[Cholestasis in pregnancy].

Minerva Ginecol

Istituto di Ginecologia ed Ostetricia, Cattedra A, Università degli Studi di Torino.

Published: June 1993

The authors report the main morphological and functional alterations of the liver during the course of pregnancy. The size of the organ does not change and there is a slight (20%) reduction of hepatic flow. Hepatic function is partially modified in view of the following factors: reduced protein synthesis (in particular the albumin component), increased serum levels of cholesterol and triglycerides mediated by steroid hormones, inhibition of canalicular secretion and consequent diminution of the liver's excretory function, variations in serum levels of many markers of cholestasis so much so that they become unreliable due to pregnancy. The high level of sexual steroids also influences cholecystic kinetics: progesterone, in particular, negatively affects the contractile response to cholecystokinin-pancreozymin stimulus. The paper then reports some historical data including those which led to the definition of "gravidic cholestasis" as a clinical condition. The incidence of the disease varies considerably in relation to the geographical area and genetic factors. In Sweden and Finland the percentage ranges between 1 and 3%, whereas much higher values (12-22%) are reported in Chile and among the American Indians. The latest data for Italy reveal an incidence of 0.34%. The onset of disease is conditioned by familial predisposition due to an enhanced sensitivity to estrogens or excessive production of estrogenic metabolites. Among the hepatocytic changes induced by estrogens are the reduced fluidity of sinusoidal plasmatic membranes and the inhibition of vasolateral Na+K+ ATPase pump activity. The last months of gestation are characterized by a "cholestatic state" which may vary in severity from slight symptoms, to itching and idiopathic jaundice.(ABSTRACT TRUNCATED AT 250 WORDS)

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