose. Jashin J. Wu,* MD, served as a consultant for Abbvie, Allergan, Almirall, Amgen, Bristol-Myers Squibb, Celgene, Dermira, Dr Reddy's Laboratories, Eli Lilly and Company, Janssen Biotech, LEO Pharma, Novartis, Ortho Dermatologics, Pfizer, Inc, Promius Pharma, Regeneron, Sun Pharmaceutical Industries, Ltd, UCB, and Valeant Pharmaceuticals North America, LLC, receiving fees and/or honoraria; as a speaker for Abbvie, Celgene, Novartis, Regeneron, Sanofi Genzyme, Sun Pharmaceutical Industries Ltd, UCB, and Valeant Pharmaceuticals North America LLC, receiving honoraria; and as a principal/investigator for AbbVie, Amgen, AstraZeneca, Boehringer Ingelheim, Coherus Biosciences, Dermira, Eli Lilly and Company, Janssen Pharmaceuticals, Inc, Merck & Co, Inc, Novartis, Pfizer, Inc, Regeneron, Sandoz (a Novartis Company), and Sun Pharmaceutical Industries Ltd, receiving research and/or grant funding. Vidhya Hariharan, PhD, has no relationships to disclose. Adherence to these guidelines will not ensure successful treatment in every situation. Furthermore, these guidelines should not be interpreted as setting a standard of care, nor should they be deemed either inclusive of all proper methods of care or exclusive of other methods of care reasonably directed toward obtaining the same results. The ultimate judgment regarding the propriety of any specific therapy must be made by the physician and the patient in light of all the circumstances presented by the individual patient and the known variability and biologic behavior of the disease. Furthermore, the treatment dosages used in clinical trials may not be effective in certain cases, and some patients may require shorter intervals between doses and/or higher treatment doses of a particular treatment methodology. This guideline reflects the best available data at the time the guideline was prepared. The results of future studies will likely require revisions to the recommendations in this guideline to reflect new data. Although many patients with psoriasis may be capable of adequately controlling their disease with the use of topical treatments alone, often these interventions are insufficient and disease severity dictates the need for alternative options. While systemic and biologic treatments are heavily relied on for severe and widespread skin disease, these medications do come with risks of systemic side effects and immunosuppression that many patients may not be willing or able to assume. Phototherapy serves as a reasonable and effective treatment option for patients requiring more than topical medications and/or those wishing to avoid systemic medications or simply seeking an adjunct to a failing regimen. See Appendix 1 for definitions. This section covers the use of phototherapy in the treatment of psoriasis in adults; psoriasis treatment in the pediatric population is addressed in the Joint American Academy of Dermatology–National Psoriasis Foundation Guidelines of Care for the Management and Treatment of Psoriasis in Pediatric Population (in preparation). An evidence-based model was used, and evidence was obtained by using a search of the PubMed and MEDLINE databases from January 1, 2008, to December 31, 2017, for all newly identified clinical questions (Table I). Searches were limited to publications in the English language. Medical Subject Heading (MeSH) terms used alone or in various combinations in the search included psoriasis (plaque, vulgaris, guttate, erythrodermic, inverse, pustular), phototherapy, ultraviolet (short-wave, long-wave), targeted phototherapy (excimer laser), narrowband ultraviolet B (NB-UVB), photochemotherapy, psolaren ultraviolet A, broadband ultraviolet B (BB-UVB), grenz ray, climatotherapy, photodynamic therapy, visible light (red/blue), TURBO-UVB, intense pulsed light, and Goeckerman therapy.Table IClinical questionWhat are the efficacy, effectiveness, and adverse effects of the following phototherapy/photochemotherapy modalities used as monotherapy or in combination with other psoriasis therapies to treat psoriasis in adults?1)Narrowband ultraviolet B (NB-UVB)2)Broadband ultraviolet B (BB-UVB)3) Targeted phototherapy (excimer laser and excimer lamp)4)Psoralen plus ultraviolet A (PUVA) therapya.Topicalb.Bathc.Oral5)Photodynamic therapy6)Grenz ray therapy7)Climatotherapy8)Visible light therapy9)Goeckerman therapy10)Pulsed dye laser and Intense pulsed light Open table in a new tab For detailed methodology, see Appendix I. NB-UVB refers to wavelengths ranging from 311 to 313 nm, which are widely used for the treatment of generalized plaque psoriasis.1Almutawa F. Alnomair N. Wang Y. Hamzavi I. Lim H.W. Systematic review of UV-based therapy for psoriasis.Am J Clin Dermatol. 2013; 14: 87-109Crossref PubMed Scopus (55) Google Scholar, 2Archier E. Devaux S. Castela E. et al.Efficacy of psoralen UV-A therapy vs. narrowband UV-B therapy in chronic plaque psoriasis: a systematic literature review.J Eur Acad Dermatol Venereol. 2012; 26: 11-21Crossref PubMed Scopus (48) Google Scholar, 3Dayal S. Mayanka Jain V.K. Comparative evaluation of NBUVB phototherapy and PUVA photochemotherapy in chronic plaque psoriasis.Indian J Dermatol Venereol Leprol. 2010; 76: 533-537Crossref PubMed Scopus (9) Google Scholar, 4El-Mofty M. Mostafa W.Z. Bosseila M. et al.A large scale analytical study on efficacy of different photo(chemo)therapeutic modalities in the treatment of psoriasis, vitiligo and mycosis fungoides.Dermatol Ther. 2010; 23: 428-434Crossref PubMed Scopus (17) Google Scholar As outlined in Table II,5Mehta N.N. Shin D.B. Joshi A.A. et al.Effect of 2 psoriasis treatments on vascular inflammation and novel inflammatory cardiovascular biomarkers: a randomized placebo-controlled trial.Circ Cardiovasc Imaging. 2018; 11: e007394Crossref PubMed Scopus (41) Google Scholar, 6Ward W.H. Lambreton F. Goel N. Yu J.Q. Farma J.M. Clinical presentation and staging of melanoma.in: Ward W.H. Farma J.M. Cutaneous Melanoma: Etiology and Therapy. Codon Publications, Brisbane, Australia2017Crossref Google Scholar, 7Zanolli M. Feldman S.R. Phototherapy Treatment Protocols for Psoriasis and Other Photoherapy Responsive Dermatoses.2nd ed. Taylor & Francis, Milton, Abingdon, UK2005Google Scholar, 8Boztepe G. Karaduman A. Sahin S. Hayran M. Kolemen F. The effect of maintenance narrow-band ultraviolet B therapy on the duration of remission for psoriasis: a prospective randomized clinical trial.Int J Dermatol. 2006; 45: 245-250Crossref PubMed Scopus (23) Google Scholar, 9Menter A. Korman N.J. Elmets C.A. et al.Guidelines of care for the management of psoriasis and psoriatic arthritis: section 5. Guidelines of care for the treatment of psoriasis with phototherapy and photochemotherapy.J Am Acad Dermatol. 2010; 62: 114-135Abstract Full Text Full Text PDF PubMed Scopus (247) Google Scholar the starting dose for NB-UVB therapy can be based on skin phototype or minimal erythema dose (MED).2Archier E. Devaux S. Castela E. et al.Efficacy of psoralen UV-A therapy vs. narrowband UV-B therapy in chronic plaque psoriasis: a systematic literature review.J Eur Acad Dermatol Venereol. 2012; 26: 11-21Crossref PubMed Scopus (48) Google Scholar, 9Menter A. Korman N.J. Elmets C.A. et al.Guidelines of care for the management of psoriasis and psoriatic arthritis: section 5. Guidelines of care for the treatment of psoriasis with phototherapy and photochemotherapy.J Am Acad Dermatol. 2010; 62: 114-135Abstract Full Text Full Text PDF PubMed Scopus (247) Google Scholar, 10Parlak N. Kundakci N. Parlak A. Akay B.N. Narrowband ultraviolet B phototherapy starting and incremental dose in patients with psoriasis: comparison of percentage dose and fixed dose protocols.Photodermatol Photoimmunol Photomed. 2015; 31: 90-97Crossref PubMed Scopus (8) Google Scholar, 11Dawe R.S. Cameron H.M. Yule S. Ibbotson S.H. Moseley H.H. Ferguson J. A randomized comparison of methods of selecting narrowband UV-B starting dose to treat chronic psoriasis.Arch Dermatol. 2011; 147: 168-174Crossref PubMed Scopus (12) Google Scholar A frequency of twice or thrice weekly is effective and is therefore recommended.1Almutawa F. Alnomair N. Wang Y. Hamzavi I. Lim H.W. Systematic review of UV-based therapy for psoriasis.Am J Clin Dermatol. 2013; 14: 87-109Crossref PubMed Scopus (55) Google Scholar, 12Cameron H. Dawe R.S. Yule S. Murphy J. Ibbotson S.H. Ferguson J. A randomized, observer-blinded trial of twice vs. three times weekly narrowband ultraviolet B phototherapy for chronic plaque psoriasis.Br J Dermatol. 2002; 147: 973-978Crossref PubMed Scopus (0) Google Scholar, 13Dawe R.S. Wainwright N.J. Cameron H. Ferguson J. Narrow-band (TL-01) ultraviolet B phototherapy for chronic plaque psoriasis: three times or five times weekly treatment?.Br J Dermatol. 1998; 138: 833-839Crossref PubMed Scopus (83) Google Scholar A frequency greater than thrice weekly results in little added benefit, while at the same time exposing the patient to a higher total dose of UVB radiation and greater risk of ultraviolet (UV)-induced erythema.13Dawe R.S. Wainwright N.J. Cameron H. Ferguson J. Narrow-band (TL-01) ultraviolet B phototherapy for chronic plaque psoriasis: three times or five times weekly treatment?.Br J Dermatol. 1998; 138: 833-839Crossref PubMed Scopus (83) Google Scholar Although both twice-weekly treatment and thrice-weekly treatment eventually achieve clearance in equal proportions, twice-weekly treatments appear to take about 1.5 times longer to achieve skin disease clearance as compared with thrice-weekly treatments.12Cameron H. Dawe R.S. Yule S. Murphy J. Ibbotson S.H. Ferguson J. A randomized, observer-blinded trial of twice vs. three times weekly narrowband ultraviolet B phototherapy for chronic plaque psoriasis.Br J Dermatol. 2002; 147: 973-978Crossref PubMed Scopus (0) Google Scholar More specifically, patients receiving twice-weekly NB-UVB treatments achieve clearance in a mean of 88 days compared with 58 days for those receiving 3 treatments per week.12Cameron H. Dawe R.S. Yule S. Murphy J. Ibbotson S.H. Ferguson J. A randomized, observer-blinded trial of twice vs. three times weekly narrowband ultraviolet B phototherapy for chronic plaque psoriasis.Br J Dermatol. 2002; 147: 973-978Crossref PubMed

ABSTRACT Background Few population‐based studies have reported the prevalence of psoriatic disease. Objective We validated computerized diagnoses to estimate the prevalence of psoriasis and psoriatic arthritis. Method We identified adults with ≥1 ICD‐9 diagnosis codes of 696.0 (psoriatic arthritis) or 696.1 (psoriasis) in clinical encounter data during 1996–2009 and used chart review to confirm the diagnoses in random samples of patients. We then used the best performing case‐finding algorithms to estimate the point prevalence of psoriasis and psoriatic arthritis. Results The number of persons with a diagnosis for psoriasis (ICD‐9 code 696.1) was 87 827. Chart review of a random sample of 101 cases with at least one dermatologist‐rendered psoriasis code revealed a positive predictive value (PPV) of 90% (95% CI, 83–95) with sensitivity of 88% (95% CI, 80–93). Psoriatic arthritis (code 696.0) was recorded for 5187 patients, with the best performing algorithm requiring ≥2 diagnoses recorded by a rheumatologist or ≥1 diagnosis recorded by a rheumatologist together with ≥1 psoriasis diagnoses recorded by a dermatologist; the PPV was 80% (95% CI, 70–88) with sensitivity 73% (95% CI, 63–82). Among KPNC adults, the point prevalence of psoriasis, with or without psoriatic arthritis, was 939 (95% CI, 765–1142) per 100 000, and the overall prevalence of psoriatic arthritis, with or without psoriasis, was 68 (95% CI, 54–84) per 100 000. Conclusion Within an integrated health care delivery system, the use of computerized diagnoses rendered by relevant disease specialists is a valid method for identifying individuals with psoriatic disease. Copyright © 2013 John Wiley &amp; Sons, Ltd.

Background Psoriasis is associated with increased risk for cardiovascular disease. Objective To compare major cardiovascular event risk in psoriasis patients receiving methotrexate or tumor necrosis factor-α inhibitor (TNFi) and to assess TNFi treatment duration impact on major cardiovascular event risk. Methods Adult psoriasis patients with ≥2 TNFi or methotrexate prescriptions in the Truven MarketScan Databases (Q1 2000–Q3 2011) were classified as TNFi or methotrexate users. The index date for each of these drugs was the TNFi initiation date or a randomly selected methotrexate dispensing date, respectively. Cardiovascular event risks and cumulative TNFi effect were analyzed by using multivariate Cox proportional-hazards models. Results By 12 months, TNFi users (N = 9148) had fewer cardiovascular events than methotrexate users (N = 8581) (Kaplan-Meier rates: 1.45% vs 4.09%: P < .01). TNFi users had overall lower cardiovascular event hazards than methotrexate users (hazard ratio = 0.55; P < .01). Over 24 months' median follow-up, every 6 months of cumulative exposure to TNFis were associated with an 11% cardiovascular event risk reduction (P = .02). Limitations Lack of clinical assessment measures. Conclusions Psoriasis patients receiving TNFis had a lower major cardiovascular event risk compared to those receiving methotrexate. Cumulative exposure to TNFis was associated with a reduced risk for major cardiovascular events. Psoriasis is associated with increased risk for cardiovascular disease. To compare major cardiovascular event risk in psoriasis patients receiving methotrexate or tumor necrosis factor-α inhibitor (TNFi) and to assess TNFi treatment duration impact on major cardiovascular event risk. Adult psoriasis patients with ≥2 TNFi or methotrexate prescriptions in the Truven MarketScan Databases (Q1 2000–Q3 2011) were classified as TNFi or methotrexate users. The index date for each of these drugs was the TNFi initiation date or a randomly selected methotrexate dispensing date, respectively. Cardiovascular event risks and cumulative TNFi effect were analyzed by using multivariate Cox proportional-hazards models. By 12 months, TNFi users (N = 9148) had fewer cardiovascular events than methotrexate users (N = 8581) (Kaplan-Meier rates: 1.45% vs 4.09%: P < .01). TNFi users had overall lower cardiovascular event hazards than methotrexate users (hazard ratio = 0.55; P < .01). Over 24 months' median follow-up, every 6 months of cumulative exposure to TNFis were associated with an 11% cardiovascular event risk reduction (P = .02). Lack of clinical assessment measures. Psoriasis patients receiving TNFis had a lower major cardiovascular event risk compared to those receiving methotrexate. Cumulative exposure to TNFis was associated with a reduced risk for major cardiovascular events.

Abstract Background Sparse information is available concerning mental health issues in psoriasis, psoriatic arthritis (PsA) and ankylosing spondylitis ( AS ) patients. Objective To estimate risk of depression, suicidal ideation and suicide attempt in patients with psoriasis, PsA and AS , respectively, compared with the general population. Methods This population‐based cohort study analysed 36 214 psoriasis patients, 5138 PsA patients and 1878 AS patients who were frequency‐matched with a general population cohort. Annual incidence rate of depression, suicidal ideation and suicide attempt was calculated separately for psoriasis, PsA and AS . Results There was an increased risk of depression in the three cohorts; adjusted IRR : psoriasis, 1.14 (95% CI , 1.11, 1.17); PsA, 1.22 (95% CI , 1.16, 1.29); AS , 1.34 (95% CI , 1.23, 1.47). There was no significantly increased risk for suicidal ideations or suicide attempt among psoriasis, PsA or AS patients. Limitations Patients were not excluded if previously diagnosed with depression, suicidal ideation or suicide attempt. Suicide attempt and completed suicide analyses were not adjusted for presence of depression. Use of systemic psoriasis treatment to measure severe psoriasis could lead to psoriasis severity misclassification. Conclusion The risk of depression, but not suicidal ideation or suicide attempt, was significantly increased in patients with psoriasis, PsA and AS .

Nail psoriasis can be difficult to treat and has a significant effect on quality of life. Relatively few controlled trials evaluating treatments for nail psoriasis have been published. There is an unmet need for treatment recommendations to guide therapeutic decisions.To develop treatment recommendations for nail psoriasis from the Medical Board of the National Psoriasis Foundation.A PubMed search for publications on nail psoriasis treatments was performed from January 1, 1947, through May 11, 2014, without language restrictions.Treatment recommendations for 4 clinical nail psoriasis scenarios were developed based on the evidence reviewed in this study and expert opinion of the Medical Board of the National Psoriasis Foundation. Treatment of nail psoriasis should balance consideration of the extent of skin disease, psoriatic arthritis, and severity of nail disease with concomitant impairment of quality of life. All patients should be evaluated for onychomycosis because this may complicate psoriatic nail disease. For disease limited to the nails, high-potency topical corticosteroids with or without calcipotriol are initial options. For patients with significant nail disease for whom topical therapy has failed, treatment with adalimumab, etanercept, intralesional corticosteroids, ustekinumab, methotrexate sodium, and acitretin are recommended. For patients with significant skin and nail disease, adalimumab, etanercept, and ustekinumab are strongly recommended, and methotrexate, acitretin, infliximab, and apremilast are recommended. Finally, for a patient with significant nail, skin, and joint disease, adalimumab, etanercept, ustekinumab, infliximab, methotrexate, apremilast, and golimumab are recommended.Treatment of nail psoriasis poses a clinical challenge. Clinical trial data are limited, and results are reported inconsistently, making comparisons among treatment options difficult. The treatment recommendations from the Medical Board of the National Psoriasis Foundation will help guide treatment decisions for clinicians who are treating patients with nail psoriasis.

Abstract Background Previous studies have demonstrated that patients with psoriasis have higher rates of comorbidities compared to the general population. Despite the clinical and economic burden of psoriatic disease, there have been few large‐scale observational studies focused on this condition. Objective To assess rates of cardiovascular, autoimmune, infectious and other conditions in patients with psoriasis or psoriatic arthritis ( PSA ). Methods The data for this retrospective study were obtained from the Clinical Practice Research Datalink ( CRPD ). Cohorts of patients with psoriasis ( n = 27 672; mild, n = 22 174, severe, n = 5498) and PSA ( n = 1952) were generated based on the diagnosis made by general practitioner or specialist recorded in CPRD between 2006 and 2010. Frequencies of comorbidities at baseline and incidence rate ratios ( IRR ) of medical conditions occurring during follow‐up were calculated and compared between groups. Cox proportional hazard models were employed to compare hazard ratios ( HR ) of comorbidities across the same subpopulations previously described. Results Significant differences in the unadjusted risk of cardiovascular disease, hyperlipidaemia, diabetes, skin cancer and autoimmune diseases were observed between patients with differing severity of psoriasis or between PSA and psoriasis patients. The adjusted HR analyses confirmed patients with severe psoriasis had significantly higher rates of several conditions including diabetes (1.23; 95% CI : 1.01–1.51) and rheumatoid arthritis (2.88; 95% CI : 2.25–3.67) compared to patients with mild psoriasis. Patients with PSA had significantly higher adjusted rates of hypertension (1.30; 95% CI : 1.01–1.68), rheumatoid arthritis (6.93; 95% CI : 5.45–8.80) and ankylosing spondylitis (6.98; 95% CI : 2.37–20.58) compared to those with severe psoriasis. Conclusion Patients with mild psoriasis are less affected by comorbid conditions than those with severe psoriasis, and patients with psoriasis are less affected by comorbidities than those with PSA . Given the differences observed across severities of psoriasis and between psoriasis and PSA , each patient subgroup should be taken into consideration in clinical practice and future research.

Background Psoriasis is associated with risk of cardiovascular (CV) disease (CVD) and a major adverse CV event (MACE). Whether psoriasis duration affects risk of vascular inflammation and MACEs has not been well characterized. Objectives We utilized two resources to understand the effect of psoriasis duration on vascular disease and CV events: (1) a human imaging study and (2) a population-based study of CVD events. Methods First, patients with psoriasis (N = 190) underwent fludeoxyglucose F 18 positron emission tomography/computed tomography (duration effect reported as a β-coefficient). Second, MACE risk was examined by using nationwide registries (adjusted hazard ratios in patients with psoriasis (n = 87,161) versus the general population (n = 4,234,793). Results In the human imaging study, patients were young, of low CV risk by traditional risk scores, and had a high prevalence of cardiometabolic diseases. Vascular inflammation by fludeoxyglucose F 18 positron emission tomography/computed tomography was significantly associated with disease duration (β = 0.171, P = .002). In the population-based study, psoriasis duration had strong relationship with MACE risk (1.0% per additional year of psoriasis duration [hazard ratio, 1.010; 95% confidence interval, 1.007-1.013]). Limitations These studies utilized observational data. Conclusion We found detrimental effects of psoriasis duration on vascular inflammation and MACE, suggesting that cumulative duration of exposure to low-grade chronic inflammation may accelerate vascular disease development and MACEs. Providers should consider inquiring about duration of disease to counsel for heightened CVD risk in psoriasis. Psoriasis is associated with risk of cardiovascular (CV) disease (CVD) and a major adverse CV event (MACE). Whether psoriasis duration affects risk of vascular inflammation and MACEs has not been well characterized. We utilized two resources to understand the effect of psoriasis duration on vascular disease and CV events: (1) a human imaging study and (2) a population-based study of CVD events. First, patients with psoriasis (N = 190) underwent fludeoxyglucose F 18 positron emission tomography/computed tomography (duration effect reported as a β-coefficient). Second, MACE risk was examined by using nationwide registries (adjusted hazard ratios in patients with psoriasis (n = 87,161) versus the general population (n = 4,234,793). In the human imaging study, patients were young, of low CV risk by traditional risk scores, and had a high prevalence of cardiometabolic diseases. Vascular inflammation by fludeoxyglucose F 18 positron emission tomography/computed tomography was significantly associated with disease duration (β = 0.171, P = .002). In the population-based study, psoriasis duration had strong relationship with MACE risk (1.0% per additional year of psoriasis duration [hazard ratio, 1.010; 95% confidence interval, 1.007-1.013]). These studies utilized observational data. We found detrimental effects of psoriasis duration on vascular inflammation and MACE, suggesting that cumulative duration of exposure to low-grade chronic inflammation may accelerate vascular disease development and MACEs. Providers should consider inquiring about duration of disease to counsel for heightened CVD risk in psoriasis.

<h3>Background</h3> Pruritus (itch) is a cardinal symptom in atopic dermatitis (AD). <h3>Objective</h3> To evaluate the timing and effect of dupilumab on itch. <h3>Methods</h3> Analysis of data from 1505 patients with moderate to severe AD included in 4 randomized controlled studies, treated for up to 52 weeks. Adults received dupilumab 300 mg every 2 weeks or placebo monotherapy (SOLO 1: NCT02277743; SOLO 2: NCT02277769), with concomitant topical corticosteroids (CHRONOS: NCT02260986); adolescents (≥12 to <18 y) were treated with dupilumab monotherapy every 2 weeks (200 mg for baseline weight of <60 kg; 300 mg for baseline weight of ≥60 kg) or placebo (AD ADOL: NCT03054428). <h3>Results</h3> Dupilumab showed significant rapid improvements from baseline in daily Peak Pruritus Numerical Rating Scale scores versus placebo, by day 2 in adults and day 5 in adolescents. At treatment end, dupilumab vs placebo/control had greater least-squares mean percent change from baseline in the weekly average of Peak Pruritus Numerical Rating Scale scores: SOLO −47.5% vs −20.5%; AD-ADOL −47.9% vs −19.0%; CHRONOS −57.3% vs −30.9% (<i>P</i> < .0001 for all). <h3>Limitations</h3> Short duration of monotherapy trials (16 weeks). <h3>Conclusion</h3> Across 4 randomized trials, dupilumab treatment showed rapid and sustained improvements in the magnitude of itch, starting with first dose; responses progressively increased and were sustained through to the end of treatment, up to 1 year.

Fingernail psoriasis is difficult to treat.The objective was to evaluate the effect of ixekizumab, a monoclonal antibody selectively targeting IL-17A, on fingernail psoriasis.This Phase 3, double-blind trial (UNCOVER-3) randomized patients to placebo, etanercept (50-mg twice weekly), or 80 mg ixekizumab as one injection every 4 (IXE Q4W) or 2 weeks (IXE Q2W) after a 160-mg starting dose. At Week 12, ixekizumab patients received open-label IXE Q4W through Week 60; placebo patients received a 160-mg starting ixekizumab dose and etanercept patients a 4-week placebo washout before starting IXE Q4W. Efficacy was assessed by mean per cent Nail Psoriasis Severity Index (NAPSI) improvement at Weeks 12 and 60.Of 1346 patients in the UNCOVER-3 trial, this subgroup analysis included only patients with baseline fingernail psoriasis: 116 (60.1%) placebo, 236 (61.8%) etanercept, 228 (59.1%) IXE Q4W and 229 (59.5%) IXE Q2W. At Week 12, greater mean per cent NAPSI improvements were achieved in IXE Q4W (36.7%) and IXE Q2W (35.2%) vs. placebo (-34.3%, P < 0.001 each comparison) and etanercept (20.0%, P = 0.048 vs. Q4W, P = 0.072 vs. Q2W). At Week 60, mean per cent NAPSI improvement was >80% regardless of initial treatment. At Week 12 (nonresponder imputation), complete resolution (NAPSI = 0) was achieved in 19.7% (IXE Q4W), 17.5% (IXE Q2W), 4.3% (placebo, P < 0.001 each comparison) and 10.2% (etanercept, P < 0.05 each comparison) of patients. By Week 60, >50% of patients achieved complete resolution.At Week 12, significant improvements in fingernail psoriasis were achieved with ixekizumab therapy. With IXE Q4W maintenance dosing, additional improvement was demonstrated through 60 weeks, and >50% of patients achieved complete resolution. Registered at clinicaltrials.gov: NCT01646177.

Background There is a significant association between psoriasis and inflammatory bowel disease (IBD). Many treatments for psoriasis and psoriatic arthritis are also used for IBD. Objective To assess therapeutic options for patients with psoriasis and concurrent IBD. Methods A systematic literature search was performed for clinical studies of biologic and systemic psoriasis medications in psoriasis, psoriatic arthritis, ulcerative colitis, and Crohn's disease, for the period from January 1, 1947, to February 14, 2017. Randomized, controlled, double-blinded studies were selected if available. If not, the next highest level of available evidence was selected. Results Of the 2282 articles identified, 132 were selected. Infliximab and adalimumab have demonstrated efficacy in psoriasis, psoriatic arthritis, ulcerative; colitis, and Crohn's disease. Ustekinumab has demonstrated efficacy in psoriasis, psoriatic arthritis, and Crohn's disease. Certolizumab has demonstrated efficacy in psoriatic arthritis and Crohn's disease. Etanercept, secukinumab, brodalumab, and ixekizumab have demonstrated efficacy in psoriasis and psoriatic arthritis but may exacerbate or induce IBD. Guselkumab has demonstrated efficacy in psoriasis. Limitations There are no known clinical trials of treatment specifically for concurrent psoriasis and IBD. Conclusions Infliximab and adalimumab have demonstrated efficacy in psoriasis, psoriatic arthritis, ulcerative colitis, and Crohn's disease; other agents have demonstrated efficacy for some, but not all, of these indications. There is a significant association between psoriasis and inflammatory bowel disease (IBD). Many treatments for psoriasis and psoriatic arthritis are also used for IBD. To assess therapeutic options for patients with psoriasis and concurrent IBD. A systematic literature search was performed for clinical studies of biologic and systemic psoriasis medications in psoriasis, psoriatic arthritis, ulcerative colitis, and Crohn's disease, for the period from January 1, 1947, to February 14, 2017. Randomized, controlled, double-blinded studies were selected if available. If not, the next highest level of available evidence was selected. Of the 2282 articles identified, 132 were selected. Infliximab and adalimumab have demonstrated efficacy in psoriasis, psoriatic arthritis, ulcerative; colitis, and Crohn's disease. Ustekinumab has demonstrated efficacy in psoriasis, psoriatic arthritis, and Crohn's disease. Certolizumab has demonstrated efficacy in psoriatic arthritis and Crohn's disease. Etanercept, secukinumab, brodalumab, and ixekizumab have demonstrated efficacy in psoriasis and psoriatic arthritis but may exacerbate or induce IBD. Guselkumab has demonstrated efficacy in psoriasis. There are no known clinical trials of treatment specifically for concurrent psoriasis and IBD. Infliximab and adalimumab have demonstrated efficacy in psoriasis, psoriatic arthritis, ulcerative colitis, and Crohn's disease; other agents have demonstrated efficacy for some, but not all, of these indications.

Engaging global key opinion leaders, the International Psoriasis Council (IPC) held a day-long roundtable discussion with the primary purpose to discuss the treatment goals of psoriasis patients and worldwide barriers to optimal care. Setting clear expectations might ultimately encourage undertreated psoriasis patients to seek care in an era in which great gains in therapeutic efficacy have been achieved. Here, we discuss the option for early treatment of all categories of psoriasis to alleviate disease impact while emphasizing the need for more focused attention for psoriasis patients with mild and moderate forms of this autoimmune disease. In addition, we encourage policy changes to keep pace with the innovative therapies and clinical science and highlight the demand for greater understanding of treatment barriers in resource-poor countries.

Abstract Background and Aims Epidemiological studies have established an association between psoriasis and inflammatory bowel disease [IBD], i.e. ulcerative colitis [UC] and Crohn’s disease [CD], but results are inconsistent. The aim of this study was therefore to quantify the prevalences and association between IBD and psoriasis. Methods PubMed, Web of Science, and EMBASE were searched from database inception through April 2018 for studies reporting data on psoriasis among patients with IBD and vice versa. Meta-analysis was performed to estimate, respectively, the prevalences and association between IBD and psoriasis. Data extraction was according to the PRISMA guideline, and quality assessment was made using the Newcastle-Ottawa Scale. The main outcomes were the proportion of psoriasis patients with IBD and vice versa, as well as the association (odds ratio [OR]) of IBD in psoriasis and psoriasis in IBD, respectively. Results Based on quantitative analysis of 93 studies, the prevalence of psoriasis in CD and in UC was 3.6% (95% confidence interval [CI] 3.1%–4.6%) and 2.8% [95% CI 2.0%–3.8%] respectively. The prevalence of CD and UC was 0.7% [95% CI 0.2%–1.3%] and 0.5% [95% CI 0.3%–0.8%], respectively, among patients with psoriasis. Presence of CD or UC was significantly associated with psoriasis, with OR 2.0 [95% CI 1.4–2.9] and OR 1.5 [95% CI 1.2–2.0], respectively. Presence of psoriasis was significantly associated with CD: OR 2.2 [95% CI 1.6–3.1] and with UC: OR 1.6 [95% CI 1.3–2.0]. Conclusions We found significant bidirectional associations between psoriasis and IBD, warranting increased awareness among clinicians in the diagnostic process, especially in children and adolescents with IBD. Last, this study showed an increased frequency of paradoxical psoriasis in patients treated with biologics.

The emergence of data from clinical trials of biologics, the approval of new biologics, and our improved understanding of psoriasis pathogenesis have increased the therapeutic possibilities for the treatment of moderate-to-severe psoriasis. Biologics currently approved for the treatment of psoriasis include tumor necrosis factor inhibitors, interleukin (IL)-17 inhibitors, ustekinumab (an IL-12/23 inhibitor), and IL-23 inhibitors. Data from clinical trials and studies of the safety and efficacy of biologics provide essential information for the personalization of patient care. We discuss the benefits and disadvantages of biologics as a first-line treatment choice, update treatment recommendations according to current evidence, and propose psoriasis treatment algorithms. Our discussion includes the following comorbid conditions: psoriatic arthritis, multiple sclerosis, congestive heart failure, inflammatory bowel disease, hepatitis B, nonmelanoma skin cancer, lymphoma, and latent tuberculosis. We make evidence-based treatment recommendations for special populations, including pediatric patients, patients with coronavirus 2019 (COVID-19), and pregnant and breastfeeding patients with psoriasis. Ultimately, individualized recommendations that consider patient preferences, disease severity, comorbid conditions, and additional risk factors should be offered to patients and updated as new trial data emerges.

Risankizumab has demonstrated efficacy and safety in patients with moderate-to-severe plaque psoriasis in randomized clinical trials.To evaluate safety data from risankizumab psoriasis phase I-III clinical trials.Short-term safety (through week 16) was analysed using integrated data from five phase II and III clinical trials. Long-term safety was evaluated using integrated data from 17 phase I-III completed and ongoing trials.Short-term safety analyses included 1306 patients receiving risankizumab 150 mg and 300 patients receiving placebo [402·2 and 92·0 patient-years (PY) of exposure, respectively]. Long-term analyses included 3072 risankizumab-treated patients (exposure: 7927 PY). The median (excluding four outliers) treatment duration was 2·9 years (range 2 days to 5·9 years). Exposure-adjusted adverse event rates did not increase with long-term treatment (318 vs. 171 events per 100 PY for short- and long-term analyses). With long-term risankizumab treatment, rates of serious adverse events were 7·8 per 100 PY, serious infections 1·2 per 100 PY, nonmelanoma skin cancer (NMSC) 0·7 per 100 PY, malignant tumours excluding NMSC 0·5 per 100 PY, and adjudicated major adverse cardiovascular events 0·3 per 100 PY, with no important identified risks. Limitations include that the study inclusion and exclusion criteria varied and that three studies enrolled ≤ 50 patients.Risankizumab demonstrated a favourable safety profile over short- and long-term treatment in patients with moderate-to-severe psoriasis.

To the Editor: Generalized pustular psoriasis (GPP) is a chronic, rare, life-threatening skin disease, characterized by recurrent flares of widespread sterile pustules.1-3 There are no globally accepted treatment guidelines, and, until recently, there were no approved GPP-specific medications.2-4 Real-world GPP treatment patterns are poorly characterized. Supplementary material, available via Mendeley at https://doi.org/10.17632/t4fmhr5snv.1.

Psoriasis (PsO) and psoriatic arthritis (PsA) are chronic T cell-mediated inflammatory diseases that manifest not only in the skin and joints but also in the form of cardiometabolic disturbances, which include insulin resistance, dyslipidemia, and obesity. Thus, PsO and PsA patients are predisposed to metabolic syndrome (MetS), diabetes, and cardiovascular disease. In recent years, the introduction of targeted therapy in the form of tumor necrosis factor-alpha (TNF-alpha) antagonists, such as infliximab, etanercept, and adalimumab has been an important and effective addition to the treatment armamentarium for PsO and PsA. Although TNF-alpha antagonists have produced promising results clinically in reducing cutaneous and joint manifestations of PsO and PsA, their effects on MetS components in these patients are presently unclear. This review summarizes the current limited evidence on the effects of TNF-alpha antagonists on MetS components in PsO and PsA patients and extrapolates from related literature in rheumatoid arthritis, which is also a T cell-mediated inflammatory disease, for additional information.

To investigate whether obesity and cardiovascular risk factors are associated with psoriasis in children and adolescents.For this population-based, cross-sectional study, measured weight and height, laboratory data, and psoriasis diagnoses were extracted from electronic medical records of 710,949 patients age 2 to 19 years enrolled in an integrated health plan. Weight class was assigned on the basis of body mass index-for-age.The OR for psoriasis was 0.68, 1.00, 1.31, 1.39, and 1.78 (95% CI, 1.49 to 2.14) for underweight, normal-weight, overweight, moderately obese, and extremely obese children, respectively (P for trend < .001). The OR for psoriasis treated with systemic therapy or phototherapy as an indicator of severe or widespread psoriasis was 0.00, 1.00, 2.78, 2.93, and 4.19 (95% CI, 1.81 to 9.68) for underweight, normal-weight, overweight, moderately obese, and extremely obese children, respectively (P for trend < .003). In adolescents, mean total cholesterol, low-density lipoprotein cholesterol, triglycerides, and alanine aminotransferase were significantly higher in children with psoriasis compared with children without psoriasis after adjustment for body mass index.Overweight and obesity are associated with higher odds of psoriasis in youths. Independent of body weight, adolescent patients with psoriasis have higher blood lipids. These data suggest that pediatricians and dermatologists should screen youths with psoriasis for cardiovascular disease risk factors.

Few studies based in well-defined North American populations have examined the occurrence of juvenile idiopathic arthritis (JIA), and none has been based in an ethnically diverse population. We used computerized healthcare information from the Kaiser Permanente Northern California membership to validate JIA diagnoses and estimate the incidence and prevalence of the disease in this well-characterized population.We identified children aged ≤ 15 years with ≥ 1 relevant International Classification of Diseases, 9th edition, diagnosis code of 696.0, 714, or 720 in computerized clinical encounter data during 1996-2009. In a random sample, we then reviewed the medical records to confirm the diagnosis and diagnosis date and to identify the best-performing case-finding algorithms. Finally, we used the case-finding algorithms to estimate the incidence rate and point prevalence of JIA.A diagnosis of JIA was confirmed in 69% of individuals with at least 1 relevant code. Forty-five percent were newly diagnosed during the study period. The age- and sex-standardized incidence rate of JIA per 100,000 person-years was 11.9 (95% CI 10.9-12.9). It was 16.4 (95% CI 14.6-18.1) in girls and 7.7 (95% CI 6.5-8.9) in boys. The peak incidence rate occurred in children aged 11-15 years. The prevalence of JIA per 100,000 persons was 44.7 (95% CI 39.1-50.2) on December 31, 2009.The incidence rate of JIA observed in the Kaiser Permanente population, 1996-2009, was similar to that reported in Rochester, Minnesota, USA, but 2 to 3 times higher than Canadian estimates.

Drug survival measures the length of time until discontinuation of a drug. The length of time a patient remains on a biologic drug is impacted by several factors such as tolerability, side effects, safety profile and effectiveness. To evaluate the long-term drug survival, data of the most commonly prescribed biologic medications used in the treatment of psoriasis, a systematic review was conducted. A literature search using PubMed, the Cochrane Library and the Cumulative Index to Nursing and Allied Health Literature from January 1 2010 to October 28 2016 identified 3734 abstracts. Of which, 36 publications with over 40,000 patients met the inclusion criteria. The median overall drug survival for ustekinumab, adalimumab, infliximab and etanercept was 38.0, 36.5, 26.6 and 24.7 months, respectively. The mean annual drug survival rate of TNF inhibitors was 70%, 57%, 51%, 45% and 41% at years-1, 2, 3, 4 and 5, respectively. The 5-year mean annual drug survival rate of ustekinumab was 87%, 78%, 70%, 71% and 51%, respectively. Based on our findings, ustekinumab appears to have a longer drug survival with lower rates of discontinuation compared to tumor necrosis factor inhibitors.

Aim: The occurrence of mental health comorbidities such as depression, anxiety, and suicidal ideation or behavior is not uncommon in the context of psoriasis. The negative influence of psoriatic disease on a patient’s physical and mental well-being, in combination with overlapping pathophysiology, increase the risk for clinically significant psychiatric conditions. These psychiatric conditions, in turn, influence the patient’s outlook and potentially, prognosis. Although the healthcare community increasingly recognizes the association of mental health comorbidities with psoriasis, the extent of the correlation is not fully appreciated. To better understand the relationship between mental health comorbidities and psoriasis, including prevalence, risk factors, and response of psychiatric comorbidities to psoriasis treatment, a narrative review of the published literature was conducted.Methods: Data from epidemiologic, observational, and clinical studies demonstrate a substantially greater mental health comorbidity burden in patients with psoriasis compared with those without psoriasis or patients with other dermatologic conditions.Result: The influence of contemporary drug therapies on measures of depression and anxiety are predominantly positive, although further data are needed to better understand the effects of long-term therapy.Conclusion: Clinicians should consider the heightened potential for mental health comorbidities when determining an optimal management strategy for their patients with psoriasis.

Background Psoriasis is a risk factor for cardiovascular events. Objective To assess the risk of major cardiovascular events and the effect of cumulative treatment exposure on cardiovascular event risk in patients with psoriasis treated with tumor necrosis factor–α inhibitors (TNFis) versus phototherapy. Methods Adult patients with psoriasis were selected from a large US administrative claims database (from the first quarter of 2000 through the third quarter of 2014) and classified in 2 mutually exclusive cohorts based on whether they were treated with TNFis or phototherapy. Cardiovascular event risk was compared between cohorts using multivariate Cox proportional hazards models. Cumulative exposure was defined based on treatment persistence. Results A total of 11,410 TNFi and 12,433 phototherapy patients (psoralen plus ultraviolet A light phototherapy, n = 1117; ultraviolet B light phototherapy, n = 11,316) were included in this study. TNFi patients had a lower risk of cardiovascular events compared to phototherapy patients (adjusted hazard ratio 0.77, P < .05). The risk reduction associated with 6 months of cumulative exposure was 11.2% larger for patients treated with TNFis compared to phototherapy (P < .05). Limitations Information on psoriasis severity and mortality was limited/not available. Conclusions Patients with psoriasis who were treated with TNFis exhibited a lower cardiovascular event risk than patients treated with phototherapy. Cumulative exposure to TNFis was associated with an incremental cardiovascular risk reduction compared to phototherapy. Psoriasis is a risk factor for cardiovascular events. To assess the risk of major cardiovascular events and the effect of cumulative treatment exposure on cardiovascular event risk in patients with psoriasis treated with tumor necrosis factor–α inhibitors (TNFis) versus phototherapy. Adult patients with psoriasis were selected from a large US administrative claims database (from the first quarter of 2000 through the third quarter of 2014) and classified in 2 mutually exclusive cohorts based on whether they were treated with TNFis or phototherapy. Cardiovascular event risk was compared between cohorts using multivariate Cox proportional hazards models. Cumulative exposure was defined based on treatment persistence. A total of 11,410 TNFi and 12,433 phototherapy patients (psoralen plus ultraviolet A light phototherapy, n = 1117; ultraviolet B light phototherapy, n = 11,316) were included in this study. TNFi patients had a lower risk of cardiovascular events compared to phototherapy patients (adjusted hazard ratio 0.77, P < .05). The risk reduction associated with 6 months of cumulative exposure was 11.2% larger for patients treated with TNFis compared to phototherapy (P < .05). Information on psoriasis severity and mortality was limited/not available. Patients with psoriasis who were treated with TNFis exhibited a lower cardiovascular event risk than patients treated with phototherapy. Cumulative exposure to TNFis was associated with an incremental cardiovascular risk reduction compared to phototherapy.

Psoriasis is associated with multiple co-morbid medical conditions. The purpose of this study is to evaluate the relationships between psoriasis and cardiovascular disease, psoriatic arthritis, mental health conditions, and immune-mediated diseases, respectively. A literature search was performed during the study period January 1, 2015 to December 18, 2018. Of 2,499 records identified, 28 met our criteria selection and were included in this review. The relationships between psoriasis and these multiple comorbid disease conditions are discussed and are important to consider when developing the treatment plan and overall management of patients with psoriasis. Early recognition and treatment of comorbid disease conditions is important to help improve the quality of life for these patients.

Abstract Immunosuppressive therapies, effective in treating inflammatory disorders such as psoriasis, increase the risk of serious infections, such as tuberculosis ( TB ). For example, tumour necrosis factor ( TNF )‐alpha inhibitors significantly increase the risk of TB reactivation in patients with latent TB infection (LTBI), which has led clinicians to routinely test for TB prior to initiation of these medications. This protocol has since extended to other, newer immunomodulatory therapies for psoriasis, such as interleukin ( IL )‐17 inhibitors, including secukinumab, ixekizumab and brodalumab. We conducted a systematic review to examine whether there is any evidence that IL ‐17 inhibitor therapy for psoriasis increases the risk of TB reactivation. Using PubMed and EMBASE , our literature search resulted in 139 total articles. After manually reviewing each article for the discussion of IL ‐17 inhibitors for psoriasis, with data originating from clinical trials, and assessment for incidence of TB reactivation, 23 articles met the full inclusion criteria for our review. Overall, we found no cases of TB reactivation in patients treated with IL ‐17 inhibitors for psoriasis. This suggests that IL ‐17 inhibitors may be safely used in psoriasis patients with LTBI who receive appropriate LTBI treatment. However, long‐term real‐world studies are warranted to further evaluate this risk.

To the Editor: The dermatology community remains concerned about the risk of COVID-19 in individuals with atopic dermatitis (AD). Using Symphony Health-derived data from the COVID-19 Research Database,1 we aimed to assess the risk of contracting COVID-19 in adults with AD while controlling for demographic factors and comorbidities known or speculated to be COVID-19 risk factors and assess the risk of contracting COVID-19 in adults with AD treated with dupilumab.

Biologics are important in treating patients with hidradenitis suppurativa (HS). However, to our knowledge, data on their real-life performance and treatment patterns in HS are limited.To examine the drug survival of biologic therapies for HS in a real-world setting.This cohort study included all patients with HS between January 1, 2005, and December 31, 2018, who were treated with biologics at the 5 academic hospital clinics where all biologic treatment for HS is conducted in Denmark. Biologics included adalimumab, anakinra, certolizumab pegol, etanercept, golimumab, infliximab, secukinumab, and ustekinumab. Data were analyzed between June 1, 2021, and June 20, 2021.Drug survival was depicted through Kaplan-Meier curves, and Cox regression models were used to calculate adjusted (age, sex, previous number of biologic treatment series) hazard ratios (aHRs) with 95% CIs for the risk of treatment discontinuation. Switching patterns were visualized through a Sankey diagram.The study comprised 241 patients (176 women [61.8%]; total of 386 treatment series) with a mean (SD) age of 41.8 (12.6) years at initiation of first biologic therapy. There were a total of 256 (189 [73.8%] biologic naive), 66 (32 [48.5%] biologic naive), 23 (9 [39.1%] biologic naive), and 22 (9 [40.9%] biologic naive) treatment series with adalimumab, infliximab, etanercept, and ustekinumab, respectively. The median time to discontinuation was 36.0 (IQR, 21.9-63.0), 28.7 (IQR, 15.1-62.9), 26.0 (IQR, 16.9-155.9), and 17.9 weeks (IQR, 12.9-41.0) for adalimumab, infliximab, ustekinumab and etanercept, respectively. The risk of drug discontinuation was significantly higher for etanercept compared with adalimumab (aHR, 1.81; 95% CI, 1.16-2.82), infliximab (aHR, 1.77; 95% CI, 1.03-3.05), and ustekinumab (aHR, 2.49; 95% CI, 1.12-5.52), whereas no difference was observed when comparing these 3 therapies with each other. We found no significant differences in drug survival for biologic-naive vs nonnaive treatment series. Increasing C-reactive protein levels (aHR, 1.01; 95% CI, 1.00-1.03) and concomitant antibiotic treatment (aHR, 2.82; 95% CI, 1.36-5.86) were associated with the risk of discontinuing infliximab therapy. Men (aHR, 0.69; 95% CI, 0.51-0.91) had a reduced risk of discontinuing use of adalimumab.In this cohort study, drug survival was comparable between adalimumab, infliximab, and ustekinumab but significantly lower for etanercept. There were no differences in drug survival among biologic-naive and nonnaive patients.

Background: Clindamycin, a lincosamide antibiotic, was the 125th most prescribed medicine in the US in 2020. Topical formulations that combine clindamycin with benzoyl peroxide or a retinoid are commonly used for acne vulgaris (AV) treatment. While oral and topical clindamycin carry warnings/contraindications regarding the development of gastrointestinal (GI) adverse events (AEs), the real-world incidence of these AEs with topical clindamycin is unknown. The objective is to provide an overview of safety data for topical clindamycin when used for AV treatment.&#x0D; Methods: Safety data from published literature on PubMed® (case reports, clinical trials data, retrospective data), previously unpublished worldwide pharmacovigilance data (from January 1, 1900-December 31, 2022), and two unpublished retrospective cohort studies of US electronic medical records (EMR; January 1, 2011 to January 31, 2019) were reviewed, with a focus on inflammatory bowel disease (IBD) and GI AEs following topical clindamycin monotherapy or combination treatment&#x0D; Results: There have been only 4 published case reports of topical clindamycin-associated GI AEs, which were all published between the years 1981-1997. In 8 published pivotal phase 3 clinical trials of topical clindamycin monotherapy or combination treatment for AV, GI-related AEs were reported in 1.4% of clindamycin-treated participants (38/2,672; safety populations). According to the pharmacovigilance data, the rate of GI-related adverse drug reactions with topical clindamycin-containing products was 0.000045% (64/141,084,533). In 1 published retrospective report, there were 0 reports of colitis from the 1,124 patients estimated to have received topical clindamycin prescriptions in the years 1977-1980. In the first retrospective EMR study, results indicate that physicians prescribe topical clindamycin for AV treatment equally to patients with a history of IBD (19.0%; 98/515) or without (20.7%; 14,495/70,151). The second retrospective EMR study showed that among patients with AV and an initial prescription for topical clindamycin (monotherapy or combination; n=18,012), there were 3 (0.02%) incident cases of pseudomembranous colitis within 30 days; none of these cases had a history of IBD.&#x0D; Conclusions: A review of published case reports, clinical trials safety data, worldwide pharmacovigilance data, and retrospective US prescription data demonstrate that GI events—including colitis or pseudomembranous colitis—in patients exposed to topical clindamycin is extremely low, regardless of IBD history.&#x0D; Support: Ortho Dermatologics

ABSTRACT: Subcutaneous mycoses are caused by a variety of mostly tropical organisms, usually when they are implanted into the dermis or the subcutaneous tissue. They rarely disseminate or become systemic. Sporotrichosis, mycetoma, and chromoblastomycosis are more common subcutaneous mycoses than are rhinosporidiosis, zygomycosis, pheohyphomycosis, and lobomycosis.

Abstract Recent advances in biological therapies have proved highly effective in treating psoriasis and other inflammatory conditions, including psoriatic arthritis, rheumatoid arthritis, inflammatory bowel disease and ankylosing spondylitis. However, adverse effects related to their immunosuppression have been observed, including an increased propensity to viral infections. This review evaluates the evidence of herpes zoster ( HZ ) risk from biologics based on clinical reports, cohort studies and randomized controlled studies. The risk of HZ associated with these agents remains controversial, especially when comparing their risk with non‐biological therapy used to treat the same inflammatory conditions. This review specifically assesses the risk of the TNF inhibitors etanercept, adalimumab and infliximab, as well as interleukin‐12/23 inhibitor ustekinumab. We found multiple cohort studies, randomized controlled trials and case reports that suggest infliximab increases risk of HZ , whereas adalimumab, etanercept and ustekinumab HZ risk remain controversial. Nevertheless, HZ vaccination should be considered prior to initiation of biological therapy, particularly infliximab.

ESPRIT is an ongoing, 10-year, observational registry, evaluating long-term safety and effectiveness of adalimumab treatment in routine clinical practice for patients with moderate to severe, chronic plaque psoriasis.Initial 5-year results are reported.Two populations were analyzed: the "all-treated" population received 1 or more adalimumab doses in registry, continuing adalimumab treatment from a current prescription or previous study participation, and included the "new-prescription" population initiating adalimumab 4 weeks or earlier preregistry entry.Data were collected from September 26, 2008, through November 30, 2013, for all-treated (n = 6059), which included new-prescription (n = 2580, 42.6%); median registry exposure was 765 and 677 days, respectively. In all-treated, rate (events per 100 patient-years of total adalimumab exposure [E/100PY]) of serious treatment-emergent adverse events (inside or outside of the registry) was 4.3 E/100PY, serious infection 1.0 E/100PY, malignancies 0.9 E/100PY (nonmelanoma skin cancers 0.6 E/100PY; melanomas <0.1 E/100PY). Standardized mortality ratio was 0.30 (95% confidence interval 0.19-0.44). Physician Global Assessment clear or minimal (effectiveness parameter) was achieved by 57.0% at 12 months and 64.7% at 60 months of treatment.Observational data are subject to outcome-reporting bias.No new safety signals were observed with adalimumab treatment during this initial 5-year registry review. Observed number of deaths was below expected. As-observed effectiveness remained stable through 60 months.

AbstractIntroduction: Photodynamic therapy for psoriasis showed promise in the early 1990s with reports of plaque clearance following topical aminolevulinic acid – photodynamic therapy (ALA-PDT).Methods: In December 2013, we conducted a systematic search of the PubMed Medline database using the keywords “psoriasis” and “photodynamic therapy”.Results: Numerous clinical studies have failed to demonstrate a consistent, efficacious response to topical ALA-PDT. Furthermore, severe pain and burning sensations were repeatedly reported, many cases being intolerable for patients.Discussion: The variability in clinical response and the painful side effects have made topical ALA-PDT an unsuitable treatment option for chronic plaque psoriasis. Nonetheless, early clinical studies of other modalities such as topical hypericin and methylene blue, as well as systemic ALA and verteporfin, have shown that these photosensitizers are efficacious and much better tolerated than topical ALA.Conclusion: With the current landscape of phototherapy dominated by psoralen combined with ultraviolet A (PUVA) and narrow-band ultraviolet B (NB-UVB), an alternative light therapy utilizing the visible spectrum is certainly promising and a worthwhile endeavor to pursue.KeywordsALAaminolevulinic acidhypericinmethylene bluePpIXverteporfin Declaration of interestJ. J. W. received research funding from AbbVie, Amgen, Coherus Biosciences, Eli Lilly, Merck, Pfizer, and Sandoz; he is a consultant for Eli Lilly. Y. M. C. and L. A. do not have any potential conflicts of interest.

The introduction of biological drugs for the treatment of patients with psoriasis has revolutionized treatment paradigms and enabled numerous patients to achieve disease control with an acceptable safety profile. However, the high cost of biologics limits access to these medications for the majority of patients worldwide. In recent years, the introduction of biosimilars for inflammatory diseases has become a fast evolving field. The future use of biosimilars offers the potential for decreased cost and increased access to biologics for patients with psoriasis. For approval of biosimilars, different regulatory agencies use highly variable methods for definition, production, approval, marketing and postmarketing surveillance. Due to potential interchangeability between biologics and biosimilars, traceability and pharmacovigilance are required to collect accurate data about adverse events in patients with psoriasis; spontaneous reporting, registries and use of 'big data' should facilitate this process on a global basis. The current article describes biosimilar regulatory guidelines and examples of biosimilar uptake in clinical practice in several countries around the world. As it is apparent that biological therapy treatment decisions may become more physician independent, the International Psoriasis Council recommends that dermatologists should take an active role in the development of biosimilar prescribing policies with their respective healthcare settings and government agencies.

Head-to-head randomized studies comparing ixekizumab and secukinumab in the treatment of psoriasis are not available.To assess efficacy and quality of life using matching-adjusted indirect comparisons for treatment with ixekizumab vs. secukinumab.Psoriasis Area and Severity Index (PASI) improvement of at least 75%, 90% and 100% and Dermatology Life Quality Index (DLQI) 0/1 response rates for approved dosages of ixekizumab (160 mg at Week 0, then 80 mg every two weeks for the first 12 weeks) and secukinumab (300 mg at Weeks 0, 1, 2, 3 and 4, then 300 mg every 4 weeks) treatment were compared using data from active (etanercept and ustekinumab) and placebo-controlled studies. Comparisons were made using the Bucher (BU) method and two modified versions of the Signorovitch (SG) method (SG total and SG separate). Subsequently, results based on active treatment common comparators were combined using generic inverse-variance meta-analysis.In the meta-analysis of studies with active comparators, PASI 90 response rates were 12·7% [95% confidence interval (CI) 5·5-19·8, P = 0·0005], 10·0% (95% CI 2·1-18·0, P = 0·01) and 11·2% (95% CI 3·2-19·1, P = 0·006) higher and PASI 100 response rates were 11·7% (95% CI 5·9-17·5, P < 0·001), 12·7% (95% CI 6·0-19·4, P < 0·001) and 13·1% (95% CI 6·3-19·9, P < 0·001) higher for ixekizumab compared with secukinumab using BU, SG total and SG separate methods. PASI 75 results were comparable when SG methods were used and favoured ixekizumab when the BU method was used. Week 12 DLQI 0/1 response rates did not differ significantly.Ixekizumab had higher PASI 90 and PASI 100 responses at week 12 compared with secukinumab using adjusted indirect comparisons.

BackgroundThe impact of ixekizumab treatment for psoriasis on cardiovascular-related parameters in patients is unknown.ObjectiveTo investigate cardiovascular-related parameters in patients with psoriasis treated with ixekizumab.MethodsIn phase 3 trials, patients with moderate-to-severe psoriasis were randomized and treated with placebo, ixekizumab, or etanercept during the induction period (weeks 0-12; UNCOVER-1, UNCOVER-2, and UNCOVER-3). At week 12, responders were rerandomized to receive placebo or ixekizumab through the maintenance period (weeks 12-60; UNCOVER-1 and UNCOVER-2). Laboratory measures (fasting lipid profiles, glucose level, or high-sensitivity C-reactive protein [hsCRP] level), weight, blood pressure, and electrocardiograms were obtained through 60 weeks.ResultsBaseline parameters were within normal ranges with the exception of elevated triglyceride and hsCRP levels. After maintenance dosing, no significant changes were observed versus placebo for total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, triglyceride, apolipoprotein A1, apolipoprotein B, or fasting glucose levels or for systolic/diastolic blood pressure at 60 weeks. Importantly, low-density lipoprotein–to–high-density lipoprotein ratios remained stable during the induction and maintenance periods. HsCRP concentrations were significantly reduced versus placebo at 12 weeks and remained reduced at 60 weeks, although not significantly. Although transient changes were observed for some parameters during the induction period, these changes did not persist into the maintenance period.LimitationsA lack of echocardiogram evaluations.ConclusionsIxekizumab had a neutral impact on cardiovascular-related parameters in patients with psoriasis. The impact of ixekizumab treatment for psoriasis on cardiovascular-related parameters in patients is unknown. To investigate cardiovascular-related parameters in patients with psoriasis treated with ixekizumab. In phase 3 trials, patients with moderate-to-severe psoriasis were randomized and treated with placebo, ixekizumab, or etanercept during the induction period (weeks 0-12; UNCOVER-1, UNCOVER-2, and UNCOVER-3). At week 12, responders were rerandomized to receive placebo or ixekizumab through the maintenance period (weeks 12-60; UNCOVER-1 and UNCOVER-2). Laboratory measures (fasting lipid profiles, glucose level, or high-sensitivity C-reactive protein [hsCRP] level), weight, blood pressure, and electrocardiograms were obtained through 60 weeks. Baseline parameters were within normal ranges with the exception of elevated triglyceride and hsCRP levels. After maintenance dosing, no significant changes were observed versus placebo for total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, triglyceride, apolipoprotein A1, apolipoprotein B, or fasting glucose levels or for systolic/diastolic blood pressure at 60 weeks. Importantly, low-density lipoprotein–to–high-density lipoprotein ratios remained stable during the induction and maintenance periods. HsCRP concentrations were significantly reduced versus placebo at 12 weeks and remained reduced at 60 weeks, although not significantly. Although transient changes were observed for some parameters during the induction period, these changes did not persist into the maintenance period. A lack of echocardiogram evaluations. Ixekizumab had a neutral impact on cardiovascular-related parameters in patients with psoriasis.

Abstract Background Psoriasis is a systemic chronic inflammatory condition associated with increased risk of cardiovascular disease. Data demonstrating that decreased skin inflammation reduces cardiovascular events in patients with psoriasis may be generalizable to other chronic inflammatory states with heightened cardiovascular risk. Objective To determine whether tumour necrosis factor inhibitor ( TNF i) therapy is associated with decreased major adverse cardiovascular events ( MACE ) in patients with psoriasis. Methods In this retrospective cohort study using the KPSC health plan, patients had at least three ICD ‐9 codes for psoriasis and no antecedent MACE codes. Propensity score‐adjusted multivariable Cox regression assessed hazard ratios ( HR ) of MACE associated with TNF i use. Results After adjusting for cardiovascular risk factors, the TNF i cohort had significantly lower MACE HR compared with the topical cohort ( HR , 0.80; 95% CI , 0.66–0.98). The oral/phototherapy cohort had similar MACE HR compared with the topical cohort ( HR , 1.19 (95% CI , 0.99–1.42)). Conclusions We observed significantly lower MACE risk in patients with psoriasis receiving TNF i compared to topical or oral/phototherapy agents. TNF i therapy may have benefits beyond skin disease in mitigating cardiovascular event risk.

BackgroundThe risk of melanoma and hematologic cancers in patients with psoriasis is controversial.ObjectiveWe sought to assess the risk of melanoma and hematologic cancers in patients with psoriasis, and the association with different treatments.MethodsWe used case-control and retrospective cohort designs to determine melanoma or hematologic cancer risk in patients with psoriasis. Risk with treatment type was assessed using Fisher exact test.ResultsPatients with psoriasis had 1.53 times greater risk of developing a malignancy compared with patients without psoriasis (P < .01). There were no significant differences in malignancy risk among patients treated with topicals, phototherapy, systemics, or biologic agents. Patients with psoriasis and malignancy did not have significantly worse survival than patients without psoriasis.LimitationsIt is possible that patients developed malignancy subsequent to the follow-up time included in the study.ConclusionPatients with psoriasis may experience an elevated risk of melanoma and hematologic cancers, compared with the general population. The risk is not increased by systemic or biologic psoriasis therapies. The risk of melanoma and hematologic cancers in patients with psoriasis is controversial. We sought to assess the risk of melanoma and hematologic cancers in patients with psoriasis, and the association with different treatments. We used case-control and retrospective cohort designs to determine melanoma or hematologic cancer risk in patients with psoriasis. Risk with treatment type was assessed using Fisher exact test. Patients with psoriasis had 1.53 times greater risk of developing a malignancy compared with patients without psoriasis (P < .01). There were no significant differences in malignancy risk among patients treated with topicals, phototherapy, systemics, or biologic agents. Patients with psoriasis and malignancy did not have significantly worse survival than patients without psoriasis. It is possible that patients developed malignancy subsequent to the follow-up time included in the study. Patients with psoriasis may experience an elevated risk of melanoma and hematologic cancers, compared with the general population. The risk is not increased by systemic or biologic psoriasis therapies.

Numerous factors contribute to the onset and exacerbation of psoriasis. Genetic risk factors include HLA-Cw6 and mutations in the caspase recruitment domain family member 14 gene, CARD14. Environmental risk factors, including infectious diseases, medications, and lifestyle, also have been implicated. It is important for clinicians to be aware of these risk factors and triggers because they might provide insight into the pathogenesis of psoriasis as well as help patients understand more about their disease.

Use of Janus kinase 1 inhibitors in moderate-to-severe atopic dermatitis (AD) is associated with incident acne in adolescent and adults that is mostly mild, transient and treatable. There is a need for more knowledge about the risk and severity of acne in patients with AD.To examine the prevalence, incidence and risk of acne in adolescents and adults with AD using nationwide prescription data.A matched cohort study of 6600 adults with AD and 66 000 controls was conducted using routinely and prospectively collected nationwide administrative data. Adjusted hazard ratios (HR) are reported with 95% confidence intervals (CIs).The 12-month prevalence of acne was 3.7% in the general population and 3.9% among AD patients. The incidence rate of acne was highest among 12- to 18-year-old AD patients, and overall slightly higher in women with AD compared with males. The overall risk in patients with AD was similar with that of the general population (HR 0.96; 95% CI 0.88-1.06), whereas the risk of being treated for severe acne was reduced in AD patients (HR 0.59; 95% CI 0.47-0.73) and mainly among adolescents and young adults. The HR of acne increased with age reaching 1.41 (95% CI 1.07-1.87) for ages 30-39 years, and 2.07 (95% CI 1.42-3.03) for patients ≥40 years compared with controls.The risk and severity of acne in AD patients change with age and sex, which may be used for the risk assessment of acne following treatment with Janus kinase 1 inhibitors.

Switching therapies is common for patients with psoriasis.To quantify real-world switching rates and characteristics among patients initiating biologics over 24 months.Patients aged ≥18 years with ≥2 confirmed psoriasis diagnoses who initiated a new biologic were identified from a US-payer claims database (Merative® MarketScan®) Switching rates were reported over 24 months using Kaplan-Meier survival analysis, and multivariable Cox regression analyses were performed to identify associated patient characteristics.A total of 7997 patients were included, with overall treatment switch rates at 14.4% at 12 months and 26.0% at 24 months. IL-23 inhibitors were associated with the lowest risk of switching compared with TNF, IL-17, and IL-12/23 inhibitors over 24 months (p < 0.0001). Switch rates varied between specific biologics, with the lowest switch rates observed for patients treated with risankizumab at 8.5% followed by guselkumab at 15.7% over 24 months. Prior targeted immune modulator use, age, and female gender were predictors of switching (adjusted hazard ratio; 1.23, 1.31, and 1.40, respectively; p ≤ 0.0005).Claims data may be subject to data errors and reasons for switching cannot be determined.Switching was common in psoriasis patients using biologics over 24 months, with the lowest risk of switching observed with IL-23 inhibitors.

To the Editor: Cheent et al1Cheent K. Nolan J. Shariq S. Kiho L. Pal A. Arnold J. Case report: fatal case of disseminated BCG infection in an infant born to a mother taking infliximab for Crohn’s disease.J Crohns Colitis. 2010; 4: 603-605Abstract Full Text Full Text PDF PubMed Scopus (280) Google Scholar reported an alarming case of disseminated bacillus Calmette-Guérin (BCG) infection in an infant born to a mother who had received infliximab for Crohn’s disease throughout pregnancy. The infant was healthy and met all developmental milestones at 3 months of age when he received a routine BCG vaccine; he rapidly deteriorated after receiving the vaccination and died of disseminated BCG at 4.5 months.Treatment options for psoriasis patients in pregnancy are limited, and anti–tumor necrosis factor alpha (TNF-α) agents have been used by dermatologists in this context, given their current pregnancy category B drug label by the US Food and Drug Administration.2Katz J.A. Antoni C. Keenan G.F. Smith D.E. Jacobs S.J. Lichtenstein G.R. Outcome of pregnancy in women receiving infliximab for the treatment of Crohn’s disease and rheumatoid arthritis.Am J Gastroenterol. 2004; 99: 2385-2392Crossref PubMed Scopus (402) Google Scholar Infliximab, as a monoclonal IgG antibody to TNF-α, does not cross the placenta prior to 30 weeks’ gestation, but readily crosses in the third trimester of pregnancy. There are detectable levels in an infant’s serum from 2 to 7 months after birth.3Kane S. Ford J. Cohen R. Wagner C. Absence of infliximab in infants and breast milk from nursing mothers receiving therapy for Crohn’s disease before and after delivery.J Clin Gastroenterol. 2009; 43: 613-616Crossref PubMed Scopus (121) Google Scholar, 4Mahadevan U. Terdiman J.P. Church J. Vasiliauskas E. Gitis A. Dubinsky M.C. Infliximab levels in infants born to women with inflammatory bowel disease.Gastroenterology. 2007; 132: A44Google Scholar, 5Vasiliauskas E.A. Church J.A. Silverman N. Barry M. Targan S.R. Dubinsky M.C. Case report: evidence for transplacental transfer of maternally administered infliximab to the newborn.Clin Gastroenterol Hepatol. 2006; 4: 1255-1258Abstract Full Text Full Text PDF PubMed Scopus (242) Google ScholarThe case published by Cheent et al1Cheent K. Nolan J. Shariq S. Kiho L. Pal A. Arnold J. Case report: fatal case of disseminated BCG infection in an infant born to a mother taking infliximab for Crohn’s disease.J Crohns Colitis. 2010; 4: 603-605Abstract Full Text Full Text PDF PubMed Scopus (280) Google Scholar suggests that infants born to mothers receiving infliximab, and potentially other anti–TNF-α agents during pregnancy, in the third trimester may be unable to develop an appropriate immune response to live vaccines. We recommend postponing all live vaccines in children born to women who have used anti–TNF-α biologics for psoriasis in the third trimester until the infant is at least 7 months old. We also recommend that dermatologists consider discontinuing these biologics around 30 weeks of gestation when IgG is more likely to cross the placenta. To the Editor: Cheent et al1Cheent K. Nolan J. Shariq S. Kiho L. Pal A. Arnold J. Case report: fatal case of disseminated BCG infection in an infant born to a mother taking infliximab for Crohn’s disease.J Crohns Colitis. 2010; 4: 603-605Abstract Full Text Full Text PDF PubMed Scopus (280) Google Scholar reported an alarming case of disseminated bacillus Calmette-Guérin (BCG) infection in an infant born to a mother who had received infliximab for Crohn’s disease throughout pregnancy. The infant was healthy and met all developmental milestones at 3 months of age when he received a routine BCG vaccine; he rapidly deteriorated after receiving the vaccination and died of disseminated BCG at 4.5 months. Treatment options for psoriasis patients in pregnancy are limited, and anti–tumor necrosis factor alpha (TNF-α) agents have been used by dermatologists in this context, given their current pregnancy category B drug label by the US Food and Drug Administration.2Katz J.A. Antoni C. Keenan G.F. Smith D.E. Jacobs S.J. Lichtenstein G.R. Outcome of pregnancy in women receiving infliximab for the treatment of Crohn’s disease and rheumatoid arthritis.Am J Gastroenterol. 2004; 99: 2385-2392Crossref PubMed Scopus (402) Google Scholar Infliximab, as a monoclonal IgG antibody to TNF-α, does not cross the placenta prior to 30 weeks’ gestation, but readily crosses in the third trimester of pregnancy. There are detectable levels in an infant’s serum from 2 to 7 months after birth.3Kane S. Ford J. Cohen R. Wagner C. Absence of infliximab in infants and breast milk from nursing mothers receiving therapy for Crohn’s disease before and after delivery.J Clin Gastroenterol. 2009; 43: 613-616Crossref PubMed Scopus (121) Google Scholar, 4Mahadevan U. Terdiman J.P. Church J. Vasiliauskas E. Gitis A. Dubinsky M.C. Infliximab levels in infants born to women with inflammatory bowel disease.Gastroenterology. 2007; 132: A44Google Scholar, 5Vasiliauskas E.A. Church J.A. Silverman N. Barry M. Targan S.R. Dubinsky M.C. Case report: evidence for transplacental transfer of maternally administered infliximab to the newborn.Clin Gastroenterol Hepatol. 2006; 4: 1255-1258Abstract Full Text Full Text PDF PubMed Scopus (242) Google Scholar The case published by Cheent et al1Cheent K. Nolan J. Shariq S. Kiho L. Pal A. Arnold J. Case report: fatal case of disseminated BCG infection in an infant born to a mother taking infliximab for Crohn’s disease.J Crohns Colitis. 2010; 4: 603-605Abstract Full Text Full Text PDF PubMed Scopus (280) Google Scholar suggests that infants born to mothers receiving infliximab, and potentially other anti–TNF-α agents during pregnancy, in the third trimester may be unable to develop an appropriate immune response to live vaccines. We recommend postponing all live vaccines in children born to women who have used anti–TNF-α biologics for psoriasis in the third trimester until the infant is at least 7 months old. We also recommend that dermatologists consider discontinuing these biologics around 30 weeks of gestation when IgG is more likely to cross the placenta.

Biosimilars, sometimes called 'generic biologics', are no longer a vision for the future but a present-day reality. Drug manufacturers and regulatory authorities are charged with ensuring that these products are safe and effective. Because biologically produced medications are large, complex proteins, many factors affect the quality of the end product, including glycosylation and presence of impurities, and thus many factors need to be compared between an emerging biosimilar and its originator biologic. Indeed, preclinical analytical assessments to determine similarity to an originator biologic are critical and are considered to be the foundation for regulatory approval of biosimilars. Here, the science behind the preclinical development of biosimilars is discussed by members of the International Psoriasis Council, and suggestions are put forth to try to ensure that future biosimilars are produced in a high quality and standardized manner.

Psoriasis is a systemic inflammatory condition that is associated with a higher risk of cardiovascular (CV) disease. Tofacitinib is being investigated as a treatment for psoriasis.We sought to evaluate the effects of tofacitinib on CV risk factors and major adverse CV events (MACEs) in patients with plaque psoriasis.Changes in select CV risk factors and the incidence rate (IR) of MACEs were evaluated in patients who were treated with tofacitinib.Tofacitinib treatment was associated with small, dose-dependent increases in total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol, while the total/HDL cholesterol ratio was unchanged. There were no changes in blood pressure and glycated hemoglobin levels; C-reactive protein levels decreased. The IRs of a MACE were low and similar for both tofacitinib doses. Among 3623 subjects treated with tofacitinib, the total patient-years of exposure was 5204, with a median follow-up of 527 days, and the IR of MACEs was 0.37 (95% confidence interval, 0.22-0.57) patients with events per 100 patient-years.There was relatively short follow-up time for patients who had MACEs.While treatment with tofacitinib is associated with a small increase in cholesterol levels, the total/HDL cholesterol ratio does not change, there are no unfavorable changes in several CV risk factors, and the incidence of MACEs is low.

ESPRIT (NCT00799877) is an ongoing 10-year international prospective observational registry evaluating the long-term safety and effectiveness of originator adalimumab in routine clinical practice for adult patients with chronic plaque psoriasis. Herein, we report the long-term safety, effectiveness, and patient-reported outcomes (PROs) following adalimumab treatment over the first 7 years of the ESPRIT registry.All treatment-emergent (All-TE) adverse events (AE) since the initial (first ever) dose of adalimumab were assessed. Physician Global Assessment (PGA) and PROs (PROs for US patients only) were evaluated during registry participation.As of 30 November 2015, 6051 patients in the ESPRIT registry were analyzed, representing 23,660.1 patient-years (PY) of overall adalimumab exposure. The incidence rates for All-TE serious AEs, serious infections, and malignancies were 4.4, 1.0, and 1.0 events per 100 PY (E/100PY), respectively. The standardized mortality ratio for TE deaths in the registry was 0.27 (95% CI 0.18-0.38). During the registry's first 7 years, PGA "clear" or "minimal" was achieved by >50% of patients at each annual visit, and among US patients, the mean improvement from baseline in different PROs was maintained.No new safety signals were identified during the first 7 years of the registry, and safety was consistent with the known safety profile of adalimumab. The number of TE deaths was below the expected rate. During the registry's first 7 years, most of the patients remained free of All-TE cardiovascular events, serious infections, and malignancy. As-observed effectiveness of adalimumab and improvements from baseline in PROs were maintained through 7 years of registry participation.Abbvie.ClinicalTrials.gov identifier, NCT00799877.

Psoriasis impairs quality of life, but it is unknown whether psoriasis is also an independent risk factor for depression.To evaluate the incidence and risk of new and recurrent depression in patients with psoriasis.We used individual-level linkage of Danish administrative registers. Patients with psoriasis aged ≥ 18 years between 1 January 1997 and 31 December 2016 were matched 1 : 1 with individuals without psoriasis. Incidence rates were calculated and adjusted hazard ratios (HRs) estimated by Cox regression.There were 247 755 patients with psoriasis: 220 721 were treated with topicals (mild psoriasis), 24 771 with systemic nonbiologics (moderate psoriasis) and 2263 with biological therapy (severe psoriasis). The same number of matched referents without psoriasis were also analysed. During a maximum 20 years of follow-up, 45 641 patients with psoriasis and 36 299 referents developed depression. In adjusted models, the HRs (95% confidence interval) of depression were 1·19 (1·17-1·20), 1·19 (1·15-1·23) and 1·50 (1·23-1·84) for mild, moderate and severe psoriasis, respectively. The highest risk was observed among patients with severe psoriasis aged 40-50 years. Concurrent inflammatory bowel disease, but not psoriatic arthritis, was associated with increased risk of depression. The incidence of depression was markedly higher among patients with previous depression.Psoriasis was independently associated with risk of depression. These results may help clinicians identify particularly high-risk individuals.

With the increasing availability of biosimilars, the practice of switching therapies for non-medical reasons between an originator biologic and an analogous biosimilar has become more common. The evidence to support this practice mostly comes from single-switch randomized controlled trials (RCTs) and real-world (RW) evidence studies. However, as more biosimilars of the same originator enter the market, multiple switching events between originators and biosimilars is becoming a reality, despite limited evidence to support the efficacy and safety of such practice. Some countries have established guidelines, policies, or laws related to interchangeability and/or automatic substitution, whereas others have left these practices unregulated or controlled by other components of the healthcare system. Collectively, guidelines on single non-medical switching are often vague, with even less focus given to multiple non-medical switching, leaving this practice mostly unregulated. This narrative review will first discuss the current regulatory perspectives on non-medical switching and challenges associated with switching therapies, particularly with the availability of multiple biosimilars. We will then review the current evidence from RCTs and RW studies in the light of three different multiple-switch scenarios currently taking place in clinical practice: switching between an originator and a single biosimilar, switching between biosimilars of the same originator, and the clinical practice of switching back to the originator (i.e., switchbacks) after a failure of the initial non-medical switch to the analogous biosimilar.

To the Editor: Recent studies have linked psoriasis with emerging comorbidities, thus requiring up-to-date prevalence of psoriasis to quantify a changing disease burden.1 As a representative database of health status among US adults, the National Health and Nutrition Examination Survey (NHANES) produces reliable estimates of psoriasis prevalence and comorbidities. This study aimed to update psoriasis prevalence rates among US adults in the most recent 2013-2014 NHANES cycle.

Abstract Anti‐drug antibodies (ADAs) can form with certain biological medications, but their clinical significance is not fully understood. ADA formation in psoriasis patients treated with IL‐23 inhibitors was evaluated, looking at the incidence of ADAs, impact on clinical outcomes and association with adverse events. A systematic search of PubMed, Cochrane and Embase databases yielded 318 articles, which were manually reviewed. A total of 19 articles met the eligibility criteria. The incidence of ADAs with the IL‐23 inhibitors was as follows: 4.1–14.7% with guselkumab, 141–31% with risankizumab and 6.51–18% with tildrakizumab. The incidence of neutralizing antibodies ranged from 01–0.6% with guselkumab, 21–16% with risankizumab and 2.5 to 3.2% with tildrakizumab. There was no evidence of reduced efficacy of psoriasis treatment with ADA presence alone. However, some studies found a reduction in clinical response with high ADA titres or with the presence of neutralizing antibodies. A few studies reported that patients with ADAs to guselkumab and risankizumab had a higher incidence of injection site reactions (ISRs). There do not appear to be other adverse events associated with ADAs with IL‐23 inhibitors. Testing for presence of ADAs alone in this patient group does not appear to be predictive of treatment response. Clinically, it may be more productive to test for neutralizing antibodies or ADA titre values, although further investigation is required to show a definitive correlation.

The landscape of psoriasis treatments has undergone rapid change within the last decade and the dizzying speed of drug development has not slowed, with 4 notable entries into the psoriasis treatment armamentarium within the last year: tapinarof, roflumilast, deucravacitinib, and spesolimab. Several others are in late-stage development, and these therapies represent new mechanisms, pathways, and delivery systems, meaningfully broadening the spectrum of treatment choices for our patients. However, it can be quite difficult to keep track of all the medication options. This review aims to present the mechanisms and data on both newly available therapeutics for psoriasis and products in the pipeline that may have a notable impact on our treatment paradigm for psoriasis in the near future.

Genital herpes is one of the most common sexually transmitted diseases worldwide. Currently, there are three FDA-approved nucleoside analogs and other therapies such as foscarnet and cidofovir used to treat genital herpes. Resiquimod, the latest immune response modifier (IRM), has shown in vivo evidence of efficacy against herpes simplex virus (HSV) type 2. The first clinical trial involving resiquimod demonstrated that it reduced the recurrence rate of genital herpes, but phase III trials were suspended due to lack of efficacy. Resiquimod shows promise for other viral infections and as a vaccine adjuvant.

Phytophotodermatitis is a phototoxic reaction, occurring in skin exposed to sunlight after contact with plants containing furanocoumarins. Typical reactions are mild, showing erythema with post-inflammatory hyperpigmentation. A 6-year-old boy presented with marked, symmetric, painful erythema and edema of both hands that rapidly developed into dramatic bullae covering the entire dorsum of the hands. The history revealed that the hands had been bathed in lime juice for a prolonged period in the preparation of limeade.This report documents an unusual bullous presentation of phytophotodermatitis resulting from contact with furanocoumarins in local limes. This study was conducted to identify and measure the inciting substances from the rind and pulp of the limes.Psoralen, xanthotoxin, bergapten, and isopimpinellin content were measured by gas chromatography and high-pressure liquid chromatographyThe rind contained 6- to 182-fold concentrations of all furanocoumarins measured when compared with pulp. Bergapten was the most abundant substance in the rind.Hydration of the skin during the preparation of limeade combined with increased levels of bergapten in local limes to produce a dramatic bullous reaction. We encourage clinicians to consider the possibility of phytophotodermatitis in severe bullous skin reactions.

Bortezomib, a proteasome inhibitor approved for the treatment of multiple myeloma, has been reported to be associated with Sweet syndrome. However, careful review of the histopathology of the first reported case and our case revealed similar histologic and immunohistochemical findings (a mononuclear dermal infiltrate) and not the usual neutrophilic infiltrate of Sweet syndrome. We suggest that the dermatitis induced by bortezomib is best classified as "histiocytoid Sweet syndrome."

Little information is available on the prevalence of psoriasis in children and adolescents.We sought to estimate the prevalence of pediatric psoriasis in southern California and to investigate the validity of psoriasis diagnosis by a dermatologist compared with a nondermatologist.In a southern California population of 710,949 children who were enrolled in an integrated prepaid health plan in 2007 through 2008, cases of psoriasis were identified from electronic medical records and validated by medical chart review. Positive predictive values for valid diagnosis were reported for dermatologists and nondermatologists.The prevalence of pediatric psoriasis confirmed by medical chart review was 19/10,000 patients. The prevalence of psoriasis diagnosis (confirmed and unconfirmed) was 30/10,000 patients. The age at onset of psoriasis was slightly earlier in boys than in girls. The positive predictive value for a valid diagnosis of psoriasis was 63.7% when the diagnosis was made by any health care provider, 90.0% by a dermatologist, and 26.6% by a nondermatologist. The prevalence of psoriasis was higher in girls than in boys. Psoriasis affected 29 (95% confidence interval [CI] 27-32) non-Hispanic whites, 20 (95% CI 16-24) Asian/Pacific Islanders, 16 (95% CI 15-18) Hispanic whites, and 6 (95% CI 4-9) blacks per 10,000 patients.Information on the age at onset was estimated based on the first documented diagnosis of psoriasis.The overall prevalence of pediatric psoriasis was lower compared with other published studies. This could be in part a result of underdiagnosis because of greater sunlight exposure in southern California and a lower proportion of non-Hispanic whites in the population.

Journal of the European Academy of Dermatology and VenereologyVolume 23, Issue 1 p. 36-41 308-nm excimer laser in psoriasis vulgaris, scalp psoriasis, and palmoplantar psoriasis S Gattu, S Gattu University of California, Irvine, CA, USASearch for more papers by this authorRM Rashid, RM Rashid Department of Dermatology, MD Anderson Cancer Center, University of Texas, Houston, TX, USASearch for more papers by this authorJJ Wu, Corresponding Author JJ Wu Department of Dermatology, Kaiser Permanente, Los Angeles Medical Center, Los Angeles, CA, USA *Correspondence: JJ Wu. E-mail: [email protected]Search for more papers by this author S Gattu, S Gattu University of California, Irvine, CA, USASearch for more papers by this authorRM Rashid, RM Rashid Department of Dermatology, MD Anderson Cancer Center, University of Texas, Houston, TX, USASearch for more papers by this authorJJ Wu, Corresponding Author JJ Wu Department of Dermatology, Kaiser Permanente, Los Angeles Medical Center, Los Angeles, CA, USA *Correspondence: JJ Wu. E-mail: [email protected]Search for more papers by this author First published: 15 December 2008 https://doi.org/10.1111/j.1468-3083.2008.02942.xCitations: 32Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume23, Issue1January 2009Pages 36-41 RelatedInformation

Abstract Background Etanercept is a tumour necrosis factor‐alpha antagonist used for the treatment of moderate‐to‐severe psoriasis. Current opinion suggests that etanercept may have reduced efficacy in obese patients. Narrowband ultraviolet B (NB‐UVB) phototherapy is unaffected by body weight and the addition of NB‐UVB to etanercept therapy may supplement the efficacy of etanercept in these patients. Objective To evaluate the efficacy and safety of NB‐UVB phototherapy when administered in conjunction with 50 mg of etanercept once weekly in the treatment of obese patients with moderate‐to‐severe plaque psoriasis. Methods Thirty psoriasis patients with a body mass index (BMI) greater than 30 were enrolled into this randomized, ‘head‐to‐head’ comparison study. All subjects received 50 mg of etanercept twice weekly for 12 weeks and then randomized to receive either etanercept monotherapy or combination etanercept and NB‐UVB three times weekly for an additional 12 weeks. Treatment response was evaluated using Psoriasis Area and Severity Index (PASI), body surface area (BSA) and Physician’s Global Assessment (PGA) scores. Results Twenty‐five subjects completed the study. At 12 weeks, 48% of all patients achieved PASI 75. By Week 24, 62.5% of all patients achieved PASI 75. Patients in the etanercept monotherapy and combination etanercept and NB‐UVB phototherapy arms had similar rates of achieving PASI 75 (46.7% vs. 53.3% of each group, respectively). Conclusion Combination etanercept and NB‐UVB has similar efficacy to etanercept monotherapy in obese patients. This result indicates that even in the setting of obesity, the majority of patients respond well to etanercept, with or without NB‐UVB.

Abstract Background Psoriasis patients have relatively infrequent cutaneous viral infections compared to atopic dermatitis patients. Increased expression of four antiviral proteins ( MX 1, BST 2, ISG 15 and OAS 2) has been reported in psoriatic skin and genetic studies of psoriasis have identified susceptibility genes in antiviral pathways. Objective To determine if psoriasis is associated with pervasive expression of antiviral genes in skin and blood. Methods We performed RNA sequencing on skin samples of 18 subjects with chronic plaque psoriasis and 16 healthy controls. We examined the expression of a predefined set of 42 antiviral genes, each of which has been shown in previous studies to inhibit viral replication. In parallel, we examined antiviral gene expression in atopic dermatitis, non‐lesional psoriatic skin and psoriatic blood. We performed HIV ‐1 infectivity assays in CD 4+ peripheral blood T cells from psoriatic and healthy individuals. Results We observed significant overexpression of 16 antiviral genes in lesional psoriatic skin, with a greater than two‐fold increase in ISG 15, RSAD 2, IRF 7, MX 2 and TRIM 22 ( P &lt; 1E‐07). None of these genes was overexpressed in atopic dermatitis skin ( P &lt; 0.0001) or non‐lesional psoriatic skin. In contrast to the skin compartment, no differences in antiviral gene expression were detected in the peripheral blood of psoriasis cases compared to healthy controls. CD 4+ T cells from both psoriatic and healthy patients supported HIV ‐1 infection at a similar rate. Conclusion Our findings highlight psoriasis as an inflammatory disease with cutaneous but not systemic immune activation against viral pathogens.

<h3>Background</h3> The relationship between melanoma and chronic lymphocytic leukemia (CLL) or non-Hodgkin lymphoma (NHL) has been minimally investigated. <h3>Objective</h3> The objective of this study was to examine the incidence of melanoma in patients with a history of CLL or NHL, and their associated mortality. <h3>Methods</h3> Cohorts of Kaiser Permanente Southern California members with a history of CLL and NHL were identified. Age-adjusted incidence density rates of melanoma among patients with CLL or NHL were compared with rates of melanoma among the general population of Kaiser Permanente Southern California patients. The mortality of patients with melanoma was examined using Cox proportional hazards modeling. <h3>Results</h3> The age-adjusted incidence rate per 100,000 person-years for melanoma among patients with either CLL or NHL was 107 (95% confidence interval 84.4-129.6) versus 25.9 among the general population (95% confidence interval 84.4-129.6, <i>P</i> < .001). Patients with melanoma and a history of CLL or NHL had 2.46 greater odds of death compared with those without CLL or NHL (95% confidence interval 1.77-3.41). <h3>Limitations</h3> This study was retrospective in nature; the <i>International Classification of Diseases, Ninth Revision</i> codes used may contain diagnostic errors; and only overall survival was used in our analysis. <h3>Conclusions</h3> Patients with a history of CLL or NHL have a higher incidence of melanoma. Patients with CLL or NHL who are subsequently given the diagnosis of melanoma have a higher mortality than patients with melanoma without a preceding diagnosis of CLL.

Background: Psoriasis may or may not be associated with a higher risk for myocardial infarction (MI). We sought to assess differences in MI incidence between control, mild psoriasis and severe psoriasis patients.Methods: We performed a retrospective cohort study of Kaiser Permanente Southern California members with psoriasis between 1 January 2004 and 30 June 2012, assessing the risk and incidence rates of MI.Results: There were 50 865 control patients matched to 10 173 patients with mild psoriasis and 19 205 control patients matched to 3841 patients with severe psoriasis. The MI incidence per 1000 person-years for mild psoriasis controls, mild psoriasis, severe psoriasis controls and severe psoriasis were 4.9, 6.7, 3.7 and 5.1, respectively. Upon multivariable analysis, mild psoriasis patients had a significantly higher risk of MI compared to matched control patients {hazard ratio (HR) = 1.31 [95% confidence interval (CI): 1.14, 1.51]} and severe psoriasis patients had a significantly higher risk of MI compared to matched control patients [HR = 1.28 (95% CI: 1.02, 1.60)].Conclusion: Patients with psoriasis are at higher risk for MI compared to control patients.

Treatment with systemic immunomodulatory agents is indicated for patients with moderate to severe plaque psoriasis and psoriatic arthritis. In these patients, surgery may confer an increased risk of infectious or surgical complications. We conducted a literature review to examine studies addressing the use of methotrexate, cyclosporine, and targeted immunomodulatory agents (tumor necrosis factor-alfa inhibitors, interleukin [IL]-12/23 inhibitors, IL-17 inhibitors) in patients undergoing surgery. We examined 46 total studies; the majority were retrospective studies in patients with rheumatoid arthritis and inflammatory bowel disease. One study in patients with psoriasis and psoriatic arthritis reviewed 77 procedures and did not find an elevated risk of postoperative complications with tumor necrosis factor-alfa and IL-12/23 inhibitors even with major surgeries. Based on level III evidence, infliximab, adalimumab, etanercept, methotrexate, and cyclosporine can be safely continued through low-risk operations in patients with psoriasis and psoriatic arthritis. For moderate- and high-risk surgeries, a case-by-case approach should be taken based on the patient's individual risk factors and comorbidities.

Background Venous thromboembolism (VTE) is a major public health concern. Lupus erythematosus (LE) is a chronic autoimmune disease ranging from localized cutaneous disease (CLE) to systemic involvement (SLE). Patients with SLE have an increased risk of venous thromboembolism (VTE), but little is known about the CLE-related risk of VTE. Methods To evaluate the risk of VTE in patients with SLE and CLE as compared to the general population, a retrospective cohort study was conducted. Incidence rates and hazard ratios (HRs) with 95% confidence intervals (CIs) from multivariable Cox regression models were used to evaluate and compare the risk of VTE. Registries of hospitalizations, outpatient visits, and prescription drug use were studied to determine the risk of VTE in patients with CLE and SLE and the general population between 1997 and 2011. Results A total of 3234 patients with CLE and 3627 patients with SLE were identified and compared to 5,590,070 individuals in the reference population. The incidence rates per 1000 year of VTE were higher in patients with LE, i.e. 1.20, 3.06, and 5.24 for the reference population, CLE, and SLE, respectively. In adjusted models, both CLE (HR 1.39; 95% CI 1.10–1.78) and SLE (HR 3.32; 95% CI 2.73–4.03) were associated with a statistically significant increased risk of VTE, compared to the reference population. Conclusion In this nationwide study, both CLE and SLE were significant risk factors for VTE. The results add to our understanding of comorbidities in patients with LE, and call for further studies and increased awareness of thromboembolic complications in patients with CLE.

Three main biologics target the IL-17 pathway; these include secukinumab, ixekizumab, brodalumab, all of which are approved for treatment of moderate-to-severe plaque psoriasis. We performed a systematic review of the literature to determine if IL-17 inhibitors are prone to develop anti-drug antibodies (ADA) and how efficacy of treatment is influenced. A total of 14 papers were reviewed. Only one secukinumab trial detected treatment-emergent ADA in 4 out of 996 (0.41%) patients during the 52-week treatment period. Two of these patients (1 on 150-mg retreatment as needed and 1 on 150-mg fixed interval) were found to have neutralizing antibodies; however, they were not associated with decreased efficacy. One paper reported ADAs against ixekizumab. One out of 1150 (9%) developed titers to ixekizumab after receiving 160-mg-loading dose followed by 80 mg every 2 weeks. Nineteen out of 1150 (1.7%) developed high titer (>1:1280) which impacted clinical outcomes. Three studies did detect ADA against brodalumab; however, none were neutralizing. It is difficult to draw a conclusion from our findings given the variability in ADA development. Most trials did not develop ADA, and if they did, the majority of the time they were not neutralizing. Only ixekizumab showed decreased efficacy, but no increased adverse events in cases with neutralizing ADA.

Cutaneous pain, a very broad, subjective, and complex symptom, is prevalent in patients with psoriasis. It is prompted by neurogenic inflammation and augmented by physical and psychosocial stress. Many psoriasis patients are troubled by aching, burning, stinging, tenderness, cramping, and tingling in their skin. However, there lacks a thorough and verified metric that allows patients to adequately report their unique skin pain experiences. Limited literature exists that aims to understand cutaneous pain in psoriasis patients; most studies focus on joint pain and generalized pain, and many do not specify the location of pain. This review explores and analyzes current literature on the etiology, assessment, burden, and management of skin pain in psoriasis patients. It emphasizes the significance of appropriately quantifying the skin pain experience in psoriasis and developing therapeutics that target the underlying processes that contribute to noxious skin sensations.

Introduction: Few studies have assessed the prevalence and features of axial spondyloarthritis (axSpA) and ankylosing spondylitis in diverse, population-based, community settings.Objectives: We used computerized diagnoses to estimate the prevalence of axSpA and ankylosing spondylitis in Kaiser Permanente Northern California (KPNC).Methods: We identified persons aged 18 years or older with 1 or more International Classification of Diseases, Ninth Revision (ICD-9) diagnosis Code 720.X (ankylosing spondylitis and other inflammatory spondylopathies) in clinical encounter data from 1996 through 2009 to estimate the prevalence of axSpA and ankylosing spondylitis.We reviewed medical records to confirm the diagnosis in a random sample and estimated the positive predictive value of computerized data to identify confirmed cases using various case definitions.Results: In the computerized data, 5568 adults had diagnostic codes indicating axSpA.On the basis of our case-finding approach using a single physician diagnosis code for ICD-9 720.X, the point prevalence of these conditions, standardized to the 2000 US Census, was 2.26 per 1000 persons for axSpA and 1.07 per 1000 for ankylosing spondylitis.Less than half of suspected cases saw a rheumatologist.The most specific algorithm for confirmed ankylosing spondylitis required 2 or more computerized diagnoses assigned by a rheumatologist, with 67% sensitivity (95% confidence interval, 64%-69%) and 81% positive predictive value (95% confidence interval, 79%-83%).Conclusions: Observed prevalence in the KPNC population, compared with national estimates for axSpA and ankylosing spondylitis, suggests there is substantial underrecognition of these conditions in routine clinical practice.However, use of computerized data is able to identify true cases of ankylosing spondylitis, facilitating population-based research.

Purpose: To compare the cost-effectiveness of the newly approved biologic drug, brodalumab, with other commonly used biologics for the treatment of moderate-to-severe psoriasis in the United States.Methods: An economic model was constructed in Excel to compare average costs to achieve Psoriasis Area and Severity Index (PASI) 75, 90 and 100 among moderate-to-severe psoriasis patients treated with biologics. Total annual costs to health plans associated with treatment with five different biologics were estimated and cost-effectiveness compared using the estimated average cost per PASI 75, PASI 90 and PASI 100.Results: Total annual costs to a health plan per patient with adalimumab, brodalumab, ixekizumab, secukinumab and ustekinumab were estimated at $51,246, $38,538, $65,484, $57,510 and $57,013. Mean annual treatment costs per PASI 75, 90 and 100 were the lowest for brodalumab, with the annual cost per PASI 75 for brodalumab, adalimumab, ixekizumab, secukinumab and ustekinumab estimated at $48,782, $82,655, $77,957, $75,671 and $87,243, per PASI 90 at $51,383, $119,178, $94,904, $108,509 and $130,615, and per PASI 100 at $87,585, $284,702, $176,983, $205,393, and $366,645.Conclusions: Brodalumab, which had the lowest drug cost and high drug efficacy, was associated with the lowest cost per PASI 75, 90 and 100 among the biologics evaluated.

Abstract Background The clinical meaningfulness of improvements in the Work Productivity and Activity Impairment Questionnaire for Psoriasis ( WPAI ‐PsO) reported by patients with psoriasis in response to treatment is unknown due to the lack of any publications that report minimal clinically importance differences ( MCID ) for WPAI ‐PsO outcomes. Objective To determine the MCID s for the work productivity loss and activity impairment domains of the Work Productivity and Activity Impairment Questionnaire for Psoriasis ( WPAI ‐PsO) using results from three Phase 3 trials of ixekizumab. Methods MCID s for WPAI ‐PsO domains were derived using treatment agnostic data from patients participating in UNCOVER ‐1/‐2/‐3. The analysis included patients randomized to placebo and two ixekizumab treatment groups (ixekizumab either every 2 weeks or 4 weeks) from the trials. WPAI ‐PsO was administered at baseline and Week 12 for UNCOVER ‐1/‐2/‐3 and at Weeks 24, 36, 52 and 60 in UNCOVER ‐1/‐2. MCID s for the WPAI ‐PsO domains through Week 12 were derived using an anchor‐based method supplemented with the distribution‐based method. Anchors included 75%/90%/100% improvement in Psoriasis Area and Severity Index, Static Physicians Global Assessment ( sPGA [0] and sPGA [0,1]) and Dermatology Life Quality Index MCID ). MCID s were triangulated using receiver operating characteristics ( ROC ) and distribution‐based methods. Results The analyses included 3126 patients (Placebo: 792, Ixekizumab: 2334). All anchors were shown to be valid. Significant differences in the domains of WPAI ‐PsO were observed between patients achieving clinically meaningful improvement in the validated anchors (all P ‐values &lt; 0.001). ROC analyses suggested a 20% improvement in the work productivity loss or activity impairment components best represented the benefit of meeting a clinical meaningful improvement in the validated anchors. The distribution‐based method supported the results of the anchor‐based method. Conclusion The MCID s for both the work productivity loss and the activity impairment domains of WPAI ‐PsO were estimated to be 20% in patients with PsO.

Purpose: Crude coal tar and its derivatives have been used in modern medicine for the treatment of psoriasis since at least 1925 as part of the Goeckerman regimen. To this day, coal tar remains a safe and highly effective option for the treatment of psoriasis vulgaris. However, the mechanism by which coal tar has its therapeutic effect is unknown. This review summarizes current knowledge of the mechanism by which coal tar has its therapeutic effect in the treatment of psoriasis vulgaris.Material and methods: A Pubmed search was conducted on March 13, 2017 for relevant English language journal articles on the subject and were relevant journal articles were included in this review.Results: Crude coal tar consists of thousands of ingredients, many of which are unidentified. Of these ingredients, the most research has gone into analyzing polycyclic aryl hydrocarbons. These hydrocarbons are thought to be the most likely component of crude coal tar that leads to its effects in psoriasis. Of the aryl hydrocarbons, carbazole has been the most well studied in psoriasis and is hypothesized as being responsible for the treatment efficacy of crude coal tar.Conclusions: Polycyclic aryl hydrocarbons, and specifically carbazole, are thought to be the mechanism by which crude coal tar has its effect in psoriasis. However, further research is warranted to fully characterize the mechanism of action of crude coal tar, with the potential to create new therapies for psoriasis.

Abstract The development of monoclonal antibodies targeting IL ‐12 and IL ‐23 has enhanced the therapeutic options available for psoriasis patients. Recent research suggests that IL ‐23 alone plays a role in the pathogenesis of psoriasis. The objective was to review the phase III clinical trial data for the anti‐ IL ‐23 agents to evaluate the safety and efficacy profile of each agent. We reviewed the results of the phase III clinical trials for the anti‐ IL ‐23 agents tildrakizumab and guselkumab. The results of phase III trials on risankizumab have not yet been reported. By week 12, the proportion of patients reaching Psoriasis Area and Severity Index ( PASI 75) was &gt;60% among the most efficacious dose of each agent. The percentage of patients achieving PASI 90 at week 16 was the primary endpoint for the phase III trials for guselkumab, which was above 70%. The safety profiles of the agents were comparable, with the most commonly reported adverse events of nasopharyngitis and upper respiratory tract infections. The anti‐ IL ‐23 agents demonstrated a rapid clinical improvement that is similar or superior to the improvement seen with currently marketed IL ‐17 inhibitors with a favourable short‐term safety profile. The results of the phase III trials support the notion that IL ‐23 is a potential target in psoriasis treatment.

Chronic plaque psoriasis is a common, currently incurable, immune-mediated skin disease affecting approximately 2-3% of the population worldwide (1). Patients frequently require lifelong management...

(2021). Characteristics of hospitalizations and emergency department visits due to generalized pustular psoriasis in the United States. Current Medical Research and Opinion: Vol. 37, No. 10, pp. 1697-1703.

Many patients with atopic dermatitis (AD) have a suboptimal response to systemic therapy.This study assessed predictors of nonresponse to dupilumab in patients with AD.Data (April 2017 through June 2019) for patients aged 12 years and above with AD (International Classification of Diseases-9/10-Clinical Modification: 691.8/L20.x) who initiated dupilumab on or after April 1, 2017 (index date) were collected from an electronic health record and insurance claims database. Nonresponse indicators (dupilumab discontinuation, addition of another systemic therapy or phototherapy, addition of a high-potency topical corticosteroid, AD-related hospital visit, AD-related emergency department visit, incident skin infection) were predicted from available demographic and clinical variables using machine learning.Among 419 patients (mean age: 45 years), 145 (35%) experienced at least 1 indicator of nonresponse in the 6-month postindex period. In patients with at least 1 indicator, the most common was dupilumab discontinuation (47% [68/145]). Of note, this analysis could not capture nonmedical reasons for dupilumab discontinuation (eg, cost, access). The most common predictors of nonresponse were a claim for ibuprofen (in 69% of patients with a nonresponse indicator) and a Quan-Charlson Comorbidity Index value of 3 to 4 (59%).Systemic dupilumab therapy for AD can be associated with a relatively high prevalence of nonresponse indicators. Factors associated with these indicators-that is, predictors of nonresponse-may be used to optimize disease management.

To the Editor: Clinical trials and real-world data generally suggest that biologics do not increase susceptibility to COVID-19.1Jones M.E. Kohn A.H. Pourali S.P. et al.The use of biologics during the COVID-19 pandemic.Dermatol Clin. 2021; 39: 545-553https://doi.org/10.1016/j.det.2021.05.010Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar However, it remains unknown whether these therapies may confer a protective effect against contracting COVID-19. Therefore, we sought to assess the risk of COVID-19 infection in patients with psoriasis compared with the general population and in patients receiving systemic and topical therapies. This study used the Symphony Health dataset, a large repository of pharmacy data, inpatient and outpatient medical claims, and remittance data (over 300 million patients, 7 million COVID-19 cases, and payer information: Medicaid/Medicare/commercial/cash). Patients with at least 2 recorded International Classification of Diseases-10 diagnosis codes for psoriasis (L40.x) (n = 167,027) and controls without International Classification of Diseases-10 codes for psoriasis (n = 1,002,162) were randomly sampled in a 1:6 ratio between May 1, 2019, and January 1, 2020. Two recorded diagnosis codes for psoriasis were required to increase the positive predictive value, a strategy employed by prior studies.2Icen M. Crowson C.S. McEvoy M.T. Gabriel S.E. Maradit Kremers H. Potential misclassification of patients with psoriasis in electronic databases.J Am Acad Dermatol. 2008; 59: 981-985https://doi.org/10.1016/j.jaad.2008.08.034Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar,3Takeshita J. Gelfand J.M. Li P. et al.Psoriasis in the US Medicare population: prevalence, treatment, and factors associated with biologic use.J Invest Dermatol. 2015; 135: 2955-2963https://doi.org/10.1038/jid.2015.296Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar Each patient was assigned to 1 of 9 mutually exclusive cohorts based on the last prescription dispense (biologic: Tumor necrosis factor [TNF]-α inhibitor, ustekinumab, interleukin [IL] 17 inhibitor, and IL-23 inhibitor; oral: acitretin, cyclosporine, methotrexate, and apremilast cohorts; topical: none of the above medications). Follow-up began on January 1, 2020, and ended with the first occurrence of any of the following: (1) COVID-19 diagnosis code or (2) November 11, 2020 (the end of the study). Vaccination status was unable to be ascertained from the database because Emergency Use Authorization vaccine approved by the Food and Drug Administration did not occur until December 2020. Demographics were summarized by frequency (percentage) and mean (SD) (Table I). Logistic regression models were constructed with psoriasis status as the independent variable, COVID-19 International Classification of Diseases-10 diagnosis code as the dependent variable, and the following covariates: age, sex, race, congestive heart failure (I50.X), chronic obstructive pulmonary disease (J41/J43/J44), type-2 diabetes mellitus (E11.x/E13.x), and obesity (E66.0-E66.2/E66.8-E66.9/Z68.3-Z68.5).Table ICohort characteristicsDemographicsPsoriasis (n = 167,027)No psoriasis (n = 1,002,162)Total (n = 1,169,189)Male No. (%)77,725 (46.5)444,472 (44.3)522,197 (44.7)Age, mean (SD), y58.1 (13.6)57.7 (16.1)57.7 (15.7)Race No. (%) Caucasian132,036 (79.1)748,490 (74.7)880,526 (75.3) Hispanic15,568 (9.3)90,413 (9.0)105,981 (9.1) African American13,848 (8.3)130,392 (13.0)144,240 (12.3) Asian2894 (1.7)17,171 (1.7)20,065 (1.7) Other2681 (1.6)15,696 (1.6)18,377 (1.6)High-risk factors (ICD-10) for COVID-19, No. (%) Congestive heart failure10,354 (6.2)48,025 (4.8)58,379 (5.0) Type 1 diabetes mellitus37,975 (22.7)158,987 (15.9)196,962 (16.9) Obesity44,557 (26.7)145,347 (14.5)189,904 (16.2) Chronic obstructive pulmonary disease16,514 (9.9)64,145 (6.4)80,659 (6.9)Psoriasis treatment cohorts∗ Topical99,395 (59.5)NANASystemic treatmentsOral systemic cohort, n = 31,468 (18.8)Biologic cohort†, n = 36,164 (21.7)Total systemic treatments received, n = 67,632Oral systemics No. (%) Methotrexate21,478 (68.3)230 (0.6)21,708 (32.1) Apremilast7398 (23.5)99 (0.3)7497 (11.1) Cyclosporine1573 (5.0)7 (0.02)1580 (2.3) Acitretin1072 (3.4)5 (0.01)1077 (1.6)Biologics No. (%) TNF-α inhibitorsAdalimumab09553 (26.4)9553 (14.1)Infliximab03366 (9.3)3366 (5.0)Etanercept04201 (11.6)4201 (6.2)Certolizumab01438 (4.0)1438 (2.1) IL-12/23 inhibitorUstekinumab05085 (14.1)5085 (7.5) IL-17 inhibitorsSecukinumab06266 (17.3)6266 (9.3)Ixekizumab03135 (8.7)3135 (4.6)Brodalumab0142 (0.4)142 (0.2) IL-23 inhibitorsGuselkumab01687 (4.7)1687 (2.5)Risankizumab01021 (2.8)1021 (1.5)Tildrakizumab0312 (0.9)312 (0.5)ICD, International Classification of Diseases; IL, interleukin; NA, not available; TNF, tumor necrosis factor. Open table in a new tab ICD, International Classification of Diseases; IL, interleukin; NA, not available; TNF, tumor necrosis factor. Psoriasis was associated with 18% higher odds of incident COVID-19 (adjusted odd ratio [aOR], 1.18; 95% CI, 1.13-1.23) compared with controls (Supplementary Fig 1, available via Mendeley at https://data.mendeley.com/datasets/68fht87h68/1). In contrast to data from Northeast Italian cohorts, our results appear to align with recent findings from a global registry-based study suggesting that patients receiving no systemic therapy were estimated to have an increased risk of COVID-19 hospitalization compared with patients on biologics.4Piaserico S. Gisondi P. Cazzaniga S. Naldi L. Lack of evidence for an increased risk of severe COVID-19 in psoriasis patients on biologics: a cohort study from Northeast Italy.Am J Clin Dermatol. 2020; 21: 749-751https://doi.org/10.1007/s40257-020-00552-wCrossref PubMed Scopus (19) Google Scholar,5Mahil S.K. Dand N. Mason K.J. et al.Factors associated with adverse COVID-19 outcomes in patients with psoriasis-insights from a global registry-based study.J Allergy Clin Immunol. 2021; 147: 60-71https://doi.org/10.1016/j.jaci.2020.10.007Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar In analyses of psoriasis patients (Fig 1), TNF inhibitor (aOR, 0.87; 95% CI, 0.77-1.00), methotrexate (aOR, 0.81; 95% CI, 0.71-0.92), and apremilast (aOR, 0.70; 95% CI, 0.57-0.87) use had decreased odds of incident COVID-19 compared with patients on topical therapy. Odds ratios remained unchanged after excluding patients on concomitant biologic and oral therapy. Among the limitations, first, we cannot differentiate between the impact of psoriasis severity and systemic therapy on the risk of COVID-19, because disease severity was defined based on treatment history. Second, smoking status and other cardiovascular comorbidities were not adjusted in the logistic regression model. Nonetheless, the protective role exerted by TNF-inhibitor and methotrexate is supported by the mechanistic plausibility of proinflammatory cytokine inhibition, particularly of TNF-α, IL-6, and IL-1. Our findings suggest that these drug classes do not increase the risk of acquiring COVID-19 and, thus, are safe options for continuing psoriasis treatment during the COVID-19 pandemic. Dr Wu is or has been an investigator, consultant, or speaker for AbbVie, Almirall, Amgen, Arcutis, Aristea Therapeutics, Boehringer Ingelheim, Bristol-Myers Squibb, Dermavant, Dr Reddy's Laboratories, Eli Lilly, Galderma, Janssen, LEO Pharma, Mindera, Novartis, Regeneron, Sanofi Genzyme, Solius, Sun Pharmaceutical, UCB, Valeant Pharmaceuticals North America LLC, and Zerigo Health. With no relation to the present work, Dr Egeberg has received research funding from Pfizer, Eli Lilly, Novartis, Bristol-Myers Squibb, AbbVie, Janssen Pharmaceuticals, the Danish National Psoriasis Foundation, the Simon Spies Foundation, and the Kgl Hofbundtmager Aage Bang Foundation, and honoraria as a consultant and/or speaker from AbbVie, Almirall, Leo Pharma, Galápagos NV, Sun Pharmaceuticals, Samsung Bioepis Co, Ltd, Pfizer, Eli Lilly and Company, Novartis, Galderma, Dermavant, UCB, Mylan, Bristol-Myers Squibb, and Janssen Pharmaceuticals. Authors Liu, Thatiparthi, and Martin have no conflicts of interest to declare.

Identifying the optimal long-term biologic therapy for patients with psoriasis is often done through trial and error.To identify the optimal biologic therapy for individual patients with psoriasis using predictive statistical and machine learning models.This population-based cohort study used data from Danish nationwide registries, primarily DERMBIO, and included adult patients treated for moderate-to-severe psoriasis with biologics. Data were processed and analyzed between spring 2021 and spring 2022.Patient clusters of clinical relevance were identified and their success rates estimated for each drug. Furthermore, predictive prognostic models to identify optimal biologic treatment at the individual level based on data from nationwide registries were evaluated.Assuming a success criterion of 3 years of sustained treatment, this study included 2034 patients with a total of 3452 treatment series. Most treatment series involved male patients (2147 [62.2%]) originating from Denmark (3190 [92.4%]), and 2414 (69.9%) had finished an education longer than primary school. The average ages were 24.9 years at psoriasis diagnosis and 45.5 years at initiation of biologic therapy. Gradient-boosted decision trees and logistic regression were able to predict a specific cytokine target (eg, interleukin-17 inhibition) associated with a successful treatment with accuracies of 63.6% and 59.2%, and top 2 accuracies of 95.9% and 93.9%. When predicting specific drugs resulting in success, gradient boost and logistic regression had accuracies of 48.5% and 44.4%, top 2 accuracies of 77.6% and 75.9%, and top 3 accuracies of 89.9% and 89.0%.Of the treatment prediction models used in this cohort study of patients with psoriasis, gradient-boosted decision trees performed significantly better than logistic regression when predicting specific biologic therapy (by drug as well as target) leading to a treatment duration of at least 3 years without discontinuation. Predicting the optimal biologic could benefit patients and clinicians by minimizing the number of failed treatment attempts.

To the Editor: Atopic dermatitis (AD) is a common and chronic inflammatory dermatological condition that affects the daily life of individuals in various ways. Many studies have discussed the numerous autoimmune conditions that are potentially associated with AD.1 Recent research has suggested that the underlying pathophysiology of AD may contribute to the development of autoimmunity.2 In addition, our group has reported that psoriasis is associated with thyroid dysfunction.3 In 2012, Pedullà et al4 reported a significant association between AD and autoimmune thyroid disease in children from Naples, Italy.

To the Editor: In 2021, the American Academy of Dermatology and National Psoriasis Foundation jointly released guidelines outlining therapeutic options for psoriasis management, including topical corticosteroids, calcineurin inhibitors, vitamin D analogs, nonbiologic agents, and alternative interventions. The guidelines did not recommend a specific algorithmic hierarchy. Topical medications were identified as the most employed modality in practice.1

<h2>Abstract</h2> Viral vaccines could be considered among the most important medical achievements of the 20th century. They have prevented much suffering and saved many lives. Although some curative antiviral drugs exist, we desperately depend on efforts by academic, governmental and industrial scientists in the advancement of viral vaccines in the prevention and control of infectious diseases. In the next decade, we hope to see advancement in the development of current and investigational viral vaccines against childhood and adult infections. In this article, we will review the licensed viral vaccines, some of their safety concerns, and the advances in the development of investigational viral vaccines.

To the Editor: A 45-year-old female presented to our clinic in March of 2005 armed with several small plastic bags filled with “fibers,” her magnifying glass in hand. She had been to seven physicians the past four months, three of whom were dermatologists. “Doctor, have you heard of Morgellons disease?” I explained that I had, and to my surprise, she burst into tears. She spent the first few minutes of our conversation sobbing, relieved to have found a physician who had heard of Morgellons disease. Morgellons disease is not located in modern medical texts or online journals. But a Goggle search will produce approximately 15,400 hits. Our patient had made this self-diagnosis by performing an internet search on “bugs in the skin.” Patients regularly request information on Morgellons disease from academic centers. The Morgellons Research Foundation Web site can be found at www.morgellons.org. This site describes the foundation's mission: “dedicated to finding the cause of an emerging infectious disease, which mimics scabies and lice.” On this Web page, you will find pictures of the “mysterious fibers,” a patient registration page, a distinguished medical advisory board including six doctorates, a description of the current research efforts of scientists in Oklahoma, and a request for donations to fund this research. The website claims over 3300 registrants. They also have proposed an association with Lyme disease and encourage patients to have Lyme titers drawn. The site further explains the history behind the term Morgellons, coined in 1674 by Sir Thomas Browne in his monograph entitled “De vermiculis capillaribus infantium.”1Kellett C.E. Sir Thomas Browne and the disease called the Morgellons.Ann Med His. 1935; 7: 467-479Google Scholar To the layperson, the information on this Web site is deceptive, particularly to someone who suffers from delusions of parasitosis.2Koo J. Lebwohl A. Psycho dermatology: the mind and skin connection.Am Fam Physician. 2001; 64: 1873-1878PubMed Google Scholar, 3Koo J. Lee C.S. Delusions of parasitosis. A dermatologist's guide to diagnosis and treatment.Am J Clin Dermatol. 2001; 2: 285-290Crossref PubMed Scopus (99) Google Scholar However, because the term “Morgellons disease” does not have the word “delusions” embedded in the term, it is a useful way to communicate with patients regarding their disease. As a case in point, I have established a close relationship with the patient described above by referring to her delusions of parasitosis as Morgellons disease. After taking cultures and a biopsy, I reassured her that there were no bacterial, fungal, or parasitic infections. I emphasized that I did not doubt the authenticity of the sensations she was experiencing, and I empathized with how disconcerting it must be to feel bugs crawling and stinging her skin. I explained that sometimes medications that psychiatrists use to calm nerve signals help patients with Morgellons disease. She is currently on the anti-psychotic risperidone, followed by both dermatology and psychiatry.4Elmer K.B. George R.M. Peterson K. Therapeutic update: use of risperidone for the treatment of monosymptomatic hypochondriacal psychosis.J Am Acad Dermatol. 2000; 43: 683-686Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar As is the case with the majority of patients with delusions of parasitosis, she will likely need anti-psychotic medications long-term to keep her disease under control. We caution that the use of the term “Morgellons disease” should not validate an association with an infectious disease process. Further, in order to practice ethical patient care and to serve our patients honestly and as best we can, we stress the importance of clarifying to all delusions of parasitosis patients that their condition is not a result of an infectious agent. However, we found the term to be of paramount importance in establishing patient confidence and in developing patient–physician rapport throughout this patient's care. Morgellons disease leaves us to gently question Shakespeare's age-old adage: does that which we call a rose truly smell as sweet by any other name?

Journal of the European Academy of Dermatology and VenereologyVolume 31, Issue 11 p. e481-e482 Letter to the Editor Apremilast for a psoriasis patient with HIV and hepatitis C S.P. Reddy, S.P. Reddy University of Illinois at Chicago College of Medicine, Chicago, IL, USASearch for more papers by this authorV.V. Shah, V.V. Shah University of Missouri-Kansas City School of Medicine, Kansas City, MO, USASearch for more papers by this authorJ.J. Wu, Corresponding Author J.J. Wu jashinwu@gmail.com Department of Dermatology, Kaiser Permanente Los Angeles Medical Center, Los Angeles, CA, USACorrespondence: J.J. Wu. E-mail: jashinwu@gmail.comSearch for more papers by this author S.P. Reddy, S.P. Reddy University of Illinois at Chicago College of Medicine, Chicago, IL, USASearch for more papers by this authorV.V. Shah, V.V. Shah University of Missouri-Kansas City School of Medicine, Kansas City, MO, USASearch for more papers by this authorJ.J. Wu, Corresponding Author J.J. Wu jashinwu@gmail.com Department of Dermatology, Kaiser Permanente Los Angeles Medical Center, Los Angeles, CA, USACorrespondence: J.J. Wu. E-mail: jashinwu@gmail.comSearch for more papers by this author First published: 27 April 2017 https://doi.org/10.1111/jdv.14301Citations: 23Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume31, Issue11November 2017Pages e481-e482 RelatedInformation

Abstract In this age of expanding choices of therapy for psoriasis, topical therapies still play an important part in the management of patients. There are many knowledge gaps in topical therapy for psoriasis with regard to efficacy and safety as well as various combinations including topical therapy with phototherapy or with systemic agents. Councillors of the International Psoriasis Council comprised a topical therapy working group to describe these gaps in order to help direct future research endeavours. Herein, we present the results of this analysis, discuss topical agents in clinical development and the attributes of the ideal topical treatment for psoriasis.

Sleep is essential for overall health and well-being, yet more than one-third of adults report inadequate sleep. The prevalence is higher among people with psoriasis, with up to 85.4% of the psoriatic population reporting sleep disruption. Poor sleep among psoriasis patients is particularly concerning because psoriasis is independently associated with many of the same comorbidities as sleep dysfunction, including cardiovascular disease, obesity, and depression. Given the high prevalence and serious consequences of disordered sleep in psoriasis, it is vital to understand the nature of sleep disturbance in this population. This study was designed to help meet this need by using survey data from Citizen Pscientist, an online patient portal developed by the National Psoriasis Foundation.Our analysis included 3118 participants who identified as having a diagnosis by a physician of psoriasis alone or psoriasis with psoriatic arthritis. Demographic information, psoriasis severity and duration, sleep apnea status, smoking and alcohol consumption, itch timing, and sleep characteristics were included. Two separate multivariate logistic regression models in STATA were used to determine whether the presence of psoriatic arthritis, age, gender, body mass index, comorbid sleep apnea, psoriasis severity, timing of worst itch, smoking status, or high-risk alcohol consumption were associated with sleep difficulty or low sleep quantity, defined by the American Academy of Sleep Medicine as less than 7 h of sleep per night on average.Results from the multivariate logistic regressions found that sleep difficulty was associated with psoriatic arthritis (OR 2.15, 95% CI [1.79-2.58]), female gender (2.03 [1.67-2.46]), obese body mass index (BMI ≥ 30) (1.25 [1.00-1.56]), sleep apnea (1.41 [1.07-1.86]), psoriasis severity of moderate (1.59 [1.30-1.94]) or severe (2.40 [1.87-3.08]), and smoking (1.60 [1.26-2.02]). Low sleep quantity was associated with obese BMI (1.62 [1.29-2.03]), sleep apnea (1.30 [1.01-1.68]), psoriasis severity of moderate (1.41 [1.16-1.72]) or severe (1.40 [1.11-1.76]), and smoking (1.62 [1.31-2.00]). Sleep difficulty and low sleep quantity were not associated with age, alcohol consumption, or timing of worst itch.These results are potentially meaningful in several aspects. We identify an important distinction between sleep difficulty and sleep quantity in psoriatic disease, whereby having psoriatic arthritis and being female are each associated with sleep difficulty despite no association with low sleep quantity. Furthermore, there is conflicting evidence from prior studies as to whether psoriasis severity is associated with sleep difficulty, but this well-powered, large study revealed a strong, graded relationship between psoriasis severity and both sleep difficulty and low sleep quantity. Overall, our results show that both sleep difficulty and low sleep quantity were associated with multiple factors in this analysis of a large psoriatic cohort. These findings suggest that dermatologists may gather clinically useful information by screening psoriatic patients for trouble sleeping and low sleep quantity to identify potential comorbidities and to more effectively guide disease management.