ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Cholestyramine: Drug information

Cholestyramine: Drug information
(For additional information see "Cholestyramine: Patient drug information" and see "Cholestyramine: Pediatric drug information")

For abbreviations, symbols, and age group definitions used in Lexicomp (show table)
Brand Names: US
  • Prevalite;
  • Questran;
  • Questran Light
Brand Names: Canada
  • Cholestyramine-ODAN;
  • DOM-Cholestyramine;
  • JAMP-Cholestyramine Sugar Free;
  • Olestyr;
  • Olestyr Light
Pharmacologic Category
  • Antilipemic Agent, Bile Acid Sequestrant
Dosing: Adult

Note: Dosages are expressed in terms of anhydrous resin.

Chronic diarrhea due to bile acid malabsorption

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 (Ref).

Dyslipidemia

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) (Ref).

Enhanced elimination of leflunomide

Enhanced elimination of leflunomide (off-label use): Oral: 4 g every 6 hours for 2 weeks (Ref) 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 (Ref).

Hyperthyroidism associated with Graves disease

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 (Ref).

Oral: 4 g 2 to 4 times daily (Ref).

Pruritus associated with cholestasis

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 (Ref).

Thyroid storm

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) (Ref).

Oral: 4 g four times/day until thyroid storm resolves (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.

Note: Patients with kidney impairment (eg, eGFR <60 mL/minute/1.73 m2) may be at increased risk of hyperchloremic metabolic acidosis, especially when combined with other precipitating factors (eg, volume depletion, higher cholestyramine doses). Monitor electrolytes and anion gap frequently in patients at high risk (Ref).

Altered kidney function: No dosage adjustment necessary for any degree of kidney dysfunction (no systemic absorption) (Ref).

Hemodialysis, intermittent (thrice weekly): Unlikely to be significantly dialyzed: No supplemental dose or dosage adjustment necessary (no systemic absorption) (Ref).

Peritoneal dialysis: Unlikely to be significantly dialyzed: No dosage adjustment necessary (no systemic absorption) (Ref).

CRRT: No dosage adjustment necessary (Ref).

PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).

Dosing: Hepatic Impairment: Adult

No dosage adjustment necessary; not absorbed from the gastrointestinal tract.

Dosing: Older Adult

Refer to adult dosing.

Dosing: Pediatric

(For additional information see "Cholestyramine: Pediatric drug information")

Diaper dermatitis

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 (Ref).

Hyperlipidemia

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 (Ref). 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 (Ref); 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 (Ref); doses >8 g/day may not provide additional significant cholesterol-lowering effects, but may increase adverse effects (Ref).

Weight-directed dosing: Children and Adolescents: Oral: 240 mg/kg/day in 3 divided doses; titrate to effect, maximum daily dose: 8 g/day (Ref).

Pruritus secondary to cholestasis

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 (Ref).

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 (Ref).

Diarrhea secondary to intestinal failure, short-bowel syndrome

Diarrhea secondary to intestinal failure, short-bowel syndrome: Very limited data available (Ref):

Children and Adolescents: Oral: 240 mg/kg/day in 2 to 3 divided doses; maximum daily dose: 8 g/day has been suggested (Ref); however, robust clinical trials have not been completed in pediatric patients (Ref). 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.

Dosing: Kidney Impairment: Pediatric

There are no dosage adjustments provided in manufacturer's labeling; however, use with caution in renal impairment; may cause hyperchloremic acidosis.

Dosing: Hepatic Impairment: Pediatric

No dosage adjustment necessary; not absorbed from the gastrointestinal tract.

Adverse Reactions (Significant): Considerations
Constipation

Constipation is the most common adverse effect associated with cholestyramine therapy; most cases of constipation are mild, transient, and self-limiting. Constipation may lead to or exacerbate preexisting hemorrhoids (Ref). Patients experiencing constipation may require dosage adjustment or discontinuation of therapy; adequate water and fiber intake or the addition of a stool softener may mitigate this effect. While no direct comparisons have been conducted regarding the risk of constipation between bile acid sequestrants, the incidence of constipation reported in clinical trials is relatively higher with cholestyramine as compared to colesevelam (Ref). Gastrointestinal obstruction has also been reported in pediatric patients (Ref).

Mechanism: Dose-related; cholestyramine is a bile acid sequestrant that forms a nonabsorbable complex with bile acids in the intestine. In turn, the water content in the stool is reduced leading to constipation.

Onset: Varied; may persist for years with continued cholestyramine therapy (Ref).

Risk factors :

• Patients >60 years of age

• High dose

• Rapid dose titration

• Decreased gastrointestinal motility (Ref)

• Recent abdominal surgery (Ref)

• Prior history of gastrointestinal obstruction (Ref)

Fat-soluble vitamin/folate deficiency

Administration of bile acid sequestrants, including cholestyramine, may cause reversible fat-soluble vitamin and/or folate deficiencies in adult and pediatric patients resulting in various clinical issues (Ref). Night blindness secondary to vitamin A deficiency, osteomalacia due to vitamin D deficiency, and bleeding secondary to vitamin K deficiency have been reported (Ref). Fetal vitamin K deficiency resulting in a fatal subdural hematoma secondary to maternal vitamin K deficiency has also been reported (Ref). Vitamin supplementation or treatment discontinuation may be required.

Mechanism: Dose-related; the binding of cholestyramine to bile acids interferes with fat absorption; consequently, malabsorption of fat-soluble vitamins and folate may result in deficiencies.

Onset: Varied; a wide range of onset (ie, days to years) has been reported (Ref).

Risk factors :

• Chronic use

Hemorrhage

The use of cholestyramine has been associated with hemorrhage in adult and pediatric patients; bleeding complications have included epistaxis, bruising, genitourinary bleeding, gastrointestinal bleeding, and periarticular bleeding (Ref). Hemorrhage is reversible upon discontinuation; however, recurrence has been reported following reinitiation of therapy (Ref).

Mechanism: There are multiple mechanisms by which cholestyramine therapy may result in hemorrhage. Malabsorption of fat-soluble vitamins, including vitamin K, may occur with cholestyramine use; the subsequent hypoprothrombinemia associated with vitamin K deficiency may lead to hemorrhage and bleeding complications. In addition, crystal formation and deposition secondary to the use of ion exchange resins (eg, cholestyramine) may result in mucosal damage and bleeding complications (Ref).

Onset: Varied; a wide range of onset (ie, days to years) has been reported (Ref).

Risk factors :

• Chronic use

Hyperchloremic metabolic acidosis

Use of cholestyramine may result in reversible hyperchloremic metabolic acidosis in adult and pediatric patients, especially in the presence of precipitating conditions (eg, kidney impairment, volume depletion, concomitant administration of aldosterone antagonists) (Ref). Hyperchloremic acidosis may be severe, requiring discontinuation of cholestyramine therapy and initiation of appropriate treatment (Ref).

Mechanism: Dose-related; cholestyramine is an anion exchange resin that binds bile acids by swapping chloride anions. This exchange results in a loss of bicarbonate ions and an accumulation of chloride ions. Generally, the kidneys compensate for these changes; however, when the compensatory mechanisms are inhibited by urinary acidification (eg, due to kidney impairment, volume depletion, concomitant administration of aldosterone antagonists), hyperchloremic metabolic acidosis becomes apparent (Ref).

Onset: Varied; timing of onset may be dependent on the presence of precipitating conditions (eg, kidney impairment, volume depletion, initiation of therapy with an aldosterone antagonist [eg, spironolactone]). Onset may be rapid in the presence of precipitating factors (Ref).

Risk factors :

• Kidney impairment (Ref)

• Volume depletion (eg, secondary to diarrhea or infection) (Ref)

• Concomitant administration of an aldosterone antagonist (eg, spironolactone) (Ref)

• Younger or smaller patients whose relative dose may be higher as compared to older or larger patients

Hypertriglyceridemia

Bile acid sequestrants, including cholestyramine, may result in reversible hypertriglyceridemia, especially in patients with elevated baseline fasting triglyceride concentrations or type III hyperlipoproteinemia (Ref). Treatment should not be initiated when baseline fasting triglyceride concentrations are ≥300 mg/dL (Ref); cautious use with appropriate monitoring is recommended if baseline fasting triglyceride concentration is between 250 and 299 mg/dL (Ref). Discontinuation of therapy is warranted with severely elevated triglycerides (ie, serum triglycerides >400 mg/dL [(Ref)] or if signs and symptoms of acute pancreatitis occur (Ref); hypertriglyceridemia may persist with continued administration of cholestyramine.

Mechanism: Dose-related (Ref). Bile acids in the gastrointestinal tract activate the farnesoid X receptor (FXR), which subsequently increases the clearance of triglycerides; therefore, administration of bile acid sequestrants interrupts this feedback mechanism and may result in decreased clearance of triglycerides and hypertriglyceridemia (Ref).

Onset: Varied.

Risk factors :

• Elevated baseline fasting triglyceride concentrations (eg, ≥250 mg/dL) (Ref)

• Type III hyperlipoproteinemia (Ref)

Adverse Reactions

The following adverse drug reactions are derived from product labeling unless otherwise specified.

Postmarketing:

Cardiovascular: Edema, syncope

Dermatologic: Perianal skin irritation, skin irritation, skin rash, urticaria

Endocrine & metabolic: Hyperchloremic metabolic acidosis (Kamar 2015), vitamin A deficiency, vitamin D deficiency (Heaton 1972), vitamin K deficiency (Vroonhof 2003), weight gain, weight loss

Gastrointestinal: Abdominal distress, abdominal pain, anorexia, biliary colic, constipation, dental caries, diarrhea, diverticulitis of the gastrointestinal tract, duodenal ulcer with hemorrhage, dysphagia, eructation, flatulence, gallbladder calcification, gastric ulcer, gastrointestinal obstruction (Tonstand 1996), hiccups, nausea, pancreatitis, rectal pain, sour taste, staining of tooth, steatorrhea, tongue irritation, tooth enamel erosion, vomiting

Genitourinary: Burnt odor to urine, diuresis, dysuria

Hematologic & oncologic: Anemia, hemorrhage (Gross 1970)

Hepatic: Abnormal liver function

Nervous system: Dizziness, drowsiness, fatigue, headache, vertigo

Neuromuscular & skeletal: Arthralgia, back pain, myalgia, osteoporosis

Respiratory: Dyspnea, wheezing

Contraindications

Hypersensitivity to bile acid sequestering resins or any component of the formulation; complete biliary obstruction

Warnings/Precautions

Disease-related concerns:

• Renal impairment: Use caution in patients with renal impairment.

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.

Warnings: Additional Pediatric Considerations

With prolonged use, may potentially cause hyperchloremic 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).

Dosage Forms: US

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)

Generic Equivalent Available: US

Yes

Pricing: US

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 - $1.59

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

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Dosage Forms: Canada

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)

Administration: Adult

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, including vitamins or mineral supplements, at least 1 hour before or 4 to 6 hours after cholestyramine; consult drug interactions database for additional information.

Administration: Pediatric

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 (Ref).

Enteral tube administration: One sachet (4 g) mixed in 100 mL of water (Ref).

Use: Labeled Indications

Dyslipidemia: Adjunct in the management of primary hypercholesterolemia; regression of arteriolosclerosis

Pruritus associated with cholestasis: Treatment of pruritus associated with partial biliary obstruction

Use: Off-Label: Adult

Chronic diarrhea due to bile acid malabsorption; Enhanced elimination of leflunomide; Hyperthyroidism associated with Graves disease (adjunctive therapy); Thyroid storm

Metabolism/Transport Effects

None known.

Drug Interactions

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: Separate the administration of fluvastatin and cholestyramine to maximize fluvastatin absorption. Administer fluvastatin 2 to 4 hours, or longer, after cholestyramine administration. 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 hours prior to or one hour after bile acid sequestrants, or monitor for decreased serum concentrations and clinical effects of oral thyroid products during coadministration. 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

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

Food Interactions

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.

Reproductive Considerations

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).

Pregnancy Considerations

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.

Breastfeeding Considerations

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.

Dietary Considerations

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.

Monitoring Parameters

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 (ACC/AHA [Grundy 2018]; ACC/AHA [Stone 2013]).

Mechanism of Action

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

Pharmacokinetics (Adult Data Unless Noted)

Onset of action: Peak effect: 21 days

Absorption: None

Excretion: Feces (as insoluble complex with bile acids)

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Questran;
  • (AR) Argentina: Nivelipol resina | Questran;
  • (AU) Australia: Questran lite;
  • (BE) Belgium: Questran;
  • (BR) Brazil: Questran light;
  • (CH) Switzerland: Quantalan;
  • (CL) Chile: Questran | Questran light | Resincolestiramina;
  • (CO) Colombia: Antilip | Colestepril | Colestiramina | Questran;
  • (CZ) Czech Republic: Holestan | Questran | Vasosan;
  • (DE) Germany: Colesthexal | Colestyr | Colestyramin | Colestyramin 1 A Pharma | Colestyramin hexal | Colestyramin klast | Lipocol | Quantalan | Quantalan Beragena | Questran zuckerfrei | Vasosan p | Vasosan s;
  • (DO) Dominican Republic: Colestiramina lam;
  • (EC) Ecuador: Colestiramina | Questran;
  • (EE) Estonia: Colestyramin hexal | Colestyramin orifarm | Colestyramin ratiopharm | Quantalan | Questran | Questran light;
  • (EG) Egypt: Cholestran | Questran;
  • (ES) Spain: Resincolestiramina;
  • (FI) Finland: Cuemid | Questran;
  • (FR) France: Colestyramine Dci | Questran;
  • (GB) United Kingdom: Cholemin | Cholestyramin kent | Cholestyramine | Cholestyramine cox | Cuemid | Questran;
  • (GR) Greece: Questran | Resincolestiramina | Vasosan p;
  • (HK) Hong Kong: Apt Cholestyramine | Pms-Cholestyramine | Questran | Resincolestiramina;
  • (HU) Hungary: Cholestyramine supremex | Colestyramin hexal | Questran;
  • (ID) Indonesia: Questran;
  • (IE) Ireland: Questran;
  • (IL) Israel: Cholless | Questran;
  • (IN) India: Choltran | Co diet;
  • (IT) Italy: Colestrol | Questran;
  • (JO) Jordan: Questran;
  • (JP) Japan: Questran aventis | Questran bristol myers;
  • (KR) Korea, Republic of: Bitran | Questran;
  • (KW) Kuwait: Questran;
  • (LB) Lebanon: Questran | Resincolestiramina;
  • (LT) Lithuania: Cholestyramin | Cholestyramine | Colestyr | Colestyramin ratiopharm | Holestan | Resincolestiramina | Vasosan;
  • (LU) Luxembourg: Questran;
  • (LV) Latvia: Cholestyramin | Colestyramin | Colestyramin hexal | Colestyramin ratiopharm | Holestan | Quantalan | Questran | Questran light | Vasosan;
  • (MA) Morocco: Questran;
  • (MX) Mexico: Glibofhen | Lhibre | Lipiramina | Nozacol | Questran;
  • (MY) Malaysia: Pms cholestyramine | Questran;
  • (NL) Netherlands: Colestyramin ratiopharm | Colestyramine gf | Questran | Questran-a;
  • (NO) Norway: Colestyramin orifarm | Quantalan | Questran | Questran light | Questran loc;
  • (NZ) New Zealand: Questran;
  • (PE) Peru: Colestiramina;
  • (PL) Poland: Cholestyramin | Colestyramin hexal | Colestyramin ratiopharm | Quantalan | Questran | Questran light | Vasosan p | Vasosan s;
  • (PR) Puerto Rico: Cholestyramine | Cholestyramine light | Locholest | Prevalite | Questran | Questran light;
  • (PT) Portugal: Quantalan | Questran;
  • (RO) Romania: Questran;
  • (RU) Russian Federation: Questran;
  • (SA) Saudi Arabia: Pms cholestyramine | Questran;
  • (SE) Sweden: Kolestyramin Alternova | Questran | Questran loc;
  • (SG) Singapore: Cholestyramine | Questran | Resincolestiramina;
  • (SI) Slovenia: Quantalan | Resincolestiramina | Sevit;
  • (SK) Slovakia: Questran;
  • (TH) Thailand: Questran light | Resincolestiramina;
  • (TN) Tunisia: Pms cholestyramine | Questran;
  • (TR) Turkey: Kolestran;
  • (TW) Taiwan: Choles | Cholestyramine | Questran | Questran light | Semide;
  • (UY) Uruguay: Cinecolex | Resincolestiramina;
  • (ZA) South Africa: Questran | Questran lite
  1. Allard JP, Jeejeebhoy KN. Nutritional support and therapy in the short bowel syndrome. Gastroenterol Clin North Am. 1989;18(3):589-601. [PubMed 2509356]
  2. Alswat KA. Role of cholestyramine in refractory hyperthyroidism: a case report and literature review. Am J Case Rep. 2015;16:486-490. [PubMed 26207323]
  3. Andrade Luz I, Pereira T, Catorze N. Thyroid storm: a case of haemodynamic failure promptly reversed by aggressive medical therapy with antithyroid agents and steroid pulse. BMJ Case Rep. 2018;11(1):e226669. doi:10.1136/bcr-2018-226669 [PubMed 30567262]
  4. Arava (leflunomide) [prescribing information]. Bridgewater, NJ: Sanofi-Aventis; October 2016.
  5. Arnold MA, Swanson BJ, Crowder CD, et al. Colesevelam and colestipol: novel medication resins in the gastrointestinal tract. Am J Surg Pathol. 2014;38(11):1530-1537. doi:10.1097/PAS.0000000000000260 [PubMed 24921636]
  6. Avis HJ, Hutten BA, Twickler MT, et al. Pregnancy in women suffering from familial hypercholesterolemia: a harmful period for both mother and newborn? Curr Opin Lipidol. 2009;20(6):484-490. doi: 10.1097/MOL.0b013e3283319127. Review. [PubMed 19741526]
  7. Bays HE, Davidson M, Jones MR, Abby SL. Effects of colesevelam hydrochloride on low-density lipoprotein cholesterol and high-sensitivity C-reactive protein when added to statins in patients with hypercholesterolemia. Am J Cardiol. 2006;97(8):1198-1205. doi:10.1016/j.amjcard.2005.11.039. Erratum in: Am J Cardiol. 2006;98(3):428. [PubMed 16616026]
  8. Bernsten B, Zoger S. Hyperchloremic metabolic acidosis with cholestyramine therapy for biliary cholestasis. Am J Dis Child. 1978;132(12):1220. doi:10.1001/archpedi.1978.02120370072021 [PubMed 717343]
  9. Borghede MK, Schlütter JM, Agnholt JS, Christensen LA, Gormsen LC, Dahlerup JF. Bile acid malabsorption investigated by selenium-75-homocholic acid taurine ((75)SeHCAT) scans: causes and treatment responses to cholestyramine in 298 patients with chronic watery diarrhoea. Eur J Intern Med. 2011;22(6):e137-140. [PubMed 22075299]
  10. Brent RL. Teratogen update: reproductive risks of leflunomide (Arava); a pyrimidine synthesis inhibitor: counseling women taking leflunomide before or during pregnancy and men taking leflunomide who are contemplating fathering a child. Teratology. 2001;63(2):106-112. doi:10.1002/1096-9926(200102)63:2<106::AID-TERA1017>3.0.CO;2-R [PubMed 11241434]
  11. Btaiche IF and Khalidi N, "Parenteral Nutrition-Associated Liver Complications in Children," Pharmacotherapy, 2002, 22(2):188-211. [PubMed 11837558]
  12. Carney LN, Nepa A, Cohen SS, et al, “Parenteral and Enteral Nutrition Support: Determining the Best Way to Feed,” In: Corkins MR, Balint J, Bobo E, et al, eds, The A.S.P.E.N Pediatric Nutrition Support Core Curriculum, Silver Spring: MD: American Society of Parenteral and Enteral Nutrition, 2010, 433-47.
  13. Carroll R, Matfin G. Endocrine and metabolic emergencies: thyroid storm. Ther Adv Endocrinol Metab. 2010;1(3):139-145. doi:10.1177/2042018810382481 [PubMed 23148158]
  14. Chambers CD, Johnson DL, Robinson LK, et al; Organization of Teratology Information Specialists Collaborative Research Group. Birth outcomes in women who have taken leflunomide during pregnancy. Arthritis Rheum. 2010;62(5):1494-1503. doi:10.1002/art.27358 [PubMed 20131283]
  15. Ching YA, Gura K, and Modi B, "Pediatric Intestinal Failure: Nutrition, Pharmacologic, and Surgical Approaches," Nutr Clin Pract, 2007, 22(6):653-63. [PubMed 18042954]
  16. Cholestyramine [prescribing information]. Maple Grove, MN: Upsher-Smith Laboratories, LLC; December 2017.
  17. Cies JJ and Giamalis JN, "Treatment of Cholestatic Pruritus in Children," Am J Health Syst Pharm, 2007, 64(11):1157-62. [PubMed 17519457]
  18. Clouston WM, Lloyd HM. Cholestyramine induced hyperchloremic metabolic acidosis. Aust N Z J Med. 1985;15(2):271. doi:10.1111/j.1445-5994.1985.tb04032.x [PubMed 3861176]
  19. Compston JE, Horton LW. Oral 25-hydroxyvitain D3 in treatment of osteomalacia associated with ileal resection and cholestyramine therapy. Gastroenterology. 1978;74(5 Pt 1):900-902. [PubMed 640344]
  20. Corkins MR, Balint J, Corkins KG, Bobo E, Plogsted S, Yaworski, JA, eds. A.S.P.E.N. Pediatric Nutrition Support Handbook. 2nd ed. Silver Spring, MD: American Society for Enteral and Parenteral Nutrition; 2015.
  21. Daniels SR, personal communication, May 2002.
  22. Desai M, Reiprich A, Khov N, Yang Z, Mathew A, Levenick J. Crystal-associated colitis with ulceration leading to hematochezia and abdominal pain. Case Rep Gastroenterol. 2016;10(2):332-337. doi:10.1159/000446575 [PubMed 27482192]
  23. Eaves ER, Korman MG. Cholestyramine induced hyperchloremic metabolic acidosis. Aust N Z J Med. 1984;14(5):670-672. doi:10.1111/j.1445-5994.1984.tb05023.x [PubMed 6597713]
  24. European Association for the Study of the Liver. EASL clinical practice guidelines: drug-induced liver injury. J Hepatol. 2019;70(6):1222-1261. doi:10.1016/j.jhep.2019.02.014 [PubMed 30926241]
  25. Expert opinion. Senior Renal Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
  26. Faergeman O. Effects and side-effects of treatment of hypercholesterolemia with cholestyramine and neomycin. Acta Med Scand. 1973;194(3):165-167. doi:10.1111/j.0954-6820.1973.tb19425.x [PubMed 4746523]
  27. Fihn SD, Gardin JM, Abrams J, et al, “2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons,” Circulation, 2012, 126(25):3097-137. [PubMed 23166211]
  28. Gal P, Reed M. Medications. In: Kliegman RM, Behrman RE, Jenson HB, et al, eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia, PA: Saunders Elsevier; 2007: 2955-2999.
  29. Gross L, Brotman M. Hypoprothrombinemia and hemorrhage associated with cholestyramine therapy. Ann Intern Med. 1970;72(1):95-96. doi:10.7326/0003-4819-72-1-95. [PubMed 5410402]
  30. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the management of blood cholesterol: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625. Erratum in: Circulation. 2019;139(25):e1182-e1186. [PubMed 30586774]
  31. Heaton KW, Lever JV, Barnard D. Osteomalacia associated with cholestyramine therapy for postileectomy diarrhea. Gastroenterology. 1972;62(4):642-646. [PubMed 5020877]
  32. Hofmann AF, Poley JR. Cholestyramine treatment of diarrhea associated with ileal resection. N Engl J Med. 1969;281(8):397-402. [PubMed 4894463]
  33. Imam MH, Gossard AA, and Sinakos E, "Pathogenesis and Management of Pruritus in Cholestatic Liver Disease," J Gastroenterol Hepatol, 2012, 27(7):1150-8. [PubMed 22413872]
  34. Jacobson TA, Armani A, McKenney JM, Guyton JR. Safety considerations with gastrointestinally active lipid-lowering drugs. Am J Cardiol. 2007;99(6A):47C-55C. doi:10.1016/j.amjcard.2006.11.022 [PubMed 17368279]
  35. Jacobson TA, Maki KC, Orringer CE, et al; NLA Expert Panel. National Lipid Association recommendations for patient-centered management of dyslipidemia: part 2. J Clin Lipidol. 2015;9(6 Suppl):S1-122.e1. doi: 10.1016/j.jacl.2015.09.002. [PubMed 26699442]
  36. Jellinger PS, Handelsman Y, Rosenblit PD, et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract. 2017;23(suppl 2):1-87. doi: 10.4158/EP171764.APPGL. [PubMed 28437620]
  37. Kamar FB, McQuillan RF. Hyperchloremic metabolic acidosis due to cholestyramine: a case report and literature review. Case Rep Nephrol. 2015;2015:309791. doi:10.1155/2015/309791 [PubMed 26425378]
  38. Kleinman PK. Letter: Cholestyramine and metabolic acidosis. N Engl J Med. 1974;290(15):861. [PubMed 4817847]
  39. Kliegman RM and St. Geme J, eds. Nelson Textbook of Pediatrics. 21st ed. Philadelphia, PA: Saunders Elsevier; 2020.
  40. Knab J, Goos M, Dissemond J. Successful treatment of a leg ulcer occurring in a rheumatoid arthritis patient under leflunomide therapy. J Eur Acad Dermatol Venereol. 2005;19(2):243-246. doi:10.1111/j.1468-3083.2005.01118.x [PubMed 15752303]
  41. Kulaksizoglu M, Gonen MS, Kebapcilar L, et al. Multiorgan dysfunction accompanied with metimazole and thyroid storm. Transfus Apher Sci. 2012;46(2):149-152. doi:10.1016/j.transci.2012.01.001 [PubMed 22284265]
  42. Laub M, Fraser R, Kurche J, Lara A, Kiser TH, Reynolds PM. Use of a cholestyramine washout in a patient with septic shock on leflunomide therapy: a case report and review of the literature. J Intensive Care Med. 2016;31(6):412-414. doi:10.1177/0885066615610108 [PubMed 26446104]
  43. Lindor KD, Bowlus CL, Boyer J, Levy C, Mayo M. Primary biliary cholangitis: 2018 practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2019;69(1):394-419. doi: 10.1002/hep.30145. [PubMed 30070375]
  44. Lindor KD, Gershwin ME, Poupon R, et al, "Primary Biliary Cirrhosis," Hepatology, 2009, 50(1):291-308. [PubMed 19554543]
  45. Lloyd-Still JD. Cholestyramine therapy and intestinal obstruction in infants. Pediatrics. 1977;59(4):626-627. [PubMed 850604]
  46. The Lipid Research Clinics Coronary Primary Prevention Trial (LRCCPPT) results. I. Reduction in incidence of coronary heart disease. JAMA. 1984;251(3):351-364. doi:10.1001/jama.1984.03340270029025 [PubMed 6361299]
  47. McCrindle BW, O'Neill MB, Cullen-Dean G, et al, “Acceptability and Compliance With Two Forms of Cholestyramine in the Treatment of Hypercholesterolemia in Children: A Randomized, Crossover Trial,” J Pediatr, 1997, 130(2):266-73. [PubMed 9042130]
  48. McCrindle BW, Urbina EM, Dennison BA, et al, "Drug Therapy of High-Risk Lipid Abnormalities in Children and Adolescents: A Scientific Statement from the American Heart Association Atherosclerosis, Hypertension, and Obesity in Youth Committee, Council of Cardiovascular Disease in the Young, With the Council on Cardiovascular Nursing," Circulation, 2007, 115(14):1948-67. [PubMed 17377073]
  49. McPherson R, Frohlich J, Fodor G, et al, “Canadian Cardiovascular Society Position Statement--Recommendations for the Diagnosis and Treatment of Dyslipidemia and Prevention of Cardiovascular Disease,” [published correction appears in Can J Cardiol. 2006, 22(12):1077]. Can J Cardiol. 2006;22(11):913-927. [PubMed 16971976]
  50. Mercado M, Mendoza-Zubieta V, Bautista-Osorio R, Espinoza-de los Monteros AL. Treatment of hyperthyroidism with a combination of methimazole and cholestyramine. J Clin Endocrinol Metab. 1996;81(9):3191-3193. doi:10.1210/jcem.81.9.8784067 [PubMed 8784067]
  51. Merten DF, Grossman H. Intestinal obstruction associated with cholestyramine therapy. AJR Am J Roentgenol. 1980;134(4):827-828. doi:10.2214/ajr.134.4.827 [PubMed 6767374]
  52. National Heart, Lung, and Blood Institute. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents. Clinical Practice Guidelines, 2011, National Institutes of Health. Available at http://www.nhlbi.nih.gov/guidelines/cvd_ped/peds_guidelines_full.pdf
  53. National Institute for Health and Care Excellence (2008) Clinical guidelines and evidence review for familial hypercholesterolaemia: the identification and management of adults and children with familial hypercholesterolaemia. London: NICE. (Clinical Guideline 71). Available at: http://www.nice.org.uk/CG71.
  54. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. 2006;35(4):663-686, vii. doi:10.1016/j.ecl.2006.09.008 [PubMed 17127140]
  55. Parekh NR, Steiger E. Short bowel syndrome. Curr Treat Options Gastroenterol. 2007;10(1):10-23. [PubMed 17298760]
  56. Preckshot J, et al, "Cholestyramine 6.5% Ointment," Int J Pharm Compound, 2001, 5(1)42.
  57. Prevalite (cholestyramine) [prescribing information]. Maple Grove, MN: Upsher-Smith Laboratories, LLC; June 2020.
  58. Questran Powder, Questran Light (cholestyramine) [prescribing information]. Chestnut Ridge, NY: Par Pharmaceuticals; April 2016.
  59. Refer to manufacturer's labeling.
  60. Robertson KE, Mueller BA. Uremic pruritus. Am J Health Syst Pharm. 1996;53(18):2159-2170; quiz 2215-2216. doi:10.1093/ajhp/53.18.2159 [PubMed 8879322]
  61. Ross DS. Thyroid storm. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed October 12, 2022.
  62. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26(10):1343-1421. doi:10.1089/thy.2016.0229 [PubMed 27521067]
  63. Sadler LC, Lane M, North R. Severe fetal intracranial haemorrhage during treatment with cholestyramine for intrahepatic cholestasis of pregnancy. Br J Obstet Gynaecol. 1995;102(2):169-170. doi:10.1111/j.1471-0528.1995.tb09077.x [PubMed 7756215]
  64. Sadowski DC, Camilleri M, Chey WD, et al. Canadian Association of Gastroenterology clinical practice guideline on the management of bile acid diarrhea. J Can Assoc Gastroenterol. 2020;3(1):e10-e27. doi:10.1093/jcag/gwz038 [PubMed 32010878]
  65. Scheel PJ Jr, Whelton A, Rossiter K, Watson A. Cholestyramine-induced hyperchloremic metabolic acidosis. J Clin Pharmacol. 1992;32(6):536-538. doi:10.1177/009127009203200608 [PubMed 1634640]
  66. Shojania AM, Grewar D. Hypoprothrombinemic hemorrhage due to cholestyramine therapy. CMAJ. 1986;134(6):609-610. [PubMed 3948073]
  67. Sjöberg BG, Straniero S, Angelin B, Rudling M. Cholestyramine treatment of healthy humans rapidly induces transient hypertriglyceridemia when treatment is initiated. Am J Physiol Endocrinol Metab. 2017;313(2):E167-E174. doi:10.1152/ajpendo.00416.2016 [PubMed 28487440]
  68. Solomon BL, Wartofsky L, Burman KD. Adjunctive cholestyramine therapy for thyrotoxicosis. Clin Endocrinol (Oxf). 1993;38(1):39-43. doi:10.1111/j.1365-2265.1993.tb00970.x [PubMed 8435884]
  69. Sprecher DL and Daniels SR, “Rational Approach to Pharmacologic Reduction of Cholesterol Levels in Children,” J Pediatr, 1996, 129(1):4-7. [PubMed 8757557]
  70. Staels B, Fonseca VA. Bile acids and metabolic regulation: mechanisms and clinical responses to bile acid sequestration. Diabetes Care. 2009;32 Suppl 2(suppl 2):S237-S245. doi:10.2337/dc09-S355 [PubMed 19875558]
  71. Stine JG, Lewis JH. Current and future directions in the treatment and prevention of drug-induced liver injury: a systematic review. Expert Rev Gastroenterol Hepatol. 2016;10(4):517-536. doi:10.1586/17474124.2016.1127756 [PubMed 26633044]
  72. Stone NJ, Robinson JG, Lichtenstein AH, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63(25 Pt B):2889-2934. doi:10.1016/j.jacc.2013.11.002. Erratum in: J Am Coll Cardiol. 2014;63(25 Pt B):3024-3025. Erratum in: J Am Coll Cardiol. 2015;66(24):2812. [PubMed 24239923]
  73. "Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)," May 2001. Available at http://www.nhlbi.nih.gov/guidelines/cholesterol.
  74. Tonstad S, Knudtzon J, Sivertsen M, Refsum H, Ose L. Efficacy and safety of cholestyramine therapy in peripubertal and prepubertal children with familial hypercholesterolemia. J Pediatr. 1996;129(1):42-49. doi:10.1016/s0022-3476(96)70188-9 [PubMed 8757561]
  75. Tsai WC, Pei D, Wang TF, et al. The effect of combination therapy with propylthiouracil and cholestyramine in the treatment of Graves' hyperthyroidism. Clin Endocrinol (Oxf). 2005;62(5):521-524. doi:10.1111/j.1365-2265.2005.02249.x [PubMed 15853819]
  76. Visintine Re, Michaels GD, Fukayama G, Conklin J, Kinsell LW. Xanthomatous biliary cirrhosis treated with cholestyramine. A bile-acid-adsorbing resin. Lancet. 1961;2(7198):341-343. doi:10.1016/s0140-6736(61)90634-1 [PubMed 13781611]
  77. Vroonhof K, van Rijn HJ, van Hattum J. Vitamin K deficiency and bleeding after long-term use of cholestyramine. Neth J Med. 2003;61(1):19-21. [PubMed 12688565]
  78. Walters JR, Pattni SS. Managing bile acid diarrhoea. Therap Adv Gastroenterol. 2010;3(6):349-357. [PubMed 21180614]
  79. West RJ, Lloyd JK. The effect of cholestyramine on intestinal absorption. Gut. 1975;16(2):93-98. doi:10.1136/gut.16.2.93. [PubMed 1168607]
  80. Westergaard H, “Bile Acid Malabsorption,” Curr Treat Options Gastroenterol, 2007, 10(1):28-33. [PubMed 17298762]
  81. White R, Bradnam V; British Pharmaceutical Nutrition Group. Handbook of Drug Administration via Enteral Feeding Tubes. 3rd ed. London, England: Pharmaceutical Press; 2015.
  82. White CM, Kalus JS, Caron MF, et al, "Cholestyramine Ointment Used on an Infant for Severe Buttocks Rash Resistant to Standard Therapeutic Modalities," J Pharm Technol, 2003, 19:11-3.
  83. Wilcox C, Turner J, Green J. Systematic review: the management of chronic diarrhoea due to bile acid malabsorption. Aliment Pharmacol Ther. 2014;39(9):923-939. [PubMed 24602022]
  84. Williams KD and Williams L, "Diaper Rash Relief, Common Sense Remedies and Treatment," Int J Pharm Compound, 2011, 15(6):464-9.
  85. Wise DM. Suppressed wound healing in a patient with rheumatoid arthritis taking leflunomide (arava). Perm J. 2011;15(4):70-74. doi:10.7812/tpp/11-044 [PubMed 22319420]
  86. Wong SP, Chu CM, Kan CH, Tsui HS, Ng WL. Successful treatment of leflunomide-induced acute pneumonitis with cholestyramine wash-out therapy. J Clin Rheumatol. 2009;15(8):389-392. doi:10.1097/RHU.0b013e3181c3f87e [PubMed 19955995]
  87. Writing Committee; Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2022 ACC expert consensus decision pathway on the role of nonstatin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk: A report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022;80(14):1366-1418. doi:10.1016/j.jacc.2022.07.006 Erratum in: J Am Coll Cardiol. 2023;81(1):104. [PubMed 36031461]
Topic 9258 Version 392.0

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟