The experience of the Washington University Lipid Research Center in the treatment of type III hyperlipoproteinemia is reported. Six women and seven men were prescribed a type III diet and/or clofibrate over periods of two to eight months. Mean total plasma cholesterol and triglyceride levels declined by 51 and 74 per cent, respectively, whereas mean levels of high-density lipoprotein (HDL) cholesterol rose from 34 to 50 mg/dl (p < 0.001). Rises in HDL cholesterol levels were seen in every subject, whereas levels of HDL triglycerides fell. Plasma concentrations of apolipoproteins (Apo) A-I and A-II, which make up 90 per cent of the protein moieties of the HDL, were also measured for the first time in the patients with type III hyperlipoproteinemia by radioimmunoassay. Levels of both apoproteins rose with therapy (from 83 to 108 mg/dl and from 35 to 43 mg/dl, respectively, p < 0.02 for both). The sums of triglyceride + cholesterol in the HDL, + A-I + A-II in plasma, were increased by therapy from 170 to 211 mg/dl (p < 0.05). There was a significant negative correlation between the change in HDL cholesterol and the change in very low-density lipoprotein (VLDL) triglyceride (r = - 0.720; p < 0.01). Low-density lipoprotein (LDL) (density (d) 1.006 to 1.063 g/ml) cholesterol remained unchanged but LDL triglycerides decreased. Therefore, both the levels and compositions of the low- and high-density lipoproteins were affected by therapy. Levels of cholesterol and triglycerides in the d < 1.006 g/ml lipoproteins both decreased but without changes in their ratios. Visible regression of xanthomas occurred in six of six patients. Intermittent claudication and angina pectoris diminished in five of five and two of two patients, respectively. Thus, alterations in plasma lipoproteins were associated with clinical improvement. It is not known which of the changes in lipoproteins were most beneficial-the lowering of the d < 1.006 class, which is directly related to high coronary risk, or the elevation of high-density lipoproteins, which are inversely related to risk. Perhaps both contributed to the unique responsiveness of clinical signs and symptoms to therapy in patients with type III hyperlipoproteinemia. © 1979.
