Pruritus is a common symptom that has multifactorial etiologies that range from skin to neural and systemic diseases, and its pathophysiology has been, until recently, poorly understood. In this issue of Clinics and research in hep-atolosv and gastroenterotosy, Kremer et al. present the state-of-art knowledge of pathophysiology and management of cholestasis-induced pruritus. Evidence for a specific pathway for itch was generated by the findings of neurons expressing a gastrin-releasing pep-tide receptor (GRPR) gene that transmit only itch and not pain [1]. GRPR is a G protein-coupled receptor for gastrin-releasing peptide (GRP), a bombesin-like peptide that is widely distributed in the gastrointestinal tract and central nervous system. In a model of chronic itch and atopic dermatitis-like skin lesions in mice, the mice pretreated with a GRPR antagonist presented no scratching [2]. The role of this receptor in humans remains to be defined.
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