Lipid parameters predicting liver function in patients with cirrhosis and after liver transplantation

BACKGROUND/AIMS: The liver plays a central role in the production and metab olism of lipoproteins, regulating their synthesis and degradation. The prot ein content of the lipoproteins are the so-called apolipoproteins. Some of the apolipoproteins serve as cofactors for enzymatic reactions, as ligands for interaction with specific receptors, and as structural proteins. Apolip oprotein B (apoB) is the primary structural component of the atherogenic lo w density lipoprotein (LDL) particles and has a specific binding region for interacting with the LDL-receptor. In contrast, apolipoprotein A-I (apoA-I ) represents the primary protein content of the high density lipoprotein (H DL) particles, which interacts with the putative HDL-receptor, and stimulat es the enzymatic reaction of lecithin-cholesterol acyltransferase (LCAT) re sulting in esterified cholesterol, which is the essential step in the proce ss of reverse cholesterol transport. METHODOLOGY: We studied lipid parameters in arterial and hepatic venous ser um samples from 52 patients with cirrhosis and from 16 patients in the clin ically stable long-term course after liver transplantation. Splanchnic bloo d flow was measured (indocyanine-green steady-state infusion) and hepatic e xtraction/production rates were calculated. To assess the influence of the clinical stage of established cirrhosis, the quantitated parameters were st atistically analyzed. RESULTS: In cirrhosis, apolipoprotein A-I levels are decreased depending on the clinical stage (p<0.01). This parameter showed excellent correlations to liver function tests. Triglycerides (TG) (p<0.05) and cholesterol (Chol) (p<0.05) were reduced as well, whereas apolipoprotein B levels did not cha nge. In cirrhosis, hepatic production of both cholesterol and triglycerides were decreased (p<0.05 each), as well as hepatic extraction of free fatty acids (FFA) (p<0.01). Except for cholestatic liver disease with raised seru m cholesterol (p<0.05) and apolipoprotein B levels (p<0.001), the etiology of cirrhosis had no impact on the observed serum lipid alterations. CONCLUSIONS: The serum concentrations of the determined lipid parameters de pend primarily on liver function. Decreased liver function was associated w ith reduced extraction of free fatty acids and reduced cholesterol and trig lyceride synthesis. Liver transplantation restored the lipid abnormalities to normal. Finally, apolipoprotein A-I served as an excellent parameter for predicting liver function in the studied patients.