EFFECTS OF BEZAFIBRATE AND OF 2 HMG-COA REDUCTASE INHIBITORS ON LIPOPROTEIN-(A) LEVEL IN HYPERCHOLESTEROLEMIC PATIENTS

Lp(a) level is relatively stable in each individual and is mainly unde r genetic control. Attempts made to lower Lp(a) with pharmacological m eans gave conflicting results. In order to further evaluate the effect of hypocholesterolemic drugs on Lp(a) level, 66 patients with primary hypercholesterolemia were selected. The vast majority of the patients had Lp(a) concentration at the low end of the range of distribution, 7 had undetectable Lp(a) levels and only 2 had Lp(a) higher than 30 mg /dl. No relationship was found between Lp(a) level and serum and lipop rotein lipids. In 12 patients serum cholesterol was well controlled by diet alone and the patients continued the diet for up to 8 months. Th e other patients were randomly subdivided into 3 groups of therapy. Th e first group received slow release bezafibrate 400 mg once a day, the second one pravastatin 20 mg once a day and the third one simvastatin 10 - 40 mg once a day. Drug therapy lasted for 8 months. At the end o f the period, 22 of 29 patients treated with the 2 HMG-CoA reductase i nhibitors had Lp(a) higher than baseline. The difference was statistic ally significant in both groups of patients. No significant change in Lp(a) was observed in diet and in bezafibrate group. Serum and LDL cho lesterol significantly decreased in all the 3 drug groups. The increas e in Lp(a) after the 2 HMG-CoA reductase was small enough to have negl igible effects on cardiovascular risk, but raises the problem of the r ole of LDL receptor in the catabolism of Lp(a).