Mediators of Chronic Pruritus in Atopic Dermatitis

Authors: Nicholas K Mollanazar Peter K Smith Gil Yosipovitch

Publish Date: 2015/05/01

Volume: 51, Issue: 3, Pages: 263-292

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Abstract

For centuries itch was categorized as a submodality of pain Recent research over the last decade has led to the realization that itch is in fact a separate and distinct albeit closely related sensation Chronic itch is a common complaint and has numerous etiologies Various receptors TRPA1 TRPV1 PAR2 gastrinreleasing peptide receptor GRPR Masrelated G proteins secreted molecules histamine nerve growth factor NGF substance P SP proteases and cytokines/chemokines thymic stromal lymphopoietin TSLP IL2 IL4 IL13 and IL31 are implicated as mediators of chronic pruritus While much remains unknown regarding the mechanisms of chronic itch this much is certain there is no singular cause of itch Rather itch is caused by a complex interface between skin keratinocytes cutaneous nerve fibers pruritogenic molecules and the peripheral and central nervous systems Atopic dermatitis is one of the most itchy skin dermatoses and affects millions worldwide The sensation of atopic itch is mediated by the interplay between epidermal barrier dysfunction upregulated immune cascades and the activation of structures in the central nervous system Clinicians are in possession of an arsenal of different treatment options ranging from moisturizers topical immunomodulators topical anesthetic ion channel inhibitors systemic immunomodulators as well as oral drugs capable of reducing neural hypersensitization Emerging targeted therapies on the horizon such as dupilumab promise to usher in a new era of highly specific and efficacious treatments Alternative medicine stress reduction techniques and patient education are also important treatment modalities This review will focus on the mediators of chronic pruritus mainly associated with atopic dermatitis atopic itch as well as numerous different therapeutic options

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