Diaper dermatitis: Limited data available: Topical: 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; 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).
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: 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: 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: 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.
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.
(For additional information see "Cholestyramine: Drug information")
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 (Ref).
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).
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: Oral: Initial: 4 g once or twice daily; may increase dose gradually up to 16 g/day in 2 divided doses (Ref).
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.
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).
No dosage adjustment necessary; not absorbed from the gastrointestinal tract.
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)
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
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
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
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)
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), hypertriglyceridemia, 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
Hypersensitivity to bile acid sequestering resins or any component of the formulation; complete biliary obstruction
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.
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.
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
Pack (Cholestyramine Light Oral)
4 g (per each): $1.54 - $4.43
Pack (Cholestyramine Oral)
4 g (per each): $1.72 - $4.43
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.
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 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).
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.
Store at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F).
Adjunct to diet in the management of primary hypercholesterolemia (FDA approved in adults); pruritus associated with elevated levels of bile acids associated with biliary obstruction (FDA approved in adults); has also been used to manage diarrhea associated with excess fecal bile acids; applied topically to treat diaper dermatitis and as a skin-protectant around enterostomy fistula sites.
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 drug interactions program by clicking on the “Launch drug interactions program” link above.
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 drug interactions program
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
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.
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.
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.
Pediatric patients: Fasting lipid profile (baseline, 4 to 6 weeks after initiation, and then every 6 to 12 months), growth, maturation, number of stools per day (NHLBI 2011); nutritional status for vitamin (eg, fat-soluble, folic acid) and nutrient deficiencies (eg, Ca, Fe) (Allard 1989; Parekh 2007).
Adults: Fasting lipid profile before initiating treatment, 3 months after initiation (within 4 to 6 weeks if baseline fasting triglycerides of 250 to 299 mg/dL), and every 6 to 12 months thereafter (ACC/AHA [Stone 2013]).
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)
Do you want to add Medilib to your home screen?