St John’s Institute of Dermatology, King’s College London and Guy’s and St Thomas’ NHS Foundation Trust, London SE1 9RT U.K. *Department of Dermatology, Royal Gwent Hospital, Newport NP20 2UB, U.K. Department of Dermatology, Western Infirmary, Glasgow G11 6NT, U.K. The Dermatology Centre, Salford Royal Hospital, University of Manchester, Manchester Academic Health Science Centre, Manchester M6 8HD, U.K. §Psoriasis and Psoriatic Arthritis Alliance, PO Box 111, St Albans AL2 3JQ, U.K. –Department of Dermatology, Cardiff University, School of Medicine, Heath Park, Cardiff CF14 4XN, U.K. **Royal National Hospital for Rheumatic Diseases, Bath BA1 1RL, U.K. Department of Dermatology, Belfast City Hospital, Belfast BT9 7AB, U.K. Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, U.K. §§Department of Dermatology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen AB9 2ZB, U.K.

/pdf/british-association-of-dermatologists-guidelines-for-230azgd36m.pdf

British Association of Dermatologists’ guidelines for biologic interventions for psoriasis 2009

Background A task force of the National Psoriasis Foundation Medical Board was convened to evaluate treatment options for pustular psoriasis. Meetings were held by teleconference. Consensus on treatment of pustular psoriasis was achieved. Pustular psoriasis has been classified into localized and generalized forms. There are a number of treatment modalities, but there is little evidence-based information to guide the management of this type of psoriasis. Objectives The purpose of this article was to present treatment recommendations to aid in the treatment of patients with pustular psoriasis. Methods A literature review was conducted to examine treatment options for pustular psoriasis and assess the strength of the literature for each option. Results Overall the quality of the literature about the treatment of pustular psoriasis is weak. Treatment should be governed by the extent of involvement and severity of disease. Acitretin, cyclosporine, methotrexate, and infliximab are considered to be first-line therapies for those with generalized pustular psoriasis. Adalimumab, etanercept, and psoralen plus ultraviolet A are second-line modalities in this setting. Pustular psoriasis in children, in pregnant women, and in localized forms alter which agents are first-line modalities as concerns such as teratogenicity need to be factored into the decisionmaking for the individual patient. Limitations There are few high-quality studies examining treatment options for pustular psoriasis. Conclusions Treatment of patients with pustular psoriasis depends on the severity of presentation and patient's underlying risk factors. The data are extremely limited for this type of psoriasis and we encourage further exploration.

https://www.jaad.org/article/S0190-9622(11)00304-5/pdf

Treatment of pustular psoriasis: from the Medical Board of the National Psoriasis Foundation.

Psoriasis is a chronic disease, the severity of which varies among patients and changes unpredictably over time in individual patients. Psoriasis can be exacerbated during treatment by infection, endocrine factors, hypocalcemia, medications, psychologic stress, skin trauma, or other factors. Patients who discontinue treatments may experience a return of disease—relapse—or worsening of disease—rebound. The National Psoriasis Foundation (NPF) proposed standardized definitions of relapse and rebound. Efalizumab, a recombinant humanized immunoglobulin G-1 monoclonal antibody, is approved for the management of psoriasis. During efalizumab clinical trials, a small percentage of patients experienced protocol-defined adverse events related to psoriasis. After publication of the NPF definition of rebound, post hoc exploratory analyses of the efalizumab clinical trial data were performed. The efalizumab clinical trial investigators discussed their observations, the analyses, and their individual approaches to the treatment of patients receiving or discontinuing efalizumab therapy, the conclusions of which are described herein.

https://www.jaad.org/article/S0190-9622(05)03316-5/pdf

Relapse, rebound, and psoriasis adverse events: An advisory group report

Psoriasis is a chronic inflammatory skin disease that can lead to significant physical and psychologic distress for patients. Psoriatic arthritis (PsA), originally thought to be quite a mild disorder, is now recognized as a progressive and destructive arthritis. To date, therapies for both these conditions have been non-specific and unable to maintain long-lasting remission. In addition, many of the current therapies have significant adverse effects, limiting their usefulness. However, elucidation of the pathogenesis of psoriasis and PsA at a molecular level and the development of selective biologic agents have led to an enormous expansion of the armamentarium available to psoriasis patients. Two agents (infliximab and etanercept) selectively block the role of the cytokine tumor necrosis factor (TNF)-α and have proved effective in clinical trials in the treatment of both the skin and the joint manifestations of psoriasis. A third anti-TNFα agent (adalimumab Humira®) is licensed for the treatment of rheumatoid arthritis; however, no studies have been published to date on its use in PsA or psoriasis. It is known that TNFα is elevated in both the skin and synovium of psoriatic patients and the effectiveness of its blockade by these two agents in psoriasis and PsA confirms its role in their pathogenesis. Randomized, double-blind, placebo-controlled trials have been performed with both agents in the treatment of psoriasis and PsA; in the case of etanercept these have been to support US FDA approval for use in psoriatic arthropathy. These studies are supported by smaller cohorts in open-label studies and anecdotal reports in the literature. Anti-TNFα therapy has proved to have disease-reducing activity in PsA and psoriasis and appears to be well tolerated. These studies have generally featured small numbers of patients and, until a larger cohort of treated patients is available, vigilance must be exercised. A considerable body of post-marketing safety data exists on the use of infliximab in rheumatoid arthritis and Crohn disease and for etanercept in rheumatoid arthritis and PsA. Certain issues, particularly the risk of infection, have emerged as features of the use of these agents. It remains to be seen whether effects seen in other disease entities may be extrapolated to psoriatic patients. More long-term data and experience are needed to define the role of anti-TNFα agents in the management of psoriasis and PsA. In particular, more studies are required to elucidate the finer points of co-medication; in some studies both agents have been used with other medications but there have been no formal trials of various possible combinations.

TNF alpha inhibitors in the treatment of psoriasis and psoriatic arthritis.

Mycosis fungoides: A great imitator.

We report a 50-year-old male patient with a 15-year history of psoriasis including mutilating psoriatic arthritis, in whom the withdrawal of cyclosporin A induced a generalised pustular exacerbation and a aggravation of the joint condition. Two weekly injections of 25 mg of the tumour necrosis factor alpha inhibitor etanercept led to a rapid improvement of his psoriatic arthritis, as well as regression of the pustular eruption, while residual erythema was still present. The clinical response was reflected by an increase in circulating interleukin (IL) 10 and a decrease in IL-6 and IL-8 serum levels during treatment. We conclude that etanercept may be a safe and effective therapy not only in severe psoriatic arthritis, but also in cases of pustular rebound after withdrawal of immunosuppressive agents.

Generalised Pustular Psoriasis Induced by Cyclosporin A Withdrawal Responding to the Tumour Necrosis Factor Alpha Inhibitor Etanercept

Lichenoid pigmented purpuric dermatitis of Gougerot-Blum belongs to a group of closely related disorders which are termed pigmented purpuric dermatoses. It clinically manifests itself with grouped lichenoid papules in association with purpuric lesions. We report a case of lichenoid pigmented purpuric dermatitis of Gougerot-Blum with a heavy band-like CD4-positive lymphocytic infiltrate and clonal rearrangements of the γ-chain of the T cell receptors as detected by polymerase chain reaction/denaturing gradient gel electrophoresis. Monoclonal expansion of T cells in combination with certain histological features of mycosis fungoides (MF) might support a biological relationship between lichenoid pigmented purpuric dermatitis of Gougerot-Blum and MF. However, prompt clinical response to topical steroid therapy supports the benign clinical nature of our case.

Monoclonal Rearrangement of the T Cell Receptor Gamma-Chain in Lichenoid Pigmented Purpuric Dermatitis of Gougerot-Blum Responding to Topical Corticosteroid Therapy

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Generalised Pustular Psoriasis Induced by Cyclosporin A Withdrawal Responding to the Tumour Necrosis Factor Alpha Inhibitor Etanercept

Monoclonal Rearrangement of the T Cell Receptor Gamma-Chain in Lichenoid Pigmented Purpuric Dermatitis of Gougerot-Blum Responding to Topical Corticosteroid Therapy