Lipoproteins, HDL-apolipoproteins, activities of hepatic lipase and lecithin-cholesterol acyltransferase in the plasma of patients with post-alcoholic end-stage liver cirrhosis

Abstract

12 patients with unequivocal post-alcoholic end-stage liver cirrhosis were compared with 12 healthy controls with regard to the plasma concentrations of lipids, lipoproteins (by rate zonal ultra-centrifugation) and apolipoproteins of high-density-lipoproteins (HDL) (by disc electrophoresis), as well as to the activities of lecithin-cholesterol acyltransferase (LCAT) in plasma and of hepatic lipase (HL) in post-heparin plasma. The cirrhotic group showed the following differences (all significant at the p less than 0.01 level) from the control group: Total cholesterol, HDL-cholesterol, very-low-density-lipoproteins (VLDL), HDL, and HL were decreased. Intermediate-density-lipoproteins (IDL) were not detectable in the cirrhotic group. Low-density-lipoproteins (LDL) did not differ significantly from controls. However, LDL from cirrhotic patients contained more triglycerides but less esterified and free cholesterol (all p less than 0.01). The percentage apolipoprotein composition of HDL did not differ significantly between controls and cirrhotics. Surprisingly, LCAT activity in plasma as well as the ratios between esterified and free cholesterol in plasma, LDL, and HDL were nearly identical in both groups. It seems likely that LCAT activity decreases only in the states of acute or subacute liver injury or of biliary obstruction. Severe chronic liver injury or of biliary obstruction. Severe chronic liver damage as in our cases of end-stage liver cirrhosis without any signs of acute liver injury exhibits apparently no defect in cholesterol esterification.

Circulating sterols as predictors of early allograft dysfunction and clinical outcome in patients undergoing liver transplantation

“…The LCAT, secreted by the liver into the blood, influences sterol esterification in circulating lipoproteins (Glomset and Verdery 1977; Dobiasova and Frohlich 1999; Jonas 2000). LCAT activity itself is a sensitive parameter for the severity of the liver disease (Borowsky et al 1980; Breier et al 1983). Thus, the esterification ratio of circulating sterols correlates to the number of intact hepatocytes.…”

“…Conversion of free sterols into sterol esters is catalyzed by the lecithin cholesterol acyltransferase (LCAT). This enzyme is synthesized in the liver and its activity is a sensitive parameter of liver disease (Borowsky et al 1980; Breier et al 1983). Using our LC–MS/MS approach, we are able to determine sterol esterification by simultaneous quantification of the free and esterified sterol including cholesterol, endogenous and non-endogenous sterols.…”

31P NMR spectroscopy of blood plasma: determination and quantification of phospholipid classes in patients with renal cell carcinoma

“…The activity of the lysolecithin acyltransferase was increased. Breier et al 45 found an increase in plasma LCAT activity, as well as significantly higher plasma levels of phospholipids in patients with nephrotic syndrome. However, enzyme activities in plasma of our patients will have to be investigated further.…”

A cross-sectional observational study of lipid profile of cirrhosis of liver patients in a teaching hospital in North Odisha, India

“…24 Brier C et al study conducted on lipoproteins in the plasma of patients with post alcoholic liver cirrhosis, showed that in alcoholic cirrhosis of liver, total cholesterol, HDL, VLDL, HDL-cholesterol were all decreased. 25 The study, conducted by Selimoglu and colleagues showed that variables like serum HDL, LDL level decreased in cirrhotics with the exception of serum triglyceride levels. 26 This finding has some resemblance with our results and hypolipidemia is anticipated in severe liver disease due to decline in synthetic function.…”