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Efalizumab‐induced aseptic meningitis
Author(s) -
Kluger N.,
Girard C.,
Gonzalez V.,
Guillot B.,
Bessis D.
Publication year - 2007
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2006.07594.x
Subject(s) - library science , humanities , art , computer science
of relapses after subsequent reintroduction of adalimumab. Reiter syndrome is a rare systemic reactive process to urogenital (including Chlamydia trachomatis and U. urealyticum) or intestinal (such as Yersinia and Shigella) bacterial agents, mostly in HLAB27-positive patients. Clinical manifestations include ocular involvement (conjunctivitis, uveitis), articular manifestations (reactive arthritis consistent with an asymmetrical monoor polyarticular involvement, enthesopathies, spondylitis and sacroileitis) and urogenital manifestations (urethritis, salpingitis) consecutive to a reactive inflammatory process. Cutaneous manifestations consist of a psoriasiform rash, endobuccal erosions, palmoplantar keratoderma and circinate balanitis or vulvitis. There is no clear consensus with wellrecognized diagnostic criteria. Atypical clinical manifestations, as in our case, are usually the rule. Although we cannot formally exclude that our patient developed a psoriasiform eruption directly related to an antiTNF-a therapy, our case may represent the first observation of acute cutaneous manifestations related to Reiter syndrome that developed under adalimumab and leflunomide therapy. As the pathogenic mechanism of the cutaneous manifestations seems to be similar to the pathogenesis of psoriasis, the emergence of this syndrome in a patient treated by two immunomodulating agents is paradoxical considering that these molecules are effective for the treatment of psoriasis. We suppose that concomitant immunosuppression and immunomodulation by adalimumab and leflunomide may have supported the triggering role of U. urealyticum in this patient who has a genetic predisposition to develop Reiter syndrome. The lack of recurrence after the initiation of antibiotic treatment and topical steroid therapy and after the reintroduction of adalimumab and leflunomide supports this hypothesis. This evolution does not support the hypothesis of a psoriasiform eruption induced by TNF-a antagonism considering that the lesions would probably persist or recur during the treatment. As paradoxical psoriasiform eruptions have been observed under TNF-a antagonists, this report illustrates the need to determine in the future if these cutaneous manifestations correspond to a reactive process that is consecutive to a latent infection and that may have been triggered by concomitant immunosuppression. Consequently, further investigations to exclude infection should be recommended in these patients.

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