Serum TNF-α in psoriasis after treatment with propylthiouracil, an antithyroid thioureylene

The present study examined the effect of treatment with propylthiouracil, given in a dose of 100 mg every 8 hours for 3 months, on the serum levels of TNF-α in 9 patients with plaque psoriasis.Propylthiouracil therapy did not result in a significant decline in serum TNF-α concentrations.The findings suggest that the therapeutic effect of propylthiouracil in psoriasis appears not to be related to any change in the concentration of TNF-α but occurs via an anti-proliferative mechanism as we have previously speculated.Psoriasis is a common skin disorder that affects approximately 2.8 percent of the population and is associated with morbidity that is comparable that seen with life threatening disease [1,2]. There is a clearly established genetic predisposition to the disease [3,4] that is often triggered by the processing of bacterial, viral or chemical antigens by skin antigen presenting cells (APC) or Langerhans cells [5-9]. The disease is presently believed to be a T cell disorder that leads to keratinocyte proliferation [6,10,11]. Plaque formation in the disease reflects both the effects of accelerated proliferation as well as reduced apoptosis in proliferated keratinocytes [12,13]. The events responsible for keratinocyte proliferation have been extensively reviewed [12]. An important cytokine that is associated with keratinocyte proliferation in psoriasis is TNF-α.. TNF-α concentrations are higher in psoriatic lesions than in unaffected skin of psoriatic patients and tend to decline with clearing of the lesions after effective therapy [14-16]. This cytokine is produced by keratinocytes and leads to an increased expression of cellular adhesion molecules that promote, propagate, and amplify the immune signals that are responsible for maintaining the events that lead to psoriasis. Recently introduced therapeutic approaches in the management of psoriasis depend on blocking TNF-α binding to its receptor by using TNF-α hybrid antibodies. Patients treated with such agents