title: Hepatitis C virus-associated pruritus: Etiopathogenesis and therapeutic strategies.
abstract: In addition to its contributing role in the development of chronic liver diseases, chronic hepatitis C virus (HCV) infection is associated with extrahepatic manifestations, particularly, cutaneous-based disorders including those with pruritus as a symptom. Pruritus is frequently associated with the development of chronic liver diseases such as cholestasis and chronic viral infection, and the accumulation of bile acids in patients' sera and tissues as a consequence of liver damage is considered the main cause of pruritus. In addition to their role in dietary lipid absorption, bile acids can trigger the activation of specific receptors, such as the G protein-coupled bile acid receptor (GPBA/ TGR5). These types of receptors are known to play a crucial role in the modulation of the systemic actions of bile acids. TGR5 expression in primary sensory neurons triggers the activation of the transient receptor potential vanilloid 1 (TRPV1) leading to the induction of pruritus by an unknown mechanism. Although the pathologic phenomenon of pruritus is common, there is no uniformly effective therapy available. Understanding the mechanisms regulating the occurrence of pruritus together with the conduction of large-scale clinical and evidence-based studies, may help to create a standard treatment protocol. This review focuses on the etiopathogenesis and treatment strategies of pruritus associated with chronic HCV infection.
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Youssef
authors.initials: Y
authors.lastname: Alhmada
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Denis
authors.initials: D
authors.lastname: Selimovic
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Fadi
authors.initials: F
authors.lastname: Murad
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Sarah-Lilly
authors.initials: SL
authors.lastname: Hassan
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Youssef
authors.initials: Y
authors.lastname: Haikel
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Mossaad
authors.initials: M
authors.lastname: Megahed
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Matthias
authors.initials: M
authors.lastname: Hannig
authors.affiliation: Youssef Alhmada, Mohamed Hassan, Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, United States.
authors.forename: Mohamed
authors.initials: M
authors.lastname: Hassan
mesh_terms: D002779:Cholestasis / Q000209:etiology / Q000503:physiopathology; D016207:Cytokines / Q000378:metabolism; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D008246:Lysophospholipids / Q000378:metabolism; D010727:Phosphoric Diester Hydrolases / Q000378:metabolism; D011537:Pruritus / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D000099189:Lysophospholipase D
chemical_list: D016207:Cytokines; D008246:Lysophospholipids; D010727:Phosphoric Diester Hydrolases; D000099189:Lysophospholipase D; C032881:lysophosphatidic acid
keywords: Autotoxin; Cholestasis; Hepatitis C virus; Lysophosphatidic acid; PI3 kinase; Pruritus