erapy with cholestyramine resin, secondary causes of hypercholesterolemia (e.g., poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease, other drug therapy, alcoholism), should be excluded and a lipid profile performed to assess total cholesterol, hdl-c and triglycerides (tg). for individuals with tg less than 400 mg/dl (<4.5 mmol/l), ldl-c can be estimated using the following equation: ldl-c = total cholesterol - [(tg/5) + hdl-c] for tg levels > 400 mg/dl, this equation is less accurate and ldl-c concentrations should be determined by ultracentrifugation. in hypertriglyceridemic patients, ldl-c may be low or normal despite elevated total-c. in such cases cholestyramine resin may not be indicated. serum cholesterol and triglyceride levels should be determined periodically based on ncep guidelines to confirm initial and adequate long-term response. a favorable trend in cholesterol reduction should occur during the first month of cholestyramine resin therapy. the therapy should be continued to sustain cholesterol reduction. if adequate cholesterol reduction is not attained, increasing the dosage of cholestyramine resin or adding other lipid-lowering agents in combination with cholestyramine resin should be considered. since the goal of treatment is to lower ldl-c, the ncep4 recommends that ldl-c levels be used to initiate and assess treatment response. if ldl-c levels are not available then total-c alone may be used to monitor long-term therapy. a lipoprotein analysis (including ldl-c determination) should be carried out once a year. the ncep treatment guidelines are summarized below. definite atherosclerotic disease * two or more other risk factors † ldl-cholesterol mg/dl (mmol/l) initiation level goal no no ≥ 190 (4.9) ≥ 60 (4.1) no yes ≥ 160 (4.1) ≥ 130 (3.4) yes yes or no ≥ 130 (3.4) ≥ 100 (‑2.6) * 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; females: 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). cholestyramine resin monotherapy has been demonstrated to retard the rate of progression 2,3 and increase the rate of regression 3 of coronary atherosclerosis. 2) cholestyramine is indicated for the relief of pruritus associated with partial biliary obstruction. cholestyramine resin has been shown to have a variable effect on serum cholesterol in these patients. patients with primary biliary cirrhosis may exhibit an elevated cholesterol as part of their disease.

per day. cholestyramine powder should not be taken in its dry form. always mix the dry powder with water or other fluids before ingesting. see preparation instructions. concomitant therapy preliminary evidence suggests that the lipid-lowering effects of cholestyramine on total and ldl-cholesterol are enhanced when combined with a hmg-coa reductase inhibitor, e.g., pravastatin, lovastatin, simvastatin and fluvastatin. additive effects on ldl-cholesterol are also seen with combined nicotinic acid/cholestyramine therapy. see precautions , drug interactions for recommendations on administering concomitant therapy. preparation the color of cholestyramine for oral suspension products powder may vary somewhat from batch to batch but this variation does not affect the performance of the product. place the contents of one level scoopful of cholestyramine for oral suspension products powder in a glass or cup. add at least 2 to 3 ounces of water or the beverage of your choice. stir to a uniform consistency. cholestyramine for oral suspension products powder may also be mixed with highly fluid soups or pulpy fruits with a high moisture content such as applesauce or crushed pineapple.

n of the gallbladder, in patients to whom cholestyramine resin has been given. however, this may be a manifestation of the liver disease and not drug related. one patient experienced biliary colic on each of three occasions on which he took a cholestyramine for oral suspension product. one patient diagnosed as acute abdominal symptom complex was found to have a “pasty mass” in the transverse colon on x-ray. other events (not necessarily drug related) reported in patients taking cholestyramine resin include: gastrointestinal gi-rectal bleeding, black stools, hemorrhoidal bleeding, bleeding from known duodenal ulcer, dysphagia, hiccups, ulcer attack, sour taste, pancreatitis, rectal pain, diverticulitis. laboratory test changes liver function abnormalities. hematologic prolonged prothrombin time, ecchymosis, anemia. hypersensitivity urticaria, asthma, wheezing, shortness of breath. musculoskeletal backache, muscle and joint pains, arthritis. neurologic headache, anxiety, vertigo, dizziness, fatigue, tinnitus, syncope, drowsiness, femoral nerve pain, paresthesia. eye uveitis. renal hematuria, dysuria, burnt odor to urine, diuresis.

ts with partial biliary obstruction, the reduction of serum bile acid levels by cholestyramine resin reduces excess bile acids deposited in the dermal tissue with resultant decrease in pruritus. clinical studies in a large, placebo-controlled, multi-clinic study, lrc-cppt 1 , hypercholesterolemic subjects treated with cholestyramine resin had mean reduction in total and low-density lipoprotein cholesterol (ldl-c) which exceeded those for diet and placebo treatment by 7.2% and 10.4%, respectively. over the seven-year study period the cholestyramine resin group experienced a 19% reduction (relative to the incidence in the placebo group) in the combined rate of coronary heart disease death plus non-fatal myocardial infarction (cumulative incidences of 7% cholestyramine resin and 8.6% placebo). the subjects included in the study were men aged 35 to 59 with serum cholesterol levels above 265 mg/dl and no previous history of heart disease. it is not clear to what extent these findings can be extrapolated to females and other segments of the hypercholesterolemic population. (see also precautions , carcinogenesis, mutagenesis, impairment of fertility ). two controlled clinical trials have examined the effects of cholestyramine monotherapy upon coronary atherosclerotic lesions using coronary arteriography. in the nhlbi type ii coronary intervention trial 2 , 116 patients (80% male) with coronary artery disease (cad) documented by arteriography were randomized to cholestyramine resin or placebo for five years of treatment. final study arteriography revealed progression of coronary artery disease in 49% of placebo patients compared to 32% of the cholestyramine resin group (p<0.05). in the st. thomas atherosclerosis regression study (stars) 3 , 90 hypercholesterolemic men with cad were randomized to three blinded treatments: usual care, lipid-lowering diet, and lipid-lowering diet plus cholestyramine resin. after 36 months, follow-up coronary arteriography revealed progression of disease in 46% of usual care patients, 15% of patients on lipid-lowering diet and 12% of those receiving diet plus cholestyramine resin (p<0.02). the mean absolute width of coronary segments decreased in the usual care group, increased slightly (0.003 mm) in the diet group and increased by 0.103 mm in the diet plus cholestyramine group (p<0.05). thus in these randomized controlled clinical trials using coronary arteriography, cholestyramine resin monotherapy has been demonstrated to slow progression 2,3 and promote regression 3 of atherosclerotic lesions in the coronary arteries of patients with coronary artery disease. 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 intensive combination therapy using diet plus colestipol (an anion exchange resin with a mechanism of action and an effect similar on serum lipids to that of cholestyramine for oral suspension products) 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.