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Influence of Combined Therapy with Mevinolin and Interruption of Bile-Acid Reabsorption on Low Density Lipoproteins in Heterozygous Familial Hypercholesterolemia

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Grant support: by the Veterans Administration, Southwestern Medical Foundation, Moss Heart Foundation, and the National Institutes of Health (grants HL-29252 and GCRC grant M01-RR 00633).

▸Requests for reprints should be addressed to Dr. Scott M. Grundy, M.D., Ph.D.; Center for Human Nutrition, University of Texas Health Science Center at Dallas, Room G4-100, 5323 Harry Hines Boulevard; Dallas, TX 75235.

Dallas, Texas

© 1985 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1985;103(3):339-343. doi:10.7326/0003-4819-103-3-339
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Patients with heterozygous familial hypercholesterolemia have a 50% deficiency of receptors for plasma low density lipoproteins (LDL) that induces a marked increase in plasma LDL levels. Two therapeutic measures that seem to increase the synthesis of LDL receptors are interruption of the enterohepatic circulation of bile acids with either bile-acid sequestrants or the ileal-exclusion operation, and competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase with mevinolin or compactin. To determine the effectiveness of this combination and the mechanisms of lowering LDL levels, we measured turnover rates of LDL apoprotein (apo-LDL) before and during treatment with mevinolin and colestipol in eight patients with heterozygous familial hypercholesterolemia. Drug therapy reduced LDL cholesterol levels by an average of 52%; this response was due to a 40% increase in fractional catabolic rate of apo-LDL and a 26% decrease in its production rate. A similar response was obtained in two patients who had previously had an ileal-exclusion operation for severe hypercholesterolemia and who were treated with mevinolin.





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