Chronic hepatitis C beta-interferon-induced severe hypertriglyceridaemia with apolipoprotein E phenotype E3/2

The mechanisms of hypertriglyceridaemia and changes in plasma lipoprotein subfractions by beta-interferon treatment were studied in a hepatitis C patient with apo E phenotype E3/2. Plasma levels of triglyceride (TG) were increased by treatment with 6 x 10(6) beta-interferon and reached 8.06 mmol/l at 4 weeks of treatment. Low energy and low fat diet reduced them to half the maximal level. Plasma levels of LDL1 (1.019 < d < 1.045)-C, LDL2 (1.045 < d < 1.063)-C, HDL2-C and HDL3-C were 0.39, 0.31, 0.21 and 0.28 mmol/l, respectively, which are low, but the plasma levels of IDL, which is a remnant of TG-rich lipoproteins, was normal at 7 weeks of treatment. The distribution of plasma lipoprotein subfractions returned to normal after interferon treatment was discontinued. The mass and activity of lipoprotein lipase (LPL) were reduced to half the baseline level by interferon treatment. The activity of hepatic triglyceride lipase (HTGL) which transforms IDL to LDL was normal. The patient's apo E phenotype was E3/2; with that phenotype the removal of TG-rich lipoproteins and IDL through the receptors of the remnant and LDL is impaired. But the IDL plasma level was normal, probably because of normal HTGL activity and high LDL-receptor activity. Lymphocyte LDL-receptor activity was double that of the control. We conclude that interferon caused the low mass and activity of LPL which in turn caused the hypertriglyceridaemia. And no retention of the remnant of TG-rich lipoproteins in this patient with apo E3/2 and low levels of LDL subfractions was due to the active removal of them through LDL-receptors as well as the impaired production of them by suppression of LPL by interferon.