CHOLESTYRAMINE- cholestyramine powder, for suspension
A-S Medication Solutions


Cholestyramine for Oral Suspension USP, the chloride salt of a basic anion exchange resin, a cholesterol lowering agent, is intended for oral administration. Cholestyramine resin is quite hydrophilic, but insoluble in water. The cholestyramine resin in Cholestyramine is not absorbed from the digestive tract. Four grams of anhydrous cholestyramine resin is contained in 9 grams of Cholestyramine for Oral Suspension USP. Four grams of anhydrous cholestyramine resin is contained in 5 grams of Cholestyramine for Oral Suspension USP, Light. It is represented by the following structural formula:


Cholestyramine for Oral Suspension USP contains the following inactive ingredients: acacia, citric acid, D&C Yellow No. 10, FD&C Yellow No. 6, flavor (natural and artificial Orange), polysorbate 80, propylene glycol alginate and sucrose. Cholestyramine for Oral Suspension USP, Light contains the following inactive ingredients: aspartame, citric acid, colloidal silicon dioxide, D&C Yellow No. 10, FD&C Red No. 40, flavor (natural and artificial Orange), maltodextrin, propylene glycol alginate and xanthan gum.


Cholesterol is probably the sole precursor of bile acids. During normal digestion, bile acids are secreted into the intestines. A major portion of the bile acids is absorbed from the intestinal tract and returned to the liver via the enterohepatic circulation. Only very small amounts of bile acids are found in normal serum.

Cholestyramine resin adsorbs and combines with the bile acids in the intestine to form an insoluble complex which is excreted in the feces. This results in a partial removal of bile acids from the enterohepatic circulation by preventing their absorption.

The increased fecal loss of bile acids due to Cholestyramine administration leads to an increased oxidation of cholesterol to bile acids, a decrease in beta lipoprotein or low density lipoprotein plasma levels and a decrease in serum cholesterol levels. Although in man, Cholestyramine produces an increase in hepatic synthesis of cholesterol, plasma cholesterol levels fall.

In patients with partial biliary obstruction, the reduction of serum bile acid levels by Cholestyramine 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-CPPT1 , hypercholesterolemic subjects treated with Cholestyramine had mean reductions 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 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 and 8.6% placebo). The subjects included in the study were men aged 35-59 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 Trial2, 116 patients (80% male) with coronary artery disease (CAD) documented by arteriography were randomized to Cholestyramine 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 group (p<0.05).

In the St. Thomas Atherosclerosis Regression Study (STARS)3 , 90 hypercholesteroleic men with CAD were randomized to three blinded treatments: usual care, lipid-lowering diet, and lipid-lowering diet plus Cholestyramine. 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 (p<0.02). The mean absolute width of coronary segments decreased in the usual care group, increased slightly (0.003mm) in the diet group and increased by 0.103mm in the diet plus Cholestyramine group (p<0.05). Thus in these randomized controlled clinical trials using coronary arteriography, Cholestyramine monotherapy has been demonstrated to slow progression2,3 and promote regression3 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 on serum lipids similar to that of Cholestyramine for Oral Suspension USP and Cholestyramine for Oral Suspension USP, Light) 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.


1) Cholestyramine for Oral Suspension USP is indicated as adjunctive therapy to diet for the reduction of elevated serum cholesterol in patients with primary hypercholesterolemia (elevated low density lipoprotein [LDL] cholesterol) who do not respond adequately to diet. Cholestyramine may be useful to lower LDL cholesterol in patients who also have hypertriglyceridemia, but it is not indicated where hypertriglyceridemia is the abnormality of most concern.

Therapy with lipid-altering agents should be a component of multiple risk factor intervention in those individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Treatment should begin and continue with dietary therapy specific for the type of hyperlipoproteinemia determined prior to initiation of drug therapy. Excess body weight may be an important factor and caloric restriction for weight normalization should be addressed prior to drug therapy in the overweight.

Prior to initiating therapy with Cholestyramine, 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 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 therapy. The therapy should be continued to sustain cholesterol reduction. If adequate cholesterol reduction is not attained, increasing the dosage of Cholestyramine or adding other lipid-lowering agents in combination with Cholestyramine should be considered.

Since the goal of treatment is to lower LDL-C, the NCEP 4 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.

*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).

LDL-Cholesterol mg/dL (mmol/L)

Definite Atherosclerotic Disease*

Two or More Other Risk Factors**

Initiation Level




≥190 (≥4.9)

<160 (<4.1)



≥160 (≥4.1)

<130 (<3.4)



≥130 (≥3.4)

≤100 (≤2.6)

Cholestyramine monotherapy has been demonstrated to retard the rate of progression 2,3 and increase the rate of regression3 of coronary atherosclerosis.

2) Cholestyramine for oral suspension is indicated for the relief of pruritus associated with partial biliary obstruction. Cholestyramine for oral suspension 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.

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