Abstract

The use of anion exchange resins for the treatment of type II hyperlipoproteinemia is now well established, and one such resin, cholestyramine, has received considerable attention (1, 2). This class of drug acts by preferentially binding bile acids in the intestine and facilitating their increased excretion. Since cholesterol is the precursor of bile acids in the liver, total body cholesterol decreases and there is a subsequent fall in plasma cholesterol. Cholestyramine is found to be only moderately effective because the liver compensates by synthesizing more cholesterol from acetate (3). Also, the proportion of bile acids sequestered in the intestine is small (about 5–10%) compared with the total available (4). For these reasons, effective treatment is obtained with only large doses (12–35 g/day) of the resin. In type II hypercholesterolemic patients even 32 g/day gives a mean decrease of only 22% (5).

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