Treatment with colestipol results in a significant increase in lipoprotein LpAl. Lipoprotein LpAl is one of the two major lipoprotein particles within the high-density lipoprotein (HDL) density range³, and has been shown in cell culture to promote cholesterol efflux or removal from cells⁴. Although the significance of this finding has not been established in clinical studies, the elevation of the lipoprotein LpAl particle within the HDL fraction is consistent with an antiatherogenic effect of colestipol hydrochloride, even though little change is observed in HDL cholesterol (HDL-C).

In patients with heterozygous familial hypercholesterolemia who have not obtained an optimal response to colestipol hydrochloride alone in maximal doses, the combination of colestipol hydrochloride and nicotinic acid has been shown to further lower serum cholesterol, triglyceride, and LDL-cholesterol (LDL-C) values. Simultaneously, HDL-C values increased significantly. In many such patients it is possible to normalize serum lipid values.^5-7

Preliminary evidence suggests that the cholesterol lowering effects of lovastatin and the bile acid sequestrant, colestipol hydrochloride, are additive. The effect of intensive lipid-towering therapy on coronary atherosclerosis has been assessed by arteriography in hyperlipidemic patients. In these randomized, controlled clinical trials, patients were treated for two to four years by either conventional measures (diet, placebo, or in some cases low-dose resin), or with intensive combination therapy using diet and COLESTID Granules plus either nicotinic acid or lovastatin. When compared to conventional measures, intensive lipid-lowering combination therapy significantly reduced the frequency of progression and increased the frequency of regression of coronary atherosclerotic lesions in patients with or at risk for coronary artery disease.^8-11

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