Abstract

The pathogenesis of pruritus in psoriasis remains unclear. Many possible mediators were implicated to transmit or modulate this sensation in psoriasis, but none has been clearly proven to be a causative agent of itching. The most often discussed theory mentioned the importance of impaired innervations and neuropeptides imbalance in psoriatic skin. Other possible causes of itching might be increased expression of interleukin 2 or vascular abnormalities. Recent data indicated that pruritus could be also evoked by opioid system, prostanoids, interleukin 31, serotonin, or proteases. Whether these mechanisms are also involved in pruritus accompanying psoriasis requires further investigation. Limited knowledge of pruritus origin in psoriasis is responsible for the lack of the effective antipruritic treatments for psoriatics. Here, we summarize the current knowledge about the pathogenesis of pruritus in psoriasis and point out possible directions of future studies aiming the pathogenesis of this symptom in psoriasis.