Abstract
A clinical case is described of infliximab-induced erythrodermic psoriasis resistant to conventional topical therapy and high-dose corticosteroids. Cyclosporine therapy for some months resolved the severe psoriasis picture. Pathogenetic mechanisms are considered through which anti-TNF agents could induce psoriasis. An activation of T lymphocytes with cutaneous overexpression of a CXCR3 subset and, mainly, an increase in IFN-α due to the blockage of TNF-α could be the causes for this paradoxical adverse event of biological agents. Cyclosporine can work in psoriasis induced by biological agents thanks to its peculiar suppressive activity on T lymphocytes and the concomitant specific action on keratocytes and angiogenesis.
