Bile-acid sequestrants interactions

Drug Interactions Various drugs can decrease T absorption. Drugs such as aluminum hydroxide, ferrous sulfate, sucralfate, and calcium carbonate should be separated from T administration by 1 to 2 hours. Bile acid sequestrants (cholestyramine and colestipol) must be separated from T by at least 4 hours and preferably 6 hours. CYP450 enzyme inducing drugs such as phenytoin, carba-mazepine, rifampin, and phenobarbital can increase T requirements. 

Uses Reducdon of LDL total cholesterol alone or in combo w/ an HMG-CoA reductase inhibitor Action Bile acid sequestrant Dose 3 tabs PO bid w/ meals Caution [B, ] Severe GI motility disordei s in pts w/ triglycerides >300 mg/dL (may T levels) use not established in peds Contra Bowel obst Disp Tabs SE Constipation, dyspepsia, myalgia, weakness Interactions t Vit absoiption EMS May cause bowel obstruction, monitor for abd pain and inquii e about i ecent bowel habits OD OD is unlikely b/c dioig is not systemically absorbed but may T risk of bowel obstruction... 

Because of their mechanism of action, bile acid sequestrants can potentially bind with and decrease the oral absorption of almost any other drug. Because these anion-exchange resins contain numerous positive charges, they are much more likely to bind to acidic compounds than to basic compounds or nonelectrolytes. This is not an absolute, however, because cholestyramine and colestipol have been reported to decrease the oral absorption of propranolol (a base) and the lipid-soluble vitamins. A, D, E, and K (nonelectrolytes). As a result, the current recommendation is that all other oral medication should be administered at least 1 hour before or 4 hours after cholestyramine and colestipol. Interestingly, this drug interaction has been used in a beneficial manner to treat digitalis overdose and toxicity. 

Drug interactions The extent to which vitamin D supplementation alters drug effectiveness and toxicity in humans has been systematically reviewed. Bile acid sequestrants and lipase inhibitors were found to inhibit the absorption of vitamin D from the gut. Statins, rifampicin, isoniazid, hydroxychloroquine, antiepileptics, corticosteroids, immimo-suppressive and chemotherapeutic agents, antiretroviral drugs and H2 receptor antagonists interfered with vitamin D metabolism. The interaction between vitamin D and thiazide diuretics could result in hypercalcaetnia. Vitamin D supplementation decreases concentrations of atorvastatin, and could cause hypercalcaetnia in elderly individuals or tixose with compromised renal function or hyperparathyroidism [84 ]. 

The liver is the major organ for both synthesis and degradation of plasma cholesterol. These processes are carried out by the parenchymal cells. These cells have at least two distinct surfaces, sinusoidal and canalicular. The interaction with the plasma occurs on the sinusoidal surface biliary lipids cholesterol, bile acids and phosphatidylcholine are secreted through the canalicular surface. The rate of bile acid synthesis in vivo is determined by the efficiency of the enterohepatic circulation and the cholesterol content of the diet. Bile acid synthesis is stimulated when a high-cholesterol diet is fed or when the enterohepatic circulation is interrupted by feeding cholestyramine - a bile acid sequestrant. 

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