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妊娠期肝内胆汁淤积症的分子发病机制。

Molecular pathogenesis of intrahepatic cholestasis of pregnancy.

作者信息

Arrese Marco, Macias Rocio I R, Briz Oscar, Perez Maria J, Marin Jose J G

机构信息

Department of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.

出版信息

Expert Rev Mol Med. 2008 Mar 28;10:e9. doi: 10.1017/S1462399408000628.

Abstract

Intrahepatic cholestasis of pregnancy (ICP) occurs mainly in the third trimester and is characterised by pruritus and elevated serum bile acid levels. ICP is associated with an increased perinatal risk and higher rates of foetal morbidity and mortality. Although the pathogenesis of this disease is unknown, a genetic hypersensitivity to female hormones (oestrogen and/or progesterone) or their metabolites is thought to impair bile secretory function. Recent data suggest that mutations or polymorphisms of genes expressing hepatobiliary transport proteins or their nuclear regulators may contribute to the development and/or severity of ICP. Unidentified environmental factors may also influence pathogenesis of the disease. This review summarises current knowledge on the potential mechanisms involved in ICP at the molecular level.

摘要

妊娠肝内胆汁淤积症(ICP)主要发生在妊娠晚期,其特征为瘙痒和血清胆汁酸水平升高。ICP与围产期风险增加以及胎儿发病率和死亡率升高有关。尽管该疾病的发病机制尚不清楚,但对女性激素(雌激素和/或孕激素)及其代谢产物的遗传超敏反应被认为会损害胆汁分泌功能。最近的数据表明,表达肝胆转运蛋白或其核调节因子的基因突变或多态性可能导致ICP的发生和/或严重程度。未明确的环境因素也可能影响该疾病的发病机制。本综述总结了目前在分子水平上关于ICP潜在机制的知识。

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