For bile acid sequestrants:
Bile acid-binding resins (cholestyramine, colestipol, colesevelam) work by binding to bile acid in the gastrointestinal tract, interfering with its enterohepatic circulation. LDL is reduced as a consequence, because hepatic cholesterol is consumed in the re-synthesis of bile acids, which in turn increases the uptake of LDL from the circulation. Bile acid production and secretion is increased 10-fold because of the interruption in the enterohepatic circulation of bile acids. Bile acid-binding agents increase the cholesterol content of bile, increasing the risk of gallstone formation. Fibrates also increase the cholesterol content of bile, and thus also increase the risk for gallstones. Both fibrates and bile acid-binding resins should be used with caution in patients with preexisting gallbladder disease.
Statins on the other hand (rosuvastatin, atorvastatin, simvastatin, lovastatin, pravastatin, and fluvastatin), they can lower LDL cholesterol by inhibiting the enzyme HMG-CoA reductase in the liver. They have less effect than the fibrates or niacin in reducing triglycerides and raising HDL-cholesterol. There is limited evidence to support the use of statins for primary prevention in people with low cardiovascular risk. The most common adverse side effects are raised liver enzymes and muscle problems (rhabdomyolysis).
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