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G. Michaëlsson, U. Kajermo, A. Michaëlsson, E. Hagforsen, Infliximab can precipitate as well as worsen palmoplantar pustulosis: possible linkage to the expression of tumour necrosis factor‐α in the normal palmar eccrine sweat duct?, British Journal of Dermatology, Volume 153, Issue 6, 1 December 2005, Pages 1243–1244, https://doi.org/10.1111/j.1365-2133.2005.06977.x
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Conflicts of interest: none declared.
Sir, Palmoplantar pustulosis (PPP) is a chronic skin disease that is considered to be a variant of psoriasis, although it has both clinical1, 2 and genetic3 characteristics different from those of psoriasis vulgaris. However, in a recent study 18% of patients also displayed psoriasis of the vulgaris type.3 Ninety percent of patients with PPP are women and 95% are smokers at the onset of the disease.1 The most intense inflammation is concentrated to the acrosyringium.4
Treatment of rheumatoid arthritis (RA) with infliximab, which is a chimeric monoclonal antibody against tumour necrosis factor (TNF)‐α, is well established. However, we have recently observed two patients with RA who developed severe PPP followed by widespread pustular skin lesions during treatment with infliximab. One of these patients had no previous history of PPP. She later had a similar unfavourable response to etanercept.
Patient 1 was a 62‐year‐old woman (smoker) with RA starting in 1986 and progressing in the following years. Rheumatoid factor (RF) was positive and antinuclear antibodies (ANA) were negative. In 1991 she experienced onset of mild PPP. She had been receiving methotrexate 10 mg weekly and prednisolone 5 mg daily for 3 months when infliximab was started, and continued with this regimen during infliximab treatment. Infliximab infusions (200 mg) were begun in November 2003, with the second infusion after 2 weeks and the third after 6 weeks. The joint symptoms improved after the first infusion, but the second and third infusions had a minor effect. In January 2004 the patient reported the appearance of more pustules. A fourth infusion of infliximab in February 2004 was followed by marked worsening of her PPP and the appearance of nummular erythematopapular scaly lesions on her legs and arms. She received a fifth infliximab infusion in the middle of April 2004 and a week later she developed severe, disabling worsening of both her skin disease and her arthritis, and her general condition deteriorated with pronounced weakness/fatigue, temperature 38·2 °C, leukocytosis (total white blood cells 12·4 × 109 L−1 with neutrophils 8·8 × 109 L−1), and C‐reactive protein (CRP) 62 mg L−1. There were hundreds of pustules on the soles and palms, and confluent nummular pustular lesions were present on the lower and upper legs, gluteal region and forearms. X‐rays of the lungs revealed two 3‐cm infiltrates in the right lung, and computed tomography showed another two infiltrates in the left lung. Bronchoscopy with bronchoalveolar lavage was performed. The infiltrates were considered to be caused by opportunistic infection. The patient was treated with intravenous Tienam (imipenem + cilastatin sodium) and oral ciprofloxacin. Treatment with methotrexate was discontinued. She stopped smoking. Her PPP and pustular psoriasis had cleared completely at the end of June 2004 and there has been no recurrence to date (May 2005).