| Title | Claps | Level | Year | L/Y |
|---|---|---|---|---|
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Long‐standing remission of recalcitrant juvenile pemphigus vulgaris after adjuvant therapy with rituximab
Enno Schmidt, S. Herzog, E. Bröcker, D. Zillikens, Matthias Goebeler, Matthias Goebeler
After a relapse 4 months later the disease was controlled by several cycles of immunoadsorption therapy in combination with mycophenolate mofetil (3 g day). Infliximab is a chimeric monoclonal antibody consisting of the entire variable domain of a m…
After a relapse 4 months later the disease was controlled by several cycles of immunoadsorption therapy in combination with mycophenolate mofetil (3 g day). Infliximab is a chimeric monoclonal antibody consisting of the entire variable domain of a murine antibody (25%) attached to the human IgG1 region (75%); it binds with high affinity and specificity to TNF-a, neutralizes the biologically active soluble cytokine and also blocks the membrane-bound cytokine. It has been licensed in the U.S.A. and Europe for the treatment of Crohn disease, ankylosing spondylitis, active rheumatoid arthritis and in Europe also for psoriatic arthritis. Moreover, infliximab has proven to be effective in several TNF-a-associated inflammatory dermatoses, such as psoriasis vulgaris, subcorneal pustular dermatosis and pyoderma gangrenosum. Upon binding of pathogenetic antibodies to their desmosomal targets, TNF-a and interleukin-1 are released by epidermal keratinocytes at the site of intraepidermal loss of adhesion. In vitro cultures of human keratinocytes are resistant to the acantholytic effect of pathogenic, desmoglein (Dsg) 3-specific autoantibodies upon pretreatment with anti-TNF-a antibodies. This protective effect of TNF-a blockage can be reproduced in vivo: Feliciani et al. showed that the injection of anti-Dsg 3 IgG rendered TNF receptor 1 ⁄2 deficient mice more susceptible to blister formation than their syngenic ‘wild type’ counterparts with an intact TNF receptor. Thus, TNF-a blockade by infliximab might be a short-term therapeutic option for immediate control of refractory PV and a valuable tool to reinstall responsiveness to standard immunosuppressive treatment. However, potential side-effects due to the immunosuppressive potential of infliximab such as severe bacterial infections, viral infections and tuberculosis have to be carefully considered and constitute a serious hazard in patients on chronic immmunosuppressive therapy. A synopsis of potential serious side-effects of infliximab is listed under http://www.rheumanet.org (German, accessed 27 March 2005).
Published in
British Journal of Dermatology
|
12
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6 | 2005 |
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