Intrahepatic cholestasis of pregnancy (ICP) has an increased predisposition to occur in the third trimester of pregnancy and has a varied population incidence rates due to genetic influences. Owing to the adverse and unpredictable fetal outcomes, it poses a serious therapeutic challenge to the clinician. A rise in the incidence of iatrogenic prematurity has been observed, raising concerns over the perinatal outcomes. Excess bile acids and altered placental transport mechanisms have been strongly implicated in the pathogenesis of ICP and its complications. The exact etiology is not known; yet major underlying risk factors that are thought to contribute to the disease process include genetic, environmental, hormonal, and immunological. Newer molecular processes acting at the placental level, apart from specific histopathological changes, have assumed significance in recent times. In this review, we attempt to highlight the recent understanding of the mechanisms that operate in the placenta in patients with obstetric cholestasis that lead to poor fetal outcomes, through various studies published in the literature. Despite these additions to the existing knowledge on the etiopathogenesis of obstetric cholestasis and its possible placental origin, further studies are needed to validate the newer concepts.
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