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DOI: 10.1017/S1462399408000628; 28 March 2008
Marco Arrese, Rocio I.R. Macias, Oscar Briz, Maria J. Perez and Jose J.G. Marin (2008) Molecular pathogenesis of intrahepatic cholestasis of pregnancy. Expert Rev. Mol. Med. Vol. 10, e9, DOI: 10.1017/S1462399408000628

Molecular pathogenesis of intrahepatic cholestasis of pregnancy

Marco Arrese a1 c1, Rocio I.R. Macias a2, Oscar Briz a3, Maria J. Perez a3 and Jose J.G. Marin a2

a1 Department of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
a2 Laboratory of Experimental Hepatology and Drug Targeting (HEVEFARM)
a3 Research Unit, CIBERehd, University Hospital, University of Salamanca, Spain.

c1 Corresponding author: Marco Arrese, Departamento de Gastroenterología, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago 833-0024, Chile. Tel: + 56 2 6863820; Fax: + 56 2 6397780; E-mail: marrese@med.puc.cl

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.

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