Plasma Lipoprotein and Apolipoprotein Profile in Alcoholic Patients with and without Liver Disease: On the Relative Roles of Alcohol and Liver Injury

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Abstract
In the present study, we report on alterations in plasma lipid, lipoprotein and apolipoprotein patterns in three separate populations of alcoholic patients, one without liver damage (Group I), a second presenting steatosis or mild alcoholic hepatitis or both (Group II) and a third with alcoholic cirrhosis (Group III), using a healthy, normolipidemic, nonalcoholic group as controls (Group C). Total plasma cholesterol levels were elevated in Groups II and III when compared with Groups I and C, while the ratio of esterified to free cholesterol was considerably lower in Group III than in the other groups. Plasma apo-AI levels were higher in Groups I and II than in Group C, but varied over a wide range in Group III. Apo-AII was present at higher concentrations in Groups I and II than in both Groups III and C. In contrast, no significant differences were detected in total apo-B levels, irrespective of the group. Modifications in the chemical composition of plasma lipoproteins primarily concerned a reduction in the cholesteryl ester content of low-density lipoproteins (LDL) and high-density lipoprotein (HDL) in Group III, this being compensated by a reciprocal increase in triglyceride. In addition, Group III lipoproteins, with the exception of HDL3 (density 1.100 to 1.140 gm per ml), exhibited a greater content of phospholipids than those of corresponding density from patients in Groups I and II. No significant differences were found in very low-density lipoprotein concentrations, while LDL levels increased in parallel with the severity of liver injury. In Groups I and II, HDL2 concentrations were elevated relative to Group C, while HDL3 decreased in parallel with the degree of impairment of liver function and thus from Group C to Group III. Such opposing tendencies led to an HDL2:HDL3 ratio which was more than 5-fold higher than normal in Group III. The distribution of apoprotein B in the ultracentrifugal subfractions revealed no significant modification between the different groups. By contrast, in Groups I and II, apo-AI and apo-AII levels increased consequent to higher concentrations of HDL2. Our data suggest that abnormal HDL particles preferentially enriched in apo-AII and possibly apo-AI were present in Group I, while the lowest levels of both apo-AI and apo-AII were seen in Group III. No simple association is evident between a well-defined plasma lipid, lipoprotein and/or apolipoprotein profile and chronic alcoholism in the presence or absence of liver injury. Nonetheless, our findings suggest that measurement of the absolute concentrations and ratio of HDL2 and HDL3, as well as of the levels and ratio of apo-AI and apo-AII in these subclasses, may permit differentiation of certain of the subpopulations of chronic alcoholics described herein.