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Atromid-S (clofibrate) is an antilipidemic agent. It acts to lower elevated serum lipids by reducing the very low-density lipoprotein fraction (S f 20-400) rich in triglycerides. Serum cholesterol may be decreased, particularly in those patients whose cholesterol elevation is due to the presence of IDL as a result of Type III hyperlipoproteinemia.
The mechanism of action has not been established definitively. Clofibrate may inhibit the hepatic release of lipoproteins (particularly VLDL), potentiate the action of lipoprotein lipase, and increase the fecal excretion of neutral sterols.
Between 95% and 99% of an oral dose of clofibrate is excreted in the urine as free and conjugated clofibric acid; thus, the absorption of clofibrate is virtually complete. The half-life of clofibric acid in normal volunteers averages 18 to 22 hours (range 14 to 35 hours) but can vary by up to 7 hours in the same subject at different times. Clofibric acid is highly protein-bound (95% to 97%). In subjects undergoing continuous clofibrate treatment, 1 g q12h, plasma concentrations of clofibric acid range from 120 to 125 mcg/mL to an approximate peak of 200 mcg/mL.
Several investigators have observed in their studies that clofibrate may produce a decrease in cholesterol linoleate but an increase in palmitoleate and oleate, the latter being considered atherogenic in experimental animals. The significance of this finding is unknown at this time.
Reduction of triglycerides in some patients treated with clofibrate or certain of its chemically and clinically similar analogs may be associated with an increase in LDL cholesterol. Increase in LDL cholesterol has been observed in patients whose cholesterol is initially normal.
Animal studies suggest that clofibrate interrupts cholesterol biosynthesis prior to mevalonate formation.
Last reviewed on RxList: 12/8/2004
This monograph has been modified to include the generic and brand name in many instances.
Additional Atromid-S Information
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