Review paper
Updated knowledge on aethiopathogenesis and therapy of pruritus in chronic inflammatory dermatoses

Abstract
Aetiopathogenesis of pruritus is extremely complicated. Itching can be evoked directly by mechanical and thermal stimuli as well as chemical mediators. It may also be a result of indirect stimulation and mast cell degranulation and histamine release. Most of the itch mediators are also implicated in pain neurotransmission. Among all of the substances released during mast cell degranulation the most important are histamine, prostaglandins, proteases and serotonin. Direct stimulation of “itch receptors” is caused by histamine, acetylcholine, endothelin, prostaglandins and cytokines. Proteases, capsaicin and neuropeptides evoke enhanced mast cell degranulation and histamine release. Constant activation of nociceptors in lesional skin has been reported. Many factors such as bradykinin, serotonin, neurotrophins, prostaglandins, interleukins and leukotrienes cause nociceptor sensitization and lower the threshold of afferent nerve fibre activation by histamine. A new therapeutic approach should be a combination of agents that combat peripheral and central sensitization and chronic skin inflammation.
Key words: pruritus, nociceptors, neuropeptides, sensitization.