Abstract
Discovery of pruritus-specific mediators and receptors facilitated the neurobiological concept of pruritus: itch-specific (histamine-dependent and histamine-independent C-fibers); itch-specific receptors on cutaneous and spinal neurons; "dialogue" between the pruritus-specific neurons and cells in the skin; peripheral and central mediation of pruritus; functional "pruritus-specific matrix" in the brain with a role of pruritus center. In 10%-50% of persons without skin diseases, pruritus is considered the manifestation of a systemic disorder. Identification of pruritus within autoimmune and inflammatory diseases in dermatology is based on the clinical picture and nature of the underlying disease, implying the development of pruritus on primarily and/or secondarily inflamed skin. In the internal medicine, pruritus commonly presents on primarily non-inflamed skin., involvement of the skin and gastrointestinal tract are two independent risk factors of pruritus in systemic sclerosis, and of anal/vulvar pruritus. Classification combines etiological and clinical criteria and should be considered the only segment of a comprehensive approach to pruritus of unknown origin.
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