Abstract
Serum cholesterol esterification in vitro is usually impaired in patients with parenchymal liver disease. This abnormality roughly parallels the severity of the hepatic disorder and appears due to decreased synthesis or release of LCAT by the damaged liver. The extent to which this explains the cholesterol ester derangements observed in vivo is still unclear. but it probably plays a significant role. In contrast, cholesterol esterification in patients with cholestatic hepatobiliary disease has been variably reported as low, normal. or high. Conflicting data may partly be due to the influence of substrate on apparent LCAT activity. Further studies are needed to sort out complex interactions among LCAT, lipoprotein-X, and other factors which probably contribute to the serum lipid abnormalities of cholestasis.

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