Gemfibrozil vs



Keywords: drug-induced liver injuries, hepatotoxicity, medications, supplements, liver diseases, drugs, liver injury
Description: Clinical and research information on drug-induced liver injury.

Gemfibrozil is a fibric acid derivative used in the therapy of hypertriglyceridemia and dyslipidemia. Gemfibrozil therapy is associated with mild and transient serum aminotransferase elevations and with rare instances of acute liver injury.

Gemfibrozil (jem fye' broe zil) is a fibric acid derivative and lipid lowering agent. The lipid lowering activity of gemfibrozil is probably mediated by its interactions with the peroxisome proliferator activated receptor alpha (PPARα), which regulates gene expression of enzymes involved in fatty acid oxidation. Gemfibrozil increases lipoprotein lipase levels, which enhance clearance of triglyceride rich lipoproteins. Gemfibrozil was approved for use in the United States in 1981 and it is still widely used with more than 5 million prescritions filled yearly. Gemfibrozil is recommended for therapy of hypertriglyceridemia (Fredrickson type IV and V hyperlipidemia) and hypercholesterolemia (type IIb). Gemfibrozil therapy has been shown to lower rates of myocardial infarction and stroke, most likely as a result of its effects on HDL cholesterol and triglyceride levels. Gemfibrozil is available in multiple generic forms and under the brand name of Lopid as tablets of 600 mg. The recommended dosage is 600 mg twice daily before morning and evening meals. Common side effects of gemfibrozil include gastrointestinal upset, diarrhea, constipation and fatigue. Fibrates have multiple drug interactions requiring careful review and use.

Mild, transient serum aminotransferase elevations develop in approximately 20% of patients receiving gemfibrozil, but values above 3 times normal in 5% or less. These abnormalities are usually asymptomatic and transient, resolving even with continuation. However, there have also been rare reports of clinically apparent liver injury in patients on long term gemfibrozil. The clinical presentation was highly variable. The onset of injury varied from a few weeks to several years after starting the medication and the pattern of serum enzyme elevations ranged from hepatocellular (Case 1) to mixed to cholestatic. Cases have not been associated with signs of immunoallergic (fever, rash, eosinophilia) or autoimmune hepatitis and recovery has been prompt and complete with stopping therapy.

The mechanism of hepatotoxicity of the gemfibrozil is not known, but is likely due to an immunologic response to an intermediate of its metabolism.






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