The effects of treatment on itch in atopic dermatitis

Abstract

Pruritus causes significant impairment in the quality of life of patients suffering from atopic dermatitis. Treatments for itch in atopic dermatitis range from simple avoidance of pruritus triggers to more complicated systemic therapy. Several treatments aim to target specific mediators of itch in atopic dermatitis, while others improve pruritus by reducing inflammation. Currently, the most effective treatments for atopic dermatitis-associated itch are primarily topical or systemic anti-inflammatory agents. Better management of pruritus in atopic dermatitis is an important goal, and necessitates the development of novel targeted treatments as well as efficient use of current therapies.

Phloretin ameliorates chemokines and ICAM-1 expression via blocking of the NF-κB pathway in the TNF-α-induced HaCaT human keratinocytes

“…Steroids and non-steroidal anti-inflammatory drugs (NSAIDs) are currently used to treat atopic dermatitis and psoriasis [9]. Topical NSAIDs or steroid ointments are used to treat redness, itching, and skin desquamation.…”

A randomized, investigator‐blinded efficacy assessment study of stand‐alone emollient use in mild to moderately severe atopic dermatitis flares

“…10,27,28 Though the first-line anti-inflammatory agents such as topical steroids and calcineurin inhibitors are known to induce short-term improvement, the achievement of lasting relief is a challenge and a most important goal in disease management. 29,30 The pathogenesis of itch related to AD involves numerous factors within the skin, nervous system and the environment and recent advances indicate a critical role for different thermosensitive members of the transient receptor potential (TRP) ion channels superfamily in the transmission and modulation of itch. [31][32][33][34] Independent lines of research provide evidence that both the generation and the alleviation of itch is temperature-dependent.…”

Phloretin‐induced cytoprotective effects on mammalian cells: A mechanistic view and future directions

“…Therefore, phloretin inhibited the MAPK/NF-jB axis leading to decreased ICAM-1 expression and downregulation of cytokines and chemokines secretion by human HaCaT cells. ICAM-1 protein exerts a role in favoring adsorption of leukocyte cells in sites of inflammation in the skin, amplifying the proinflammatory signal in some cases [133,134]. Hence, decreased ICAM-1 expression may suppress skin damage during sustained inflammation.…”