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.