Note: Dosages are expressed in terms of anhydrous resin.
Chronic diarrhea due to bile acid malabsorption (off-label use): Oral: Initial: 2 to 4 g/day as a single dose or in divided doses; increase gradually (eg, by 4 g at weekly intervals) based on response and tolerability; daily doses may be administered in 1 to 4 divided doses; maximum: 24 g/day (Sadowski 2020; Wilcox 2014).
Dyslipidemia: Oral: Initial: 4 g 1 to 2 times/day; increase gradually over ≥1-month intervals; maintenance: 8 to 16 g/day divided in 2 doses; maximum: 24 g/day. Note: May be considered in patients with fasting triglyceride level ≤300 mg/dL who do not meet cholesterol treatment goals with dietary modification and other lipid-lowering therapies (eg, maximally tolerated statin and ezetimibe) (AHA/ACC [Grundy 2018]).
Enhanced elimination of leflunomide (off-label use): Oral: 4 g every 6 hours for 2 weeks (EASL 2019) or 8 g 3 times daily for 11 days (Arava prescribing information 2016). Note: In patients who do not require rapid elimination, days of administration may be nonconsecutive (Stine 2016).
Hyperthyroidism associated with Graves disease (adjunctive therapy) (off-label use):
Note: May be used as an adjunct to standard therapies in patients where euthyroidism cannot be achieved prior to thyroidectomy, there is an urgent need for thyroidectomy, or with allergies to antithyroid drugs (ATA [Ross 2016]).
Oral: 4 g 2 to 4 times daily (Mercado 1996; Solomon 1993; Tsai 2005).
Pruritus associated with cholestasis: Oral: Initial: 4 g once or twice daily; may increase dose gradually up to 16 g/day in 2 divided doses (Lindor 2018; manufacturer labeling).
Thyroid storm (adjunctive agent) (off-label use):
Note: May use in combination with other appropriate agents in patients with severe or refractory disease, particularly in patients who cannot take antithyroid drugs (eg, propylthiouracil) (Nayak 2006; Ross 2022).
Oral: 4 g four times/day until thyroid storm resolves (Nayak 2006).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling; however, use with caution in renal impairment; may cause hyperchloremic acidosis.
No dosage adjustment necessary; not absorbed from the gastrointestinal tract.
(For additional information see "Cholestyramine: Pediatric drug information")
Diaper dermatitis: Limited data available: Topical: Infants and Children: Apply to affected area with each diaper change. Note: Product not commercially available; may be prepared as an extemporaneously compounded ointment or paste in Aquaphor or polyethylene glycol; usual concentration 5% to 10%, although higher concentrations (up to 20%) have been compounded; some centers have also used petrolatum as the base for compounding (Preckshot 2001; White 2003; Williams 2011).
Hyperlipidemia: Limited data available: Note: Begin treatment after an adequate trial (6 to 12 months) of intensive lifestyle modification emphasizing body weight normalization and diet. Should not be used in pediatric patients with hypertriglyceridemia (AACE [Jellinger 2017]). Dosages are expressed in terms of anhydrous resin:
Age-directed (fixed-dosing): Children ≥6 years and Adolescents: Oral: Initial: 2 to 4 g/day for 1 week, then increase as tolerated to 8 g/day; children <10 years of age may only tolerate daily dose of 4 g (McCrindle 2007; Sprecher 1996; Tonstad 1996); lipid-lowering effects are better if dose is administered as a single daily dose with the evening meal (single daily morning doses are less effective); however, for patients unable to tolerate doses administered as a single dose, total daily doses may be divided into 2 or 3 divided doses with meals (Daniels 2002); doses >8 g/day may not provide additional significant cholesterol-lowering effects, but may increase adverse effects (Sprecher 1996).
Weight-directed dosing: Children and Adolescents: Oral: 240 mg/kg/day in 3 divided doses; titrate to effect, maximum daily dose: 8 g/day (Gal 2007).
Pruritus secondary to cholestasis: Limited data available: Note: Dosages are expressed in terms of anhydrous resin:
Children ≤10 years: Oral: 240 mg/kg/day in 2 or 3 divided doses administered in the morning around breakfast and if necessary, the third dose at lunch (see "Administration: Pediatric"); may titrate dose to effect. Some experts have suggested a maximum daily dose of 4 g/day; however, higher doses have been reported to treat pruritus in pediatric patients <10 years; in a case report (age: 9 years), the reported effective dose range was 3.3 to 6.6 g/day; in another case series (n=3; ages: 3 to 9 years), the reported range was 1.7 to 10 g/day; in some patients, higher doses were associated with increased steatorrhea and required dosage reduction (Cies 2007; Sprecher 1996).
Children >10 years and Adolescents: Oral: 240 mg/kg/day administered in the morning before breakfast; may titrate dose to effect. Some experts have suggested a maximum daily dose of 8 g/day; in adult patients, the AASLD guidelines recommend an initial dose of 4 g/day; may titrate up to 16 g/day; in some patients, higher doses have been associated with increased steatorrhea requiring dose reduction (Cies 2007; Imam 2012; Lindor 2009; Sprecher 1996).
Diarrhea secondary to intestinal failure, short-bowel syndrome: Very limited data available (ASPEN [Corkins 2015]; Kliegman 2020):
Children and Adolescents: Oral: 240 mg/kg/day in 2 to 3 divided doses; maximum daily dose: 8 g/day has been suggested (Ching 2007; manufacturer's labeling); however, robust clinical trials have not been completed in pediatric patients (ASPEN [Corkins 2015]). Note: Therapeutic effect may differ among products due to excipients (eg, sorbitol, sucrose) which could potentially worsen diarrhea.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in manufacturer's labeling; however, use with caution in renal impairment; may cause hyperchloremic acidosis.
No dosage adjustment necessary; not absorbed from the gastrointestinal tract.
Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Packet, Oral:
Prevalite: 4 g (1 ea, 42 ea, 60 ea) [contains aspartame; orange flavor]
Questran: 4 g (1 ea, 60 ea) [contains fd&c yellow #6 (sunset yellow), quinoline yellow (d&c yellow #10); orange flavor]
Generic: 4 g (1 ea, 60 ea)
Powder, Oral:
Prevalite: 4 g/dose (231 g) [contains aspartame; orange flavor]
Questran: 4 g/dose (378 g) [contains fd&c yellow #6 (sunset yellow), quinoline yellow (d&c yellow #10); orange flavor]
Questran Light: 4 g/dose (210 g) [sugar free; contains aspartame, fd&c red #40 (allura red ac dye), quinoline yellow (d&c yellow #10); orange flavor]
Generic: 4 g/dose (201.6 g, 210 g, 231 g, 239.4 g, 348.6 g, 368.76 g, 378 g)
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Packet, Oral:
Olestyr: 4 g (4 g) [contains fd&c yellow #6(sunset yellow)alumin lake, quinoline (d&c yellow #10) aluminum lake, quinoline yellow (d&c yellow #10)]
Olestyr Light: 4 g (4 g) [contains aspartame, fd&c yellow #6 (sunset yellow), quinoline yellow (d&c yellow #10)]
Generic: 4 g (4 g, 30 ea)
Oral: Administer prepared suspension orally. Not to be taken in dry form. Suspension should not be sipped or held in mouth for prolonged periods (may cause tooth discoloration or enamel decay). Administration at mealtime is recommended. Twice-daily dosing is recommended but may be administered in 1 to 6 doses daily. In general, administer other oral medications ≥1 hour before or 4 to 6 hours after cholestyramine; consult drug interactions database for additional information.
Oral: Administer as prepared suspension; not to be taken in dry form orally; suspension should not be sipped or held in mouth for prolonged periods (may cause tooth discoloration or enamel decay). Administration at mealtime is recommended. Administer other drugs including vitamins or mineral supplements at least 1 hour before or at least 4 to 6 hours after cholestyramine.
Dyslipidemia: Administer as a single dose (preferably) with the evening meal; however, some patients may require divided doses; in pediatric patients, may use 2 to 3 divided doses and in adults up to 6 doses daily.
Pruritus; cholestasis: Administer before breakfast (gall bladder has highest concentration of bile acids available for binding); for patients with an intact gall bladder, it has been suggested to administer the first dose 30 minutes before breakfast, the second dose 30 minutes after breakfast, and the final dose with lunch (Cies 2007).
Enteral tube administration: One sachet (4 g) mixed in 100 mL of water (White 2015).
Dyslipidemia: Adjunct in the management of primary hypercholesterolemia; regression of arteriolosclerosis
Pruritus associated with cholestasis: Treatment of pruritus associated with partial biliary obstruction
Chronic diarrhea due to bile acid malabsorption; Enhanced elimination of leflunomide; Hyperthyroidism associated with Graves disease (adjunctive therapy); Thyroid storm
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Frequency not defined.
Cardiovascular: Edema, syncope
Central nervous system: Anxiety, dizziness, drowsiness, fatigue, headache, neuralgia, paresthesia, vertigo
Dermatologic: Perianal skin irritation, skin irritation, skin rash, urticaria
Endocrine & metabolic: Hyperchloremic metabolic acidosis (children), increased libido, weight gain, weight loss
Gastrointestinal: Abdominal pain, anorexia, biliary colic, constipation, dental bleeding, dental caries, dental discoloration, diarrhea, diverticulitis, duodenal ulcer with hemorrhage, dysgeusia, dysphagia, eructation, flatulence, gallbladder calcification, gastric ulcer, gastrointestinal hemorrhage, hemorrhoidal bleeding, hiccups, intestinal obstruction (rare), melena, nausea, pancreatitis, rectal pain, steatorrhea, tongue irritation, tooth enamel damage (dental erosion), vomiting
Genitourinary: Diuresis, dysuria, hematuria
Hematologic & oncologic: Adenopathy, anemia, bruise, hemorrhage, hypoprothrombinemia, prolonged prothrombin time, rectal hemorrhage
Hepatic: Abnormal hepatic function tests
Neuromuscular & skeletal: Arthralgia, arthritis, back pain, myalgia, osteoporosis
Ophthalmic: Nocturnal amblyopia (rare), uveitis
Otic: Tinnitus
Respiratory: Asthma, dyspnea, wheezing
Hypersensitivity to bile acid sequestering resins or any component of the formulation; complete biliary obstruction
Concerns related to adverse effects:
• Bleeding: Chronic use may be associated with bleeding problems (especially in high doses); may be prevented with use of oral vitamin K therapy.
• Constipation: May produce or exacerbate constipation problems; initiate therapy at a reduced dose in patients with a history of constipation. Hemorrhoids may be worsened.
Disease-related concerns:
• Hypertriglyceridemia: Bile acid sequestrants should not be used in patients with baseline fasting triglyceride levels ≥300 mg/dL or type III hyperlipoproteinemia since severe triglyceride elevations may occur. Use bile acid sequestrants with caution in patients with triglyceride levels 250 to 299 mg/dL and evaluate a fasting lipid panel in 4 to 6 weeks after initiation; discontinue use if triglycerides are >400 mg/dL (Stone 2013).
• Renal impairment: Use caution in patients with renal impairment.
Concurrent drug therapy issues:
• Decreased absorption (orally administered drugs): Not to be taken simultaneously with many other medicines (decreased absorption).
• Patients susceptible to fat-soluble vitamin deficiencies: Use with caution in patients susceptible to fat-soluble vitamin deficiencies. Absorption of fat-soluble vitamins A, D, E, and K and folic acid may be decreased; patients should take vitamins 1 hour before or ≥4 hours after cholestyramine.
Dosage form specific issues:
• Phenylalanine: Some products may contain phenylalanine.
Other warnings/precautions:
• Hyperlipidemia: Secondary causes of hyperlipidemia should be ruled out prior to therapy.
With prolonged use, may potentially cause hypochloremic acidosis due to the exchange of organic anions for chloride; reported pediatric cases observed in younger patients (eg, ages reported: 1.5 days, 4 weeks, 5 weeks, 6 months, 5 years, 10 years); reported precipitating factor in pediatric cases include renal failure or volume depletion in setting of diarrhea or infection and cholestatic jaundice; in adults, concomitant spironolactone therapy identified as factor (Kamar 2015; Kleinman 1976; Scheel 1992). Prolonged exposure to tooth enamel may result in discoloration or erosion; patients should be instructed to avoid sipping or slowly swallowing cholestyramine doses and to maintain good dental hygiene practices. May increase serum triglyceride concentrations; in a trial of children and adolescents (>10 years of age); the serum triglycerides increased 6% to 9% from baseline (not statistically significant) (McCrindle 1997).
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Amiodarone: Bile Acid Sequestrants may decrease the bioavailability of Amiodarone. Management: Consider alternatives to this combination due to the risk of subtherapeutic amiodarone serum concentrations. If amiodarone is coadministered with colesevelam, administer amiodarone at least 4 hours before colesevelam. Risk D: Consider therapy modification
Cardiac Glycosides: Bile Acid Sequestrants may decrease the absorption of Cardiac Glycosides. Risk C: Monitor therapy
Chenodiol: Bile Acid Sequestrants may decrease the serum concentration of Chenodiol. Management: Administration of chenodiol 5 hours or more after bile acid sequestrants may reduce the magnitude of this interaction. Monitor for decreased therapeutic effects of chenodiol in patients receiving bile acid sequestrants. Risk D: Consider therapy modification
Cholic Acid: Bile Acid Sequestrants may decrease the absorption of Cholic Acid. Management: Administer cholic acid at least 1 hour before or 4 to 6 hours after administration of any bile acid-binding products to minimize the potential for a significant interaction. Risk D: Consider therapy modification
Corticosteroids (Oral): Bile Acid Sequestrants may decrease the absorption of Corticosteroids (Oral). Risk C: Monitor therapy
Deferasirox: Bile Acid Sequestrants may decrease the serum concentration of Deferasirox. Management: Avoid combination when possible; if the combination must be used, consider a 50% increase in initial deferasirox dose, with monitoring of serum ferritin concentrations and clinical responses to guide further dosing. Risk D: Consider therapy modification
Ethinyl Estradiol-Containing Products: Bile Acid Sequestrants may decrease the serum concentration of Ethinyl Estradiol-Containing Products. Management: Administer ethinyl estradiol-containing products 4 hours prior to the administration of a bile acid sequestrant. Risk D: Consider therapy modification
Ezetimibe: Bile Acid Sequestrants may decrease the absorption of Ezetimibe. Management: Administer ezetimibe at least 2 hours before or 4 hours after any bile acid sequestrant. Risk D: Consider therapy modification
Fibric Acid Derivatives: Bile Acid Sequestrants may decrease the absorption of Fibric Acid Derivatives. Management: Separate doses by at least 2 hours to minimize this interaction; fenofibric acid labeling recommends administration one hour prior to or 4-6 hours after a bile acid sequestrant. Risk D: Consider therapy modification
Fluvastatin: Cholestyramine Resin may decrease the serum concentration of Fluvastatin. Management: Administer fluvastatin at least 1 hour or greater (particularly with extended-release form) before, or at least 4 hours after cholestyramine to minimize the risk for any significant interaction. Risk D: Consider therapy modification
Leflunomide: Bile Acid Sequestrants may decrease serum concentrations of the active metabolite(s) of Leflunomide. Management: Unless using this combination to intentionally enhance leflunomide elimination, consider an alternative to the bile acid sequestrants when possible. Separating drug administration is not likely to be effective at avoiding this interaction. Risk D: Consider therapy modification
Lomitapide: Bile Acid Sequestrants may decrease the absorption of Lomitapide. Management: Administer lomitapide at least 4 hours before or after administration of a bile acid sequestrant. Risk D: Consider therapy modification
Loop Diuretics: Bile Acid Sequestrants may decrease the absorption of Loop Diuretics. Risk C: Monitor therapy
Maralixibat: Bile Acid Sequestrants may decrease the serum concentration of Maralixibat. Management: Bile acid sequestrants should be administered either at least 4 hours before, or 4 hours after, maralixibat. Risk D: Consider therapy modification
Methotrexate: Bile Acid Sequestrants may decrease the absorption of Methotrexate. Risk C: Monitor therapy
Multivitamins/Fluoride (with ADE): Bile Acid Sequestrants may decrease the serum concentration of Multivitamins/Fluoride (with ADE). Management: Avoid concomitant administration of multivitamins and bile acid sequestrants (eg, cholestyramine). Separate administration of these agents by several hours to minimize the risk of an interaction. Risk D: Consider therapy modification
Multivitamins/Minerals (with ADEK, Folate, Iron): Bile Acid Sequestrants may decrease the serum concentration of Multivitamins/Minerals (with ADEK, Folate, Iron). Specifically, bile acid sequestrants may impair the absorption of fat-soluble vitamins. Management: Avoid concomitant administration of multivitamins and bile acid sequestrants (eg, cholestyramine). Separate administration of these agents by several hours to minimize the risk of an interaction. Risk D: Consider therapy modification
Multivitamins/Minerals (with AE, No Iron): Bile Acid Sequestrants may decrease the serum concentration of Multivitamins/Minerals (with AE, No Iron). Management: Avoid concomitant administration of multivitamins and bile acid sequestrants (e.g., cholestyramine). Separate administration of these agents by several hours to minimize the risk of an interaction. Risk D: Consider therapy modification
Mycophenolate: Cholestyramine Resin may decrease the serum concentration of Mycophenolate. Risk X: Avoid combination
Niacin: Bile Acid Sequestrants may decrease the absorption of Niacin. Management: Consider separating the administration times of niacin and bile acid sequestrants by a few hours in order to reduce the potential for decreased efficacy of these agents. Risk D: Consider therapy modification
Nonsteroidal Anti-Inflammatory Agents: Bile Acid Sequestrants may decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Obeticholic Acid: Bile Acid Sequestrants may decrease the serum concentration of Obeticholic Acid. Management: Administer obeticholic acid at least 4 hours before or at least 4 hours after the administration of bile acid sequestrants. Risk D: Consider therapy modification
Odevixibat: Bile Acid Sequestrants may decrease the serum concentration of Odevixibat. Management: Bile acid sequestrants should be administered either at least 4 hours before, or 4 hours after, odevixibat. Risk D: Consider therapy modification
PHENobarbital: Cholestyramine Resin may decrease the serum concentration of PHENobarbital. Management: Administer phenobarbital at least 1 hour before or 4 to 6 hours after administration of cholestyramine in order to minimize the risk for any significant interaction. Risk D: Consider therapy modification
Pravastatin: Bile Acid Sequestrants may decrease the serum concentration of Pravastatin. Management: Administer pravastatin at least 1 hour before or 4 hours after administration of bile-acid resins (eg, cholestyramine, colestipol, colesevelam) to minimize the risk for any significant interaction. Risk D: Consider therapy modification
Propranolol: Bile Acid Sequestrants may decrease the serum concentration of Propranolol. Risk C: Monitor therapy
Raloxifene: Bile Acid Sequestrants may decrease the absorption of Raloxifene. Management: Consider separating the doses of raloxifene and bile acid sequestrants by at least 4 hours. Risk D: Consider therapy modification
Rosiglitazone: Cholestyramine Resin may decrease the serum concentration of Rosiglitazone. Management: Administer rosiglitazone at least 2 hours prior to cholestyramine in order to minimize the likelihood of an interaction, and monitor patients closely for evidence of reduced rosiglitazone effectiveness. Risk D: Consider therapy modification
Sincalide: Drugs that Affect Gallbladder Function may diminish the therapeutic effect of Sincalide. Management: Consider discontinuing drugs that may affect gallbladder motility prior to the use of sincalide to stimulate gallbladder contraction. Risk D: Consider therapy modification
Spironolactone: Cholestyramine Resin may enhance the adverse/toxic effect of Spironolactone. Specifically, the risks of developing metabolic acidosis and hyperkalemia may be elevated with this combination. Risk C: Monitor therapy
Taurursodiol: Bile Acid Sequestrants may decrease the absorption of Taurursodiol. Risk X: Avoid combination
Teriflunomide: Bile Acid Sequestrants may decrease the serum concentration of Teriflunomide. Management: Unless using this combination to intentionally enhance teriflunomide elimination, consider an alternative to the bile acid sequestrants when possible. Separating drug administration is unlikely to be effective at avoiding the interaction. Risk D: Consider therapy modification
Tetracyclines: Bile Acid Sequestrants may decrease the absorption of Tetracyclines. Risk C: Monitor therapy
Thiazide and Thiazide-Like Diuretics: Bile Acid Sequestrants may decrease the absorption of Thiazide and Thiazide-Like Diuretics. The diuretic response is likewise decreased. Management: Consider separating administraton of bile acid sequestrants and thiazide diuretics by at least 4 hours. Monitor for decreased therapeutic effects of thiazide diuretics if coadministered with a bile acid sequestrant. Risk D: Consider therapy modification
Thyroid Products: Bile Acid Sequestrants may decrease the serum concentration of Thyroid Products. Management: Administer oral thyroid products at least 4 h prior to colesevelam, and at least 1 h before or 4-6 h after cholestyramine. Specific recommendations for colestipol are not available. Monitor for decreased concentrations/effects of the thyroid product. Risk D: Consider therapy modification
Ursodiol: Bile Acid Sequestrants may decrease the serum concentration of Ursodiol. Management: Administer ursodiol 1 hour before or at least 4 to 5 hours after bile acid sequestrants to minimize the potential for any significant interaction. Monitor for decreased therapeutic effects of ursodiol in patients receiving bile acid sequestrants. Risk D: Consider therapy modification
Valproic Acid and Derivatives: Cholestyramine Resin may decrease the serum concentration of Valproic Acid and Derivatives. Management: Separate administration of valproic acid and cholestyramine by at least 3 hours whenever possible in order to minimize this interaction. The impact of concurrent cholestyramine on delayed- or extended-release valproic acid is uncertain. Risk D: Consider therapy modification
Vancomycin: Bile Acid Sequestrants may diminish the therapeutic effect of Vancomycin. Management: Avoid concurrent administration of oral vancomycin and bile acid sequestrants when possible. If use of both agents is necessary, consider separating doses by at least 2 hours to minimize the significance of the interaction. Risk D: Consider therapy modification
Vitamin D Analogs: Bile Acid Sequestrants may decrease the serum concentration of Vitamin D Analogs. More specifically, bile acid sequestrants may impair absorption of Vitamin D Analogs. Management: Avoid concomitant administration of vitamin D analogs and bile acid sequestrants (eg, cholestyramine). Separate administration of these agents by several hours to minimize the potential risk of interaction. Monitor plasma calcium concentrations. Risk D: Consider therapy modification
Vitamin K Antagonists (eg, warfarin): Cholestyramine Resin may decrease the serum concentration of Vitamin K Antagonists. Management: Separate the administration of vitamin K antagonists and cholestyramine by at least 3 to 4 hours. Monitor patients closely for reduced vitamin K antagonist effects (eg, decreased INR, thrombosis) when these agents are combined. Risk D: Consider therapy modification
Cholestyramine (especially high doses or long-term therapy) may decrease the absorption of folic acid, calcium, fat-soluble vitamins (vitamins A, D, E, and K), and iron. Management: Supplementation of folic acid, calcium, fat-soluble vitamins (vitamins A, D, E, and K), and iron may be necessary.
Cholestyramine is used off label to enhance leflunomide elimination. Use of the enhanced elimination procedure is recommended in all females of reproductive potential upon discontinuation of leflunomide. Pregnancy should be avoided until undetectable serum concentrations (<0.02 mg/L) of leflunomide are verified (Brent 2001).
Lipid concentrations increase during pregnancy as required for normal fetal development. When increases are greater than expected, supervised dietary intervention should be initiated. Bile acid sequestrants are recommended when treatment is needed (Avis 2009; Jacobson 2015).
Cholestyramine is not absorbed systemically, but may interfere with maternal vitamin absorption; therefore, regular prenatal supplementation may not be adequate.
Due to lack of systemic absorption, cholestyramine is not expected to be present in breast milk.
When treatment for hypercholesterolemia in breastfeeding women is needed, therapy with bile acid sequestrants may be considered (Jacobson 2015; NICE 2008). However, because use may interfere with maternal vitamin absorption, the manufacturer recommends caution be used if administered to breastfeeding women.
Supplementation of vitamins A, D, E, and K, folic acid, and iron may be required with high-dose, long-term therapy. Some products may contain phenylalanine.
ACC/AHA Blood Cholesterol Guideline recommendations (ACC/AHA [Grundy 2018]; ACC/AHA [Stone 2013]): Lipid profile (fasting or nonfasting) before initiating treatment. Fasting lipid profile should be rechecked 4 to 12 weeks after starting therapy and every 3 to 12 months thereafter.
Lipid treatment goals: May vary depending on clinical condition, different clinical practice guidelines, and expert opinion. Refer to clinical practice guidelines for specific treatment goals.
Forms a nonabsorbable complex with bile acids in the intestine, releasing chloride ions in the process; inhibits enterohepatic reuptake of intestinal bile salts and thereby increases the fecal loss of bile salt-bound low density lipoprotein cholesterol
Onset of action: Peak effect: 21 days
Absorption: None
Excretion: Feces (as insoluble complex with bile acids)
Pack (Cholestyramine Light Oral)
4 g (per each): $3.35
Pack (Cholestyramine Oral)
4 g (per each): $3.35 - $3.37
Pack (Prevalite Oral)
4 g (per each): $5.11
Pack (Questran Oral)
4 g (per each): $7.11
Powder (Cholestyramine Oral)
4 g/dose (per gram): $0.23 - $0.35
Powder (Prevalite Oral)
4 g/dose (per gram): $0.59
Powder (Questran Light Oral)
4 g/dose (per gram): $0.89
Powder (Questran Oral)
4 g/dose (per gram): $0.49
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