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BACKGROUND: Ixekizumab, a high-affinity monoclonal antibody that selectively targets interleukin (IL)-17A, is approved for the treatment of moderate-to-severe psoriasis.OBJECTIVES: This analysis represents an overview of the efficacy outcomes from three Phase 3 psoriasis studies.METHODS: Data were integrated from the 12-week induction period of three studies in which patients received ixekizumab 80 mg every 2 (IXE Q2W; N=1169) or 4 weeks (IXE Q4W; N=1165) after an initial 160-mg dose for both, etanercept (ETN) (50 mg biweekly; N=740; two studies), or placebo (PBO) (N=792). The co-primary endpoints were the percentages of patients with response of sPGA (0,1) and a 75% improvement in baseline psoriasis area severity index (PASI 75) at Week 12. Response rates were compared between treatments using the Cochran-Mantel-Haenszel test stratified by study. Treatment comparisons with placebo included data from three studies, whereas etanercept comparisons were based on two studies.RESULTS: Ixekizumab treatment was superior to placebo (pCONCLUSIONS: Ixekizumab therapy at both dosing regimens demonstrated rapid onset and superior efficacy compared with placebo and etanercept, with IXE Q2W providing better outcomes than IXE Q4W during the first 12 weeks of treatment. This article is protected by copyright. All rights reserved.

Background Efalizumab, a T-cell-targeted, recombinant, humanized, monoclonal IgG1 antibody, inhibits key T-cell-mediated steps in the pathogenesis of psoriasis. Efalizumab is approved for the treatment of moderate-to-severe chronic plaque psoriasis in adults in more than 50 countries. Objectives To evaluate the efficacy and safety of long-term, continuous efalizumab therapy in patients with psoriasis. Methods This open-label, multicentre phase III study enrolled 339 patients with moderate-to-severe chronic plaque psoriasis. During the initial 3-month phase, patients received subcutaneous efalizumab 2 mg kg−1 weekly with randomization to receive concomitant fluocinolone acetonide or placebo ointment during month 3. The second phase was a long-term observational period; patients achieving a ≥ 50% improvement in the Psoriasis Area and Severity Index (PASI) score were eligible to receive efalizumab 1 mg kg−1 weekly for up to 33 months. The final 3-month treatment period was an optional transition period for patients who completed the 33-month segment before efalizumab became commercially available. Results After 3 months, 41·3% of patients achieved a ≥ 75% improvement in PASI (PASI-75) and 13·0% achieved a ≥ 90% improvement (PASI-90). Continued improvement was observed: 45·4% and 24·5% achieved PASI-75 and PASI-90, respectively, at the end of the observational phase. The safety profile was stable, with no new or no increase in common events over 36 months of treatment. Conclusions This was the longest continuous study using a biologic therapy for psoriasis. Clinical benefit of efalizumab improved over the first 18 months and was maintained during 36 months of continuous therapy. Long-term efalizumab therapy is appropriate for many patients with plaque psoriasis. Conflicts of interest C.L. with 3M Pharmaceuticals, Abbott, Allergan, Altana, Amgen, Astellas-Biogen, Bristol Myers, Centocor, CombinatoRx, Fujisawa Healthcare, Galderma, Genentech, Merck Serono International SA, Schering Plough, RTL, Vitae and Warner Chilcott; A.M. with 3M Pharmaceuticals, Abbott, Allergan, Allermed, Amgen, Astralis, Berlex, Biogen Idec, Celgene, Centocor, Cephalon, Collagenex Pharmaceuticals, CombinatoRx, Connetics, Corixa, Dermik Laboratories, Doak Dermatologics, Dow, Ferndale Laboratories, Fujisawa Healthcare, Galderma, Genentech, Genzyme, GlaxoSmithKline, Ligand Pharmaceuticals, Medicis, MedImmune, Novartis Pharmaceuticals, Otsuka Pharmaceutical, Protein Design Labs, QLT USA, Regeneration Pharma AG, Roche, Merck Serono International SA, Sinclair, Synta Pharma, Thermosurgery, Vertex, Warner Chilcott, Wyeth, XOMA and Zars; T.H. with Genentech; A.B.G. with Abbott, Actelion, Almirall, Amgen, Beiersdorf, Biogen Idec, Bristol Myers Squibb, Can-Fite, Celera, Celgene, Centocor, DermiPsor, Eisai, Genentech, Immune Control, Incyte, Kemia, Medacorp, Medarex, Novo Nordisk, Pharmacare, Roche, RxClinical, Sankyo, Schering Plough, TEVA, UCB, Warner Chilcott and Wyeth. All income derived from these sources goes to her employer. I.C. and B.X. are employees and stockholders of Genentech.

For nearly 200 years it has been appreciated that plaque psoriasis consists of a number of distinct clinical phenotypes. However, a reliable and simple stratification of clinical presentation of psoriasis is lacking. In the era of immunogenetic association studies and an advanced understanding of the pathomechanisms of psoriasis it is important that a classification of the disease according to phenotype is readily available. Such a classification would facilitate clinically relevant interpretation of investigational data. A meeting of the International Psoriasis Council produced a consensus on clinical phenotypes of psoriasis equally relevant to clinical practitioners and psoriasis researchers.

Efalizumab is a recombinant, humanized monoclonal anti-CD11a antibody used for the treatment of moderate to severe plaque psoriasis. Immune-mediated thrombocytopenia and anaemia have previously been reported with this therapy. We describe the first case of immune-mediated pancytopenia in a patient treated with efalizumab. Close monitoring of all blood cell counts is warranted in light of this case.

Three patients, one healthy and two immunocompromised, developed cutaneous reactions that histologically mimicked granuloma annulare at sites of resolved varicella-zoster virus (VZV) reactivation infections. Variable latency periods between the infection and the granulomatous reaction were noted. As in other case reports, the presence of VZV DNA in these lesions was inconsistently demonstrated by the polymerase chain reaction (PCR) and appears more common in early, as opposed to late, post-zoster granulomas. In addition to various granulomatous reactions, vasculitic and neoplastic eruptions following resolved VZV infections have been described and are reviewed here. Therapeutically, topical, intralesional and systemic corticosteroids, as well as acyclovir, have been tried with inconsistent results. Although the pathogenesis remains unclear, the presence of VZV DNA in early lesions that histologically do not display viral cytopathic changes, suggests the virus induces an atypical delayed hypersensitivity reaction not affected by antiviral therapy.