Τόμος 25 (2007) – Τεύχος 1 – Άρθρο 4 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Ελληνική Έκδοση – Volume 25 (2007) – Issue 1– Article 4 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-Greek Edition

Εμφάνιση Ψωριασικόμορφων Εξανθημάτων σε Ασθενείς υπό Αντι-TNFα Αγωγή

Psoriasiform lesions in parients receiving anti-TNFa treatment

Ελληνικά – Greek

Άρθρο

Article

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Tumor necrosis alpha blockade has proved to be very effective in the treatment of several autoimmune disorders, including rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel diseases and psoriatic arthritis/ psoriasis. Skin abnormalities represent a significant proportion of the adverse events linked to the use of anti TNF-α agents, mainly in the form of skin infections, eczema, drug-related eruptions, vasculitis, cutaneous lupus erythematosus and skin malignancies. Lately, a continuously growing number of cases describing psoriasis development during TNF-α antagonist therapy are being reported, raising the possibility of a direct causative relationship of these agents with the induction or exacerbation of psoriasis. We report the development of psoriasiform lesions (plaques or palmoplantar pustulosis) in a series of 8 patients from a total of 200 patients receiving anti-TNFα agents for a variety of rheumatological condi­tions at our center. The puzzling observation that medications used to treat psoriasis may induce psoria­sis suggests a complex role for TNF-α antagonists in the pathogenesis of this inflammatory skin disease. The underlying mechanism responsible for this ad­verse event of the treatment remains unclear. A possi­ble explanation might be that a subpopulation of pa­tients under anti-TNFα treatment is prone to develop palmoplantar pustulosis, a condition which is charac­terized by lower levels of TNFα expression, a hypothe­sis which however, even if proven, would not account for all of the cases encountered. Further investigation is warranted towards identification of the pathophysi­ologic mechanism responsible for this phenomenon, and to determine the best therapeutic strategy for this condition regardless of the continuation or not of the TNF-α antagonist regimen.