bsorption, but had a small yet statistically significant effect on its rate of absorption; the time to reach maximum concentration was delayed approximately 30 minutes. effects on the absorption of other beta-blockers have not been determined. therefore, patients on propranolol should be observed when colestipol hydrochloride tablets are either added or deleted from a therapeutic regimen. studies in humans show that the absorption of chlorothiazide as reflected in urinary excretion is markedly decreased even when administered one hour before colestipol hydrochloride. the absorption of tetracycline, furosemide, penicillin g, hydrochlorothiazide and gemfibrozil was significantly decreased when given simultaneously with colestipol hydrochloride; these drugs were not tested to determine the effect of administration one hour before colestipol hydrochloride. no depressant effect on blood levels in humans was noted when colestipol hydrochloride was administered with any of the following drugs: aspirin, clindamycin, clofibrate, methyldopa, nicotinic acid (niacin), tolbutamide, phenytoin or warfarin. particular caution should be observed with digitalis preparations since there are conflicting results for the effect of colestipol hydrochloride on the availability of digoxin and digitoxin. the potential for binding of these drugs if given concomitantly is present. discontinuing colestipol hydrochloride could pose a hazard to health if a potentially toxic drug that is significantly bound to the resin has been titrated to a maintenance level while the patient was taking colestipol hydrochloride. bile acid binding resins may also interfere with the absorption of oral phosphate supplements and hydrocortisone. a study has shown that cholestyramine binds bile acids and reduces mycophenolic acid exposure. as colestipol also binds bile acids, colestipol may reduce mycophenolic acid exposure and potentially reduce efficacy of mycophenolate mofetil.

drug therapy. shorter periods may be considered in patients with severe elevations of ldl-c or with definite chd. according to the ncep guidelines, the goal of treatment is to lower ldl-c and ldl-c is to be used to initiate and assess treatment response. only if ldl-c levels are not available, should the total-c be used to monitor therapy. the ncep treatment guidelines are shown below. * coronary heart disease or peripheral vascular disease (including symptomatic carotid artery disease). ** other risk factors for coronary heart disease (chd) include: age (males: ≥ 45 years; female: ≥ 55 years or premature menopause without estrogen replacement therapy); family history of premature chd; current cigarette smoking; hypertension; confirmed hdl-c < 35 mg/dl (0.91 mmol/l); and diabetes mellitus. subtract one risk factor if hdl-c is ≥ 60 mg/dl (1.6 mmol/l). ldl-cholesterol mg/dl (mmol/l) definite atherosclerotic disease * two or more other risk factors ** initiation level goal no no ≥ 190 (≥ 4.9) < 160 (< 4.1) no yes ≥ 160 (≥ 4.1) < 130 (< 3.4) yes yes or no ≥ 130 (≥ 3.4) ≤ 100 (≤ 2.6)

ochloride tablets to minimize possible interference with their absorption. (see drug interactions .) before administration of colestipol hydrochloride tablets define the type of hyperlipoproteinemia, as described in ncep guidelines. institute a trial of diet and weight reduction. establish baseline serum total and ldl-c and triglyceride levels. during administration of colestipol hydrochloride tablets the patient should be carefully monitored clinically, including serum cholesterol and triglyceride levels. periodic determinations of serum cholesterol levels as outlined in the ncep guidelines should be done to confirm a favorable initial and long-term response. failure of total or ldl-c to fall within the desired range should lead one to first examine dietary and drug compliance. if these are deemed acceptable, combined therapy or alternate treatment should be considered. significant rise in triglyceride level should be considered as indication for dose reduction, drug discontinuation or combined or alternate therapy.

stitis and cholelithiasis have been rarely reported in patients receiving colestid granules and are not necessarily drug related. difficulty swallowing and transient esophageal obstruction have been rarely reported in patients taking colestipol hydrochloride tablets. transient and modest elevations of aspartate aminotransferase (ast, sgot), alanine aminotransferase (alt, sgpt) and alkaline phosphatase were observed on one or more occasions in various patients treated with colestipol hydrochloride. the following nongastrointestinal adverse reactions have been reported with generally equal frequency in patients receiving colestipol hydrochloride tablets, colestid granules or placebo in clinical studies: cardiovascular chest pain, angina and tachycardia have been infrequently reported. hypersensitivity rash has been infrequently reported. urticaria and dermatitis have been rarely noted in patients receiving colestid granules. musculoskeletal musculoskeletal pain, aches and pains in the extremities, joint pain and arthritis and backache have been reported. neurologic headache, migraine headache and sinus headache have been reported. other infrequently reported complaints include dizziness, light-headedness and insomnia. miscellaneous anorexia, fatigue, weakness, shortness of breath and swelling of the hands or feet, have been infrequently reported. to report suspected adverse reactions, contact zydus pharmaceuticals (usa) inc., at 1-877-993-8779 or fda at 1-800-fda-1088 or www.fda.gov/medwatch.

bsorption, but had a small yet statistically significant effect on its rate of absorption; the time to reach maximum concentration was delayed approximately 30 minutes. effects on the absorption of other beta-blockers have not been determined. therefore, patients on propranolol should be observed when colestipol hydrochloride tablets are either added or deleted from a therapeutic regimen. studies in humans show that the absorption of chlorothiazide as reflected in urinary excretion is markedly decreased even when administered one hour before colestipol hydrochloride. the absorption of tetracycline, furosemide, penicillin g, hydrochlorothiazide and gemfibrozil was significantly decreased when given simultaneously with colestipol hydrochloride; these drugs were not tested to determine the effect of administration one hour before colestipol hydrochloride. no depressant effect on blood levels in humans was noted when colestipol hydrochloride was administered with any of the following drugs: aspirin, clindamycin, clofibrate, methyldopa, nicotinic acid (niacin), tolbutamide, phenytoin or warfarin. particular caution should be observed with digitalis preparations since there are conflicting results for the effect of colestipol hydrochloride on the availability of digoxin and digitoxin. the potential for binding of these drugs if given concomitantly is present. discontinuing colestipol hydrochloride could pose a hazard to health if a potentially toxic drug that is significantly bound to the resin has been titrated to a maintenance level while the patient was taking colestipol hydrochloride. bile acid binding resins may also interfere with the absorption of oral phosphate supplements and hydrocortisone. a study has shown that cholestyramine binds bile acids and reduces mycophenolic acid exposure. as colestipol also binds bile acids, colestipol may reduce mycophenolic acid exposure and potentially reduce efficacy of mycophenolate mofetil.

drochloride is hydrophilic, but it is virtually water insoluble (99.75%) and it is not hydrolyzed by digestive enzymes. the high molecular weight polymer in colestipol hydrochloride apparently is not absorbed. in humans, less than 0.17% of a single 14 c-labeled colestipol hydrochloride dose is excreted in the urine when given following 60 days of dosing of 20 grams of colestipol hydrochloride per day. the increased fecal loss of bile acids due to colestipol hydrochloride administration leads to an increased oxidation of cholesterol to bile acids. this results in an increase in the number of low-density lipoprotein (ldl) receptors, increased hepatic uptake of ldl and a decrease in beta lipoprotein or ldl serum levels and a decrease in serum cholesterol levels. although colestipol hydrochloride produces an increase in the hepatic synthesis of cholesterol in man, serum cholesterol levels fall. there is evidence to show that this fall in cholesterol is secondary to an increased rate of clearance of cholesterol-rich lipoproteins (beta or low-density lipoproteins) from the plasma. serum triglyceride levels may increase or remain unchanged in colestipol hydrochloride treated patients. the decline in serum cholesterol levels with colestipol hydrochloride treatment is usually evident by one month. when colestipol hydrochloride is discontinued, serum cholesterol levels usually return to baseline levels within one month. periodic determinations of serum cholesterol levels as outlined in the national cholesterol education program (ncep) guidelines, should be done to confirm a favorable initial and long-term response. 1 in a large, placebo-controlled, multiclinic study, the lrc-cppt 2 , hypercholesterolemic subjects treated with cholestyramine, a bile-acid sequestrant with a mechanism of action and an effect on serum cholesterol similar to that of colestipol hydrochloride, had reductions in total and ldl-c. over the 7 year study period the cholestyramine group experienced a 19% reduction (relative to the incidence in the placebo group) in the combined rate of coronary heart disease (chd) death plus nonfatal myocardial infarction (cumulative incidences of 7% cholestyramine and 8.6% placebo). the subjects included in the study were middle-aged men (aged 35 to 59) with serum cholesterol levels above 265 mg/dl, ldl-c above 175 mg/dl on a moderate cholesterol-lowering diet and no history of heart disease. it is not clear to what extent these findings can be extrapolated to other segments of the hypercholesterolemic population not studied. treatment with colestipol results in a significant increase in lipoprotein lpai. lipoprotein lpai is one of the two major lipoprotein particles within the high-density lipoprotein (hdl) density range 3 and has been shown in cell culture to promote cholesterol efflux or removal from cells 4 . although the significance of this finding has not been established in clinical studies, the elevation of the lipoprotein lpai particle within the hdl fraction is consistent with an antiatherogenic effect of colestipol hydrochloride, even though little change is observed in hdl cholesterol (hdl-c). in patients with heterozygous familial hypercholesterolemia who have not obtained an optimal response to colestipol hydrochloride alone in maximal doses, the combination of colestipol hydrochloride and nicotinic acid has been shown to further lower serum cholesterol, triglyceride and ldl-cholesterol (ldl-c) values. simultaneously, hdl-c values increased significantly. in many such patients it is possible to normalize serum lipid values. 5–7 preliminary evidence suggests that the cholesterol-lowering effects of lovastatin and the bile acid sequestrant, colestipol hydrochloride, are additive. the effect of intensive lipid-lowering therapy on coronary atherosclerosis has been assessed by arteriography in hyperlipidemic patients. in these randomized, controlled clinical trials, patients were treated for two to four years by either conventional measures (diet, placebo or in some cases low-dose resin) or with intensive combination therapy using diet and colestid granules plus either nicotinic acid or lovastatin. when compared to conventional measures, intensive lipid-lowering combination therapy significantly reduced the frequency of progression and increased the frequency of regression of coronary atherosclerotic lesions in patients with or at risk for coronary artery disease. 8–11

act your doctor. do not take colestipol hydrochloride tablets again without your doctor's advice. if you are taking other medications, you should take them at least one hour before or four hours after taking colestipol hydrochloride tablets.