HDL and its subfractions in patients with chronic liver diseases.

Serum lipids, lipids (cholesterol, triglycerides and phospholipids) and apo-A in d.>1. 063 fraction, HDL2, HDL8 and VHDL of 10 normal subjects and 34 patients with chronic liver diseases (chronic aggressive hepatitis 2A and 2B, and liver cirrhosis in the compensated and decompensated stages) were analyzed. The analysis of d.>1. 063 and its subfractions (HDL2, HDL8 and VHDL) was achieved by relatively simple procedures with combination of precipitation method and ultracentrifugal technique. Many lipids and apo-A in HDL decreased in these diseases, particularly in liver cirrhosis in the decompensated stage. Triglycerides were exceptional and tended to increase. Lipids and apo-A in both HDL2 and HDL3 tended to decrease but the magnitude of their decrease in HDL3 exceeded that in HDL2• Phospholipids in VHDL also decreased in these patients. The above results demonstrated, therefore, that the decrease in HDL-cholesterol and apo-A is mainly due to their decrease in HDL8, and the decrease in phospholipids in d.>1. 063 is mainly due to their decrease in both HDL and VHDL fractions. These results totally differed from what was seen in atherosclerotic patients in whom the decrease in d.>L 063 fraction chiefly resulted from the decrease in HDL2 fraction. Among the patients with liver diseases there was no significant inverse correlation between serum triglycerides and HDL-cholesterol, as observed in atherosclerotic patients. The LCA T activity and VHDL-phospholipids that contain plentiful lysolecithin produced during the LCAT reaction, were also not correlated. 273