Various liver disorders are often associated with decreased concentrations of serum a-and pre-b-lipoproteins. The decreased concentrations of high density lipoproteins (HDL) is primarily due to an impaired lipid binding capacity of apolipoprotein A (apo -4), the major protein moiety of HDL.

Indirect evidence suggests that lecithin : cholesterol acyltransferase (LCAT) is synthesized in the liver. There are, however, controversial reports in the literature correlating LCAT activity with various forms of liver disease. The purpose of this study was to determine LCAT activity in icteric patients. These were classified not only by the aonventional methods, but also with respect to the presence or absence of LP-X, an abnormal plasma lipoprotein, highly specific for demonstrating or excluding cholestasis. LCAT was measured a t different stages of the disease. The patients were divided into 4 groups: I. Hepatitis with cholestasis (LP-X pos.) [li]; 11. Hepatitis without cholestsis (LP-X neg.) [12]; 111. Extrahepatic biliary obstruction (LP-9 pos.) [lo]; IV. Chronic liver failure (LP-5 neg./pos.) [ll]. Compared to normal controls [lJ], patients from group I had low, group I1 had normal, group I11 had normal and group IV had low LC$T activity.In vitro studies clearly excluded the existence of circulating inhibitors of LCST. From these data it is suggested that the ratio of esterified to unesterified cholesterol in liver disease depends on two factors: LCXT activity and the occurrence of the abnormal lipoprotein-X. Furthermore these results indicate that combined determinations of LCAT and LP-X may prove to be useful techniques for differentiating intra-and extrahepatic cholestasis.K e y words: LCAT. LP-S, lipids in liver disease.

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