Since cholesterol is the major precursor of bile acids, the removal of bile acids from the enterohepatic circulation increases the catabolism of cholesterol to form bile acids. The loss of bile acids stimulates a compensatory increase in the hepatic production of cholesterol. It is postulated that the increased hepatic production of cholesterol falls short of the amount lost, leading to a net decrease in circulating cholesterol. This effect, however, has not been clearly shown. Clinically, colestipol lowers LDL and total cholesterol, but has little effect on HDL cholesterol.
Triglycerides increase with colestipol therapy.
Thus, colestipol is appropriate for type II hyperlipoproteinemia in patients without hypertriglyceridemia. Colestipol can bind to substances other than bile acids, especially if they undergo enterohepatic recirculation as does digitoxin. Fab fragments are probably preferred agents for this use. Other agents that bind readily with colestipol include chenodiol, chlorothiazide, digoxin, fat-soluble vitamins, penicillin G, and tetracycline. Colestipol is not affected by digestive enzymes.