The role of immunosuppression in the pathogenesis of basal cell carcinoma.

effect of thalidomide on TNF-a is not clear. Immune stimulation has been reported in scleroderma patients treated with thalidomide. In a randomized study comparing thalidomide vs. placebo in toxic epidermal necrolysis there was a paradoxical overproduction of TNF-a leading to excess mortality. There was a similar observation of increased plasma TNF-a and soluble TNF-a receptors with thalidomide treatment for oral aphthous ulcers in human immunodeficiency virus-1infected patients. Thalidomide, at a concentration achieved in vivo, could either enhance or suppress the synthesis of TNF-a in vitro depending on the type of cells stimulated. This leads to the suggestion that, in certain circumstances, thalidomide could paradoxically enhance the production of TNF-a. We hypothesize that the flare of our patient’s psoriasis was due to a thalidomide-induced increase in TNF-a. We suggest cautious use of thalidomide in patients with coexisting psoriasis.