E. Daudén

European S3-Guidelines on the systemic treatment of psoriasis vulgaris - Update 2015 - Short version - EDF in cooperation with EADV and IPC

European S3-Guidelines on the systemic treatment of psoriasis vulgaris – Update 2015 – Short version – EDF in cooperation with EADV and IPC A. Nast,* P. Gisondi, A.D. Ormerod, P. Saiag, C. Smith, P.I. Spuls, P. Arenberger, H. Bachelez, J. Barker, E. Dauden, E.M. de Jong, E. Feist, A. Jacobs, R. Jobling, L. Kem eny, M. Maccarone, U. Mrowietz, K.A. Papp, C. Paul, K. Reich, S. Rosumeck, T. Talme, H.B. Thio, P. van de Kerkhof, R.N. Werner, N. Yawalkar Division of Evidence Based Medicine, Department of Dermatology, Charit e – Universit€ atsmedizin Berlin, Berlin, Germany Section of Dermatology and Venereology, Department of Medicine, University of Verona, Verona, Italy Department of Dermatology, Aberdeen Royal Infirmary, Aberdeen, UK Service de Dermatologie, Hôpital Ambroise Par e Universit e Paris V, Boulogne, France Clinical Lead for Dermatology, St Johns Institute of Dermatology, St Thomas’ Hospital, London, UK Department of Dermatology, Academic Medical Center, Amsterdam, The Netherlands Third Faculty of Medicine, Department of Dermatology, Charles University, Prague, Czech Republic Department of Dermatology, Hôpital Saint-Louis, Paris, France St. Johns Institute of Dermatology, St. Thomas’ Hospital, London, UK Hospital Universitario de la Princesa, Madrid, Spain University Medical Center Nijmegen St Radboud, Nijmegen, The Netherlands Medizinische Klinik mit Schwerpunkt Rheumatologie u. klinische Immonologie, Charit e – Universit€atsmedizin Berlin, Berlin, Germany Cambridge, UK SZTE Borgyogyaszati Klinika, Szeged, Hungary Roma, Italy Department of Dermatology, Psoriasis-Center University Medical Center Schleswig Holstein, Kiel, Germany Waterloo, Canada Department of Dermatology, Paul Sabatier University, Toulouse, France Dermatologikum Hamburg, Hamburg, Germany Section of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden Department of Dermatology, Erasmus University, Rotterdam, The Netherlands Department of Dermatology, University Hospital Nijmegen, Nijmegen, The Netherlands Department of Dermatology, Inselspital, Universit€ atsklinik f€ ur Dermatologie, Bern, Switzerland *Correspondence: A. Nast. E-mail: alexander.nast@charite.de Received: 22 June 2015; Accepted: 7 July 2015

Risk of Serious Adverse Events Associated With Biologic and Nonbiologic Psoriasis Systemic Therapy: Patients Ineligible vs Eligible for Randomized Controlled Trials

OBJECTIVE To describe the use of systemic therapy for psoriasis (biologic and nonbiologic [classic] drugs) in patients not adequately represented in randomized controlled trials (RCTs) and the risk of serious adverse events (SAEs) in these patients. DESIGN A registry inception cohort was used. SETTING Thirteen dermatology departments in Spain participated. PATIENTS A consecutive sample of patients treated with biologics and a systematic sample of patients treated with classic systemic therapy were evaluated. A total of 1042 patients (2179 person-years) were included. EXPOSURE Inadequate representation in trials was defined as the presence of any of the following factors: elderly age (>70 years); type of psoriasis other than chronic plaque psoriasis; history of infection caused by hepatitis B, hepatitis C, or human immunodeficiency virus; history of cancer (excluding nonmelanoma skin cancer); and chronic renal or hepatic disease. MAIN OUTCOME MEASURES Serious adverse events as defined by the International Conference on Harmonization were evaluated. RESULTS In all, 29.8% of patients receiving systemic therapy for psoriasis would not have been eligible for RCTs. These individuals had an increased risk of SAEs (incidence rate ratio, 2.7; 95% CI, 1.5-4.7). Patients exposed to biologics had an adjusted increased risk of SAEs (incidence rate ratio, 2.3; 95% CI, 1.1-4.8) that was similar in patients eligible and ineligible for RCTs. CONCLUSIONS Patients ineligible for RCTs are an important proportion (30%) of those receiving systemic therapy for psoriasis. These patients have a higher risk of SAEs and should be closely monitored. Patients exposed to biologics (whether these patients are eligible for RCTs or ineligible) are susceptible to the same increase in risk of SAEs, but biologics add to a higher baseline risk in patients who are ineligible for RCTs. The risk-benefit ratio in ineligible patients receiving biologics might be different from the ratio in eligible patients.

Improvements in patient-reported outcomes in moderate-to-severe psoriasis patients receiving continuous or paused etanercept treatment over 54 weeks: the CRYSTEL study.

Objective  To assess patient‐reported outcomes (PRO) in patients with moderate‐to‐severe plaque psoriasis receiving continuous or paused etanercept treatment.

Clinical practice guideline for an integrated approach to comorbidity in patients with psoriasis

Background  The relationship between psoriasis and associated diseases has drawn particular interest in recent years. To provide appropriate management of psoriasis from an early stage, it is necessary to include prompt diagnosis of concomitant disease and to prevent and treat any comorbidity found. Such an integrated approach also serves to ensure that the drugs used to treat associated diseases do not interfere with the management of psoriasis, and vice versa.

Helicobacter pylori and idiopathic chronic urticaria.

Background Different studies have shown a high prevalence of Helicobacter pylori (HP) infection in patients with chronic urticaria (CU), and occasional remission of the skin lesions after eradication therapy. Recent investigations, however, have failed to find a significant relationship between the two conditions. We designed a case–control study to assess the prevalence of HP infection and the effect of bacterium eradication on the outcome of the skin disease in patients affected by CU. The literature is reviewed.

Flare and change of psoriasis morphology during the course of treatment with tumour necrosis factor blockers

Tumour necrosis factor (TNF) blockers represent an exciting advance in the management of psoriasis. However, the safety profile of these drugs is not completely established. We present a review of the literature, and report on eight patients: two with the unexpected appearance of psoriasis, and the remaining six with exacerbation and change in morphology of their existing psoriasis, all of which occurred during treatment with the TNF blockers adalimumab, etanercept and infliximab. The two new cases, neither of whom had any personal or family history of psoriasis, developed pustular psoriasis on the palms and/or soles. The other six patients, previously diagnosed with severe chronic plaque psoriasis (four patients), generalized pustular psoriasis (one) and erythrodermic psoriasis (one), developed eruptive guttate psoriasis between 15 days and 18 months after the beginning of therapy. These patients had never before presented guttate‐type psoriatic lesions, and the lesions appeared in areas of the body that were free of psoriatic plaques at baseline.

Gene polymorphisms that can predict response to anti-TNF therapy in patients with psoriasis and related autoimmune diseases.

Psoriasis (Ps) is a chronic inflammatory disease with an important genetic component. It shares pathophysiological mechanisms with other autoimmune diseases such as psoriatic arthritis (PsA), rheumatoid arthritis (RA) and Crohn’s disease (CD). These conditions can be treated using biological drugs such as infliximab, adalimumab and etanercept, which selectively block the proinflammatory cytokine tumor necrosis factor (TNF)-α. Although these agents have greatly improved the prognosis of Ps, PsA, RA and CD, they do not cure the disease and are expensive; in addition, significant proportions of patients do not respond or develop serious adverse effects. Therefore, it is important to investigate biomarkers, such as gene polymorphisms, that can predict which patients will respond best to a specific drug. Some polymorphisms in genes TNF, TNF receptor superfamily 1B (TNFR1B) and TNFα-induced protein 3 gene (TNFAIP3) have been associated with response to anti-TNF therapy in patients with Ps. The present article reviews other polymorphisms that could also play a role in prediction of response to these treatments.

Safety and effectiveness of ustekinumab and antitumour necrosis factor therapy in patients with psoriasis and chronic viral hepatitis B or C: a retrospective, multicentre study in a clinical setting

Background  Both the safety and efficacy of biologic therapy may be affected in the presence of highly prevalent chronic viral hepatitis.

Leishmaniasis presenting as a dermatomyositis-like eruption in AIDS.

Three patients are described with leishmaniasis and AIDS, with cutaneous lesions mimicking dermatomyositis. Leishmania organisms were observed in great numbers in the dermis of lesional skin biopsy specimens. They were also present inside keratinocytes in all layers of the epidermis in one patient. Skin cultures from all patients and bone marrow culture in patients 1 and 3 revealed Leishmania infantum. Leishmania organisms were also found in nonlesional skin. The absence of proximal symmetric muscle weakness, elevated muscle enzymes, myopathic electromyograms, or characteristic histopathologic and immunologic features of dermatomyositis, and the rapid and complete clearance or marked improvement of the cutaneous lesions after treatment for leishmaniasis, make us consider true dermatomyositis unlikely. We suggest that leishmaniasis be included in the list of diseases capable of inducing a dermatomyositis-like eruption.

The relationship between tumour necrosis factor (TNF)-α promoter and IL12B/IL-23R genes polymorphisms and the efficacy of anti-TNF-α therapy in psoriasis: a case–control study

Antitumour necrosis factor (anti‐TNF)‐α agents can be used successfully to treat patients with psoriasis and other inflammatory diseases. However, very few studies have examined the relationship between TNF‐α polymorphisms and the response to anti‐TNF‐α agents.