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Pronunciation
(ra NI ti deen)
Generic Available (U.S.)
Yes: Excludes effervescent tablet, premixed infusion
Index Terms
Brand Names: U.S.
Brand Names: Canada
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Zantac®: Short-term and maintenance therapy of duodenal ulcer, gastric ulcer, gastroesophageal reflux disease (GERD), active benign ulcer, erosive esophagitis, and pathological hypersecretory conditions; as part of a multidrug regimen for H. pylori eradication to reduce the risk of duodenal ulcer recurrence
Zantac 75® [OTC]: Relief of heartburn, acid indigestion, and sour stomach
Use: Unlabeled
Recurrent postoperative ulcer, upper GI bleeding, prevention of acid-aspiration pneumonitis during surgery, and prevention of stress-induced ulcers
Pregnancy Risk Factor
B
Pregnancy Considerations
Adverse events were not observed in animal studies; therefore, ranitidine is classified as pregnancy category B. Ranitidine crosses the placenta. An increased risk of congenital malformations or adverse events in the newborn has generally not been observed following maternal use of ranitidine during pregnancy. Histamine H2 antagonists have been evaluated for the treatment of gastroesophageal reflux disease (GERD) as well as gastric and duodenal ulcers during pregnancy. If needed, ranitidine is the agent of choice. Histamine H2 antagonists may be used for aspiration prophylaxis prior to cesarean delivery.
Lactation
Enters breast milk/use caution
Breast-Feeding Considerations
Ranitidine is excreted into breast milk. The manufacturer recommends that caution be exercised when administering ranitidine to nursing women. Peak milk concentrations of ranitidine occur ~5.5 hours after the dose (case report).
Contraindications
Hypersensitivity to ranitidine or any component of the formulation
Warnings/Precautions
Concerns related to adverse effects:
• B12 deficiency: Long-term therapy may be associated with vitamin B12 deficiency.
• Confusion: Reversible confusional states (rare), usually clearing within 3-4 days after discontinuation, have been linked to use. Increased age (>50 years) and renal or hepatic impairment are thought to be associated.
Disease-related concerns:
• Gastric malignancy: Relief of symptoms does not preclude the presence of a gastric malignancy.
• Hepatic impairment: Use with caution in patients with hepatic impairment.
• Porphyria: Avoid use in patients with a history of acute porphyria; may precipitate attacks.
• Renal impairment: Use with caution in patients with renal impairment; dosage adjustment recommended.
Dosage form specific issues:
• Phenylalanine: EFFERdose® formulation contains phenylalanine.
Adverse Reactions
Frequency not defined.
Cardiovascular: Asystole, atrioventricular block, bradycardia (with rapid I.V. administration), premature ventricular beats, tachycardia, vasculitis
Central nervous system: Agitation, dizziness, depression, hallucinations, headache, insomnia, malaise, mental confusion, somnolence, vertigo
Dermatologic: Alopecia, erythema multiforme, rash
Endocrine & metabolic: Prolactin levels increased
Gastrointestinal: Abdominal discomfort/pain, constipation, diarrhea, nausea, necrotizing enterocolitis (VLBW neonates; Guillet, 2006), pancreatitis, vomiting
Hematologic: Acquired immune hemolytic anemia, acute porphyritic attack, agranulocytosis, aplastic anemia, granulocytopenia, leukopenia, pancytopenia, thrombocytopenia
Hepatic: Cholestatic hepatitis, hepatic failure, hepatitis, jaundice
Local: Transient pain, burning or itching at the injection site
Neuromuscular & skeletal: Arthralgia, involuntary motor disturbance, myalgia
Ocular: Blurred vision
Renal: Acute interstitial nephritis, serum creatinine increased
Respiratory: Pneumonia (causal relationship not established)
Miscellaneous: Anaphylaxis, angioneurotic edema, hypersensitivity reactions (eg, bronchospasm, fever, eosinophilia)
Metabolism/Transport Effects
Substrate of CYP1A2 (minor), CYP2C19 (minor), CYP2D6 (minor), P-glycoprotein; Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits CYP1A2 (weak), CYP2D6 (weak)
Drug Interactions
ARIPiprazole: CYP2D6 Inhibitors (Weak) may increase the serum concentration of ARIPiprazole. Management: Monitor for increased aripiprazole pharmacologic effects. Aripiprazole dose adjustments may or may not be required based on concomitant therapy and/or indication. Consult product labeling for specific recommendations. Risk C: Monitor therapy
Atazanavir: H2-Antagonists may decrease the absorption of Atazanavir. Management: Specific dose limitations and administration guidelines exist; consult full interaction monograph or atazanavir prescribing information. Risk D: Consider therapy modification
Cefditoren: H2-Antagonists may decrease the serum concentration of Cefditoren. Management: Concomitant use of cefditoren with H2-antagonists and antacids is not recommended. Consider alternative methods to control acid reflux (eg, diet modification) or alternative antimicrobial therapy if use of H2-antagonists can not be avoided. Risk D: Consider therapy modification
Cefpodoxime: H2-Antagonists may decrease the absorption of Cefpodoxime. Separate oral doses by at least 2 hours. Risk C: Monitor therapy
Cefuroxime: H2-Antagonists may decrease the absorption of Cefuroxime. Separate oral doses by at least 2 hours. Risk C: Monitor therapy
Cyproterone: May decrease the serum concentration of CYP1A2 Substrates. Risk C: Monitor therapy
Dasatinib: H2-Antagonists may decrease the absorption of Dasatinib. Management: Avoid concurrent use of H2-receptor antagonists with dasatinib. Antacids (taken 2 hours before or after dasatinib administration) should be used in place of these agents if some acid-reducing therapy is needed. Risk D: Consider therapy modification
Delavirdine: H2-Antagonists may decrease the serum concentration of Delavirdine. Management: Chronic therapy with H2-antagonists should be avoided in patients who are being treated with delavirdine. The clinical significance of short-term H2-antagonist therapy with delavirdine is uncertain, but such therapy should be undertaken with caution. Risk X: Avoid combination
Dexmethylphenidate: H2-Antagonists may increase the absorption of Dexmethylphenidate. Specifically, H2-antagonists may interfere with the normal release of drug from the extended-release capsules (Focalin XR brand), which could result in both increased absorption (early) and decreased delayed absorption. Risk C: Monitor therapy
Erlotinib: H2-Antagonists may decrease the serum concentration of Erlotinib. Management: Avoid H2-antagonists in patients receiving erlotinib when possible. If concomitant treatment cannot be avoided, erlotinib should be dosed once daily, 10 hours after and at least 2 hours before H2-antagonist dosing. Risk D: Consider therapy modification
Fosamprenavir: H2-Antagonists may decrease the serum concentration of Fosamprenavir. Cimetidine may also inhibit the metabolism of the active metabolite amprenavir, making its effects on fosamprenavir/amprenavir concentrations difficult to predict. Risk C: Monitor therapy
Gefitinib: H2-Antagonists may decrease the serum concentration of Gefitinib. Risk C: Monitor therapy
Indinavir: H2-Antagonists may decrease the serum concentration of Indinavir. Risk C: Monitor therapy
Iron Salts: H2-Antagonists may decrease the absorption of Iron Salts. Exceptions: Ferric Gluconate; Ferumoxytol; Iron Dextran Complex; Iron Sucrose. Risk C: Monitor therapy
Itraconazole: H2-Antagonists may decrease the serum concentration of Itraconazole. Management: When this combination is used, the itraconazole should be administered with a cola beverage (8 ounces). Itraconazole oral suspension may be less sensitive to this interaction. Monitor patient response to itraconazole closely. Risk D: Consider therapy modification
Ketoconazole: H2-Antagonists may decrease the serum concentration of Ketoconazole. Management: Administer oral ketoconazole at least 2 hours prior to use of any H2-receptor antagonist. Monitor patients closely for signs of inadequate clinical response to ketoconazole. Risk D: Consider therapy modification
Ketoconazole (Systemic): H2-Antagonists may decrease the serum concentration of Ketoconazole (Systemic). Management: Administer oral ketoconazole at least 2 hours prior to use of any H2-receptor antagonist. Monitor patients closely for signs of inadequate clinical response to ketoconazole. Risk D: Consider therapy modification
Mesalamine: H2-Antagonists may diminish the therapeutic effect of Mesalamine. Histamine H2-Antagonist-mediated increases in gastrointestinal pH may cause the premature release of mesalamine from specific sustained-release mesalamine products. Management: Consider avoiding concurrent administration of high-dose histamine H2-receptor antagonists with sustained-release mesalamine products. Risk D: Consider therapy modification
Methylphenidate: H2-Antagonists may increase the absorption of Methylphenidate. Specifically, H2-antagonists may interfere with the normal release of drug from the extended-release capsules (Ritalin LA brand), which could result in both increased absorption (early) and decreased delayed absorption. Risk C: Monitor therapy
Nelfinavir: H2-Antagonists may decrease the serum concentration of Nelfinavir. Concentrations of the active M8 metabolite may also be reduced. Risk C: Monitor therapy
Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates. Risk C: Monitor therapy
P-glycoprotein/ABCB1 Inducers: May decrease the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
P-glycoprotein/ABCB1 Inhibitors: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
Posaconazole: H2-Antagonists may decrease the serum concentration of Posaconazole. Management: Avoid concurrent use whenever possible. Monitor patients closely for decreased antifungal effects if this combination is used. Consider using a noninteracting antifungal as appropriate. Risk D: Consider therapy modification
Prasugrel: Ranitidine may decrease serum concentrations of the active metabolite(s) of Prasugrel. Risk C: Monitor therapy
Procainamide: Ranitidine may increase the serum concentration of Procainamide. Ranitidine may also increase the concentration of the active N-acetyl-procainamide (NAPA) metabolite. Risk C: Monitor therapy
Rilpivirine: H2-Antagonists may decrease the serum concentration of Rilpivirine. Management: Administer histamine H2 receptor antagonists at least 12 hours before or 4 hours after rilpivirine. Risk D: Consider therapy modification
Saquinavir: H2-Antagonists may increase the serum concentration of Saquinavir. Risk C: Monitor therapy
Sulfonylureas: Ranitidine may increase the serum concentration of Sulfonylureas. Risk C: Monitor therapy
Varenicline: H2-Antagonists may increase the serum concentration of Varenicline. Management: Monitor for increased varenicline adverse effects with concomitant use of cimetidine or other H2-antagonists, particulary in patients with severe renal impairment. International product labeling recommendations vary. Consult appropriate labeling. Risk C: Monitor therapy
Vismodegib: H2-Antagonists may decrease the serum concentration of Vismodegib. Management: Carefully consider the need for any medication that increases the pH of the upper GI tract (PPIs, H2RAs, antacids), as these could significantly reduce vismodegib systemic exposure. Vismodegib dose increases are unlikely to compensate for this effect. Risk D: Consider therapy modification
Warfarin: Ranitidine may increase the serum concentration of Warfarin. Risk C: Monitor therapy
Ethanol/Nutrition/Herb Interactions
Ethanol: Avoid ethanol (may cause gastric mucosal irritation).
Food: Does not interfere with absorption of ranitidine.
Storage
Injection: Vials: Store between 4°C to 25°C (39°F to 77°F); excursion permitted to 30°C (86°F). Protect from light. Solution is a clear, colorless to yellow solution; slight darkening does not affect potency. Vials mixed with NS or D5W are stable for 48 hours at room temperature.
Premixed bag: Store between 2°C to 25°C (36°F to 77°F). Protect from light.
EFFERdose® formulations: Store between 2°C to 30°C (36°F to 86°F).
Syrup: Store between 4°C to 25°C (39°F to 77°F). Protect from light.
Tablets: Store in dry place, between 15°C to 30°C (59°F to 86°F). Protect from light.
Reconstitution
Vials can be mixed with NS or D5W.
Intermittent bolus injection, continuous infusion: Dilute to maximum of 2.5 mg/mL.
Intermittent infusion: Dilute to maximum of 0.5 mg/mL.
Compatibility
Stable in D51/2NS, D5W, D10W, fat emulsion 10%, LR, NS, sodium bicarbonate 5%; for injection, do not add other medications to premixed bag; variable compatibility (consult detailed reference) in D5LR, TPN.
Y-site administration: Compatible: Acyclovir, alcohol (ethyl), aldesleukin, allopurinol, amifostine, aminophylline, amsacrine, anidulafungin, atracurium, aztreonam, bivalirudin, cefazolin, cefepime, cefoxitin, ceftazidime, ciprofloxacin, cisatracurium, cisplatin, cladribine, cyclophosphamide, cytarabine, dexmedetomidine, diltiazem, dobutamine, docetaxel, dopamine, doripenem, doxapram, doxorubicin, doxorubicin liposome, enalaprilat, epinephrine, esmolol, etoposide phosphate, fenoldopam, fentanyl, filgrastim, fluconazole, fludarabine, foscarnet, furosemide, gallium nitrate, gemcitabine, granisetron, heparin, hetastarch in lactate electrolyte injection (Hextend®), hydromorphone, idarubicin, labetalol, linezolid, lorazepam, melphalan, meperidine, methotrexate, midazolam, milrinone, morphine, nicardipine, nitroglycerin, norepinephrine, ondansetron, ondansetron with paclitaxel, oxaliplatin, paclitaxel, pancuronium, pemetrexed, piperacillin, piperacillin/tazobactam, procainamide, propofol, remifentanil, sargramostim, tacrolimus, telavancin, teniposide, theophylline, thiopental, thiotepa, tigecycline, vecuronium, vinorelbine, warfarin, zidovudine. Incompatible: Amphotericin B cholesteryl sulfate complex, hetastarch in sodium chloride 0.9%, insulin (regular), pantoprazole. Variable (consult detailed reference): Drotrecogin alfa, TPN.
Compatibility in syringe: Compatible: Atropine, dexamethasone sodium phosphate, dimenhydrinate, diphenhydramine, dobutamine, dopamine, fentanyl, glycopyrrolate, heparin, hydromorphone, meperidine, metoclopramide, morphine, nalbuphine, oxymorphone, pentazocine, prochlorperazine edisylate, promethazine, scopolamine. Incompatible: Hydroxyzine, methotrimeprazine, midazolam, pantoprazole, pentobarbital, phenobarbital. Variable (consult detailed reference): Chlorpromazine, diazepam, lorazepam.
Mechanism of Action
Competitive inhibition of histamine at H2-receptors of the gastric parietal cells, which inhibits gastric acid secretion, gastric volume, and hydrogen ion concentration are reduced. Does not affect pepsin secretion, pentagastrin-stimulated intrinsic factor secretion, or serum gastrin.
Pharmacodynamics/Kinetics
Absorption: Oral: 50%
Distribution: Normal renal function: Vd: ~1.4 L/kg; Clcr 25-35 mL/minute: 1.76 L/kg minimally penetrates the blood-brain barrier
Protein binding: 15%
Metabolism: Hepatic to N-oxide, S-oxide, and N-desmethyl metabolites
Bioavailability: Oral: 48% to 50%; I.M.: 90% to 100%
Half-life elimination:
Oral: Normal renal function: 2.5-3 hours; Clcr 25-35 mL/minute: 4.8 hours
I.V.: Normal renal function: 2-2.5 hours
Time to peak, serum: Oral: 2-3 hours; I.M.: ≤15 minutes
Excretion: Urine: Oral: 30%, I.V.: 70% (as unchanged drug); feces (as metabolites)
Dosage
Children 1 month to 16 years:
Duodenal and gastric ulcer:
Oral:
Treatment: 4-8 mg/kg/day divided twice daily; maximum: 300 mg/day
Maintenance: 2-4 mg/kg/day once daily; maximum: 150 mg/day
I.V.: 2-4 mg/kg/day divided every 6-8 hours; maximum: 200 mg/day
GERD and erosive esophagitis:
Oral: 5-10 mg/kg/day divided twice daily; maximum: GERD: 300 mg/day, erosive esophagitis: 600 mg/day
I.V. (unlabeled): 2-4 mg/kg/day divided every 6-8 hours; maximum: 200 mg/day or as an alternative
Continuous infusion: Initial: 1 mg/kg/dose for one dose followed by infusion of 0.08-0.17 mg/kg/hour or 2-4 mg/kg/day
Children ≥12 years: Prevention of heartburn: Oral: Zantac 75® [OTC]: 75 mg 30-60 minutes before eating food or drinking beverages which cause heartburn; maximum: 150 mg/24 hours; do not use for more than 14 days
Adults:
Duodenal ulcer: Oral: Treatment: 150 mg twice daily, or 300 mg once daily after the evening meal or at bedtime; maintenance: 150 mg once daily at bedtime
Helicobacter pylori eradication: 150 mg twice daily; requires combination therapy
Pathological hypersecretory conditions:
Oral: 150 mg twice daily; adjust dose or frequency as clinically indicated; doses of up to 6 g/day have been used
I.V.: Continuous infusion for Zollinger-Ellison: Initial: 1 mg/kg/hour; measure gastric acid output at 4 hours, if >10 mEq or if patient is symptomatic, increase dose in increments of 0.5 mg/kg/hour; doses of up to 2.5 mg/kg/hour (or 220 mg/hour) have been used
Gastric ulcer, benign: Oral: 150 mg twice daily; maintenance: 150 mg once daily at bedtime
GERD: Oral: 150 mg twice daily
Erosive esophagitis: Oral: Treatment: 150 mg 4 times/day; maintenance: 150 mg twice daily
Prevention of heartburn: Oral: Zantac 75® [OTC]: 75 mg 30-60 minutes before eating food or drinking beverages which cause heartburn; maximum: 150 mg in 24 hours; do not use for more than 14 days
Patients not able to take oral medication:
I.M.: 50 mg every 6-8 hours
I.V.: Intermittent bolus or infusion: 50 mg every 6-8 hours
Continuous I.V. infusion: 6.25 mg/hour
Elderly: Ulcer healing rates and incidence of adverse effects are similar in the elderly, when compared to younger patients; dosing adjustments not necessary based on age alone
Dosing adjustment in renal impairment: Adults: Clcr <50 mL/minute:
Oral: 150 mg every 24 hours; adjust dose cautiously if needed
I.V.: 50 mg every 18-24 hours; adjust dose cautiously if needed
Hemodialysis: Adjust dosing schedule so that dose coincides with the end of hemodialysis
Dosing adjustment/comments in hepatic disease: Patients with hepatic impairment may have minor changes in ranitidine half-life, distribution, clearance, and bioavailability; dosing adjustments not necessary, monitor
Administration: Oral
EFFERdose®: Should not be chewed, swallowed whole, or dissolved on tongue: 25 mg tablet: Dissolve in at least 5 mL of water; wait until completely dissolved before administering
Administration: I.M.
No dilution is needed
Administration: I.V.
I.V. push: Ranitidine (usually 50 mg) should be diluted to a total of 20 mL (or a concentration not exceeding 2.5 mg/mL) with NS or D5W and administered over at least 5 minutes or a maximum rate of 10 mg/minute.
Intermittent I.V. infusion: Dilute to a maximum concentration of 0.5 mg/mL; administer over 15-20 minutes
Continuous I.V. infusion: Dilute to a maximum concentration of 2.5 mg/mL. Titrate dosage based on gastric pH.
Administration: I.V. Detail
I.V. must be diluted; may be administered I.V. push, intermittent I.V. infusion, or continuous I.V. infusion
pH: 6.7-7.3
Monitoring Parameters
AST, ALT, serum creatinine; when used to prevent stress-related GI bleeding, measure the intragastric pH and try to maintain pH >4; signs and symptoms of peptic ulcer disease, occult blood with GI bleeding, monitor renal function to correct dose
Test Interactions
False-positive urine protein using Multistix®; gastric acid secretion test; skin test allergen extracts. May also interfere with urine detection of amphetamine/methamphetamine (false-positive).
Dietary Considerations
Some products may contain phenylalanine and/or sodium. Oral dosage forms may be taken with or without food.
Patient Education
May take several days before you notice relief. Avoid excessive alcohol. May cause drowsiness, dizziness, or fatigue. Report immediately skin rash, CNS changes (mental confusion, hallucinations, somnolence), or unusual persistent weakness or lethargy.
Geriatric Considerations
Ulcer healing rates and incidence of adverse effects are similar in the elderly, when compared to younger patients; dosing adjustments not necessary based on age alone. Always adjust dose based upon creatinine clearance. Serum half-life is increased to 3-4 hours in elderly patients. H2 blockers are the preferred drugs for treating PUD in the elderly due to cost and ease of administration. These agents are no less or more effective than any other therapy. The preferred agents, due to side effects and drug interaction profile and pharmacokinetics are ranitidine, famotidine, and nizatidine. Treatment for PUD in the elderly is recommended for 12 weeks since their lesions are larger; therefore, take longer to heal. This drug is substantially cleared renally, and elderly, having decreased renal function in general, should be monitored closely for adverse effects, especially CNS.
Anesthesia and Critical Care Concerns/Other Considerations
Clinical Pearls/Comments: Ranitidine causes fewer CNS adverse reactions and drug interactions compared to cimetidine.
Evidence-Based Information: The 2008 Surviving Sepsis Campaign guidelines recommend that stress ulcer prophylaxis using an H2 blocker (Grade 1A) or proton pump inhibitor (Grade 1B) be given to patients with severe sepsis to prevent upper GI bleed. Benefit of prevention of upper GI bleed must be weighed against potential effect of increased stomach pH on development of ventilator-associated pneumonia.
Dental Health: Effects on Dental Treatment
No significant effects or complications reported
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
May cause drowsiness or dizziness
Mental Health: Effects on Psychiatric Treatment
May rarely cause agranulocytosis; use caution with clozapine and carbamazepine; concurrent use with diazepam may reduce diazepam's effectiveness
Nursing: Physical Assessment/Monitoring
Use caution in presence of renal impairment; dosage adjustment may be necessary. Monitor for CNS changes (depression, hallucinations, confusion, malaise), rash, and GI disturbance.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, oral: 150 mg, 300 mg
Infusion, premixed in 1/2 NS [preservative free]:
Zantac®: 50 mg (50 mL)
Injection, solution: 25 mg/mL (2 mL, 6 mL, 40 mL)
Zantac®: 25 mg/mL (2 mL, 6 mL, 40 mL)
Syrup, oral: 15 mg/mL (5 mL, 10 mL, 120 mL, 473 mL, 474 mL, 480 mL)
Zantac®: 15 mg/mL (480 mL) [contains ethanol 7.5%; peppermint flavor]
Tablet, oral: 75 mg, 150 mg, 300 mg
Zantac 150®: 150 mg
Zantac 150®: 150 mg [cool mint flavor]
Zantac 75®: 75 mg
Zantac 75®: 75 mg [sugar free]
Zantac®: 150 mg, 300 mg
Tablet for solution, oral [effervescent]:
Zantac® EFFERdose®: 25 mg [contains phenylalanine 2.81 mg/tablet, sodium 1.33 mEq/tablet, sodium benzoate]
Pricing: U.S. (www.drugstore.com)
Capsules (Ranitidine HCl)
150 mg (60): $50.99
300 mg (30): $30.99
Syrup (Ranitidine HCl)
15 mg/mL (30): $29.99
Syrup (Zantac)
15 mg/mL (300): $224.99
Tablet, effervescent (Zantac EFFERdose)
25 mg (60): $241.00
Tablets (Ranitidine 75)
75 mg (30): $13.99
Tablets (Ranitidine HCl)
150 mg (90): $17.99
300 mg (30): $15.99
Tablets (Zantac)
150 mg (60): $248.99
300 mg (30): $240.99
Tablets (Zantac 75)
75 mg (30): $17.99
References
“ASHP Therapeutic Guidelines on Stress Ulcer Prophylaxis. ASHP Commission on Therapeutics and Approved by the ASHP Board of Directors on November 14, 1998,” Am J Health Syst Pharm, 1999, 56(4):347-79.
Balestrazzi P, Gregori G, Bernasconi S, et al, “Bradycardia and Neurologic Disorders Associated With Ranitidine in a Child,” Am J Dis Child, 1985, 139(5):442.
Blumer JL, Rothstein FC, Kaplan BS, et al, “Pharmacokinetic Determination of Ranitidine Pharmacodynamics in Pediatric Ulcer Disease,” J Pediatr, 1985, 107(2):301-6.
Chey WD and Wong B, “American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection,” Am J Gastroenterol, 2007 102(8):1808-25.
Cook D, Guyatt G, Marshall J, et al, “A Comparison of Sucralfate and Ranitidine for the Prevention of Upper Gastrointestinal Bleeding in Patients Requiring Mechanical Ventilation. Canadian Critical Care Trials Group,” N Engl J Med, 1998, 338(12):791-7.
Dellinger RP, Levy MM, Carlet JM, et al, “Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008,” [published correction appears in Crit Care Med, 2008, 36(4):1394-6], Crit Care Med, 2008, 36(1):296-327.
Eddleston JM, Booker PD, and Green JR, “Use of Ranitidine in Children Undergoing Cardiopulmonary Bypass,” Crit Care Med, 1989, 17(1):26-9.
Fennerty MD and Higbee M, “Drug Therapy of Gastrointestinal Disease,” Geriatric Pharmacology, Bressler R and Katz MD, eds, New York, NY: McGraw-Hill, 1993, 585-608.
Fontana M, Massironi E, Rossi A, et al, “Ranitidine Pharmacokinetics in Newborn Infants,” Arch Dis Child, 1993, 68(5 Spec No):602-3.
Freeman HJ, “Ranitidine-Associated Interstitial Nephritis in a Patient With Celiac Sprue,” Can J Gastroenterol, 1988, 2:35.
Guillet R, Stoll BJ, Cotten CM, et al, "Association of H2-Blocker Therapy and Higher Incidence of Necrotizing Enterocolitis in Very Low Birth Weight Infants," Pediatrics, 2006, 117(2):137-42.
Kahrilas PJ, Shaheen NJ, Vaezi MF, et al, “American Gastroenterological Association Medical Position Statement on the Management of Gastroesophageal Reflux Disease,” Gastroenterology, 2008, 135(4):1383-91.
Kelly KL, “Ranitidine Cross-Reactivity in the EMIT D.A.U. Monocolonal Amphetamine/Methamphetamine Assay,” Clin Chem, 1990, 36(7):1391-2.
Lehmann AB, “Reversible Chorea Due to Ranitidine and Cimetidine,” Lancet, 1988, 2(8603):158.
Lopez-Herce J, Albajara L, Codoceo R, et al, “Ranitidine Prophylaxis in Acute Gastric Mucosal Damage in Critically Ill Pediatric Patients,” Crit Care Med, 1988, 16(6):591-93.
Maack DK and Spiller HA, “Rare Dystonic Reaction From Accidental Overdose of Ranitidine in a 3 Month Old,” Vet Hum Toxicol, 1993, 35:343.
Miralles ES, Nunez M, del Olmo N, et al, “Ranitidine-Related Toxic Epidermal Necrolysis in a Patient With Idiopathic Thrombocytopenic Purpura,” J Am Acad Dermatol, 1995, 32(1):133-4.
Morris DL, Markham SJ, Beechey A, et al, “Ranitidine-Bolus or Infusion Prophylaxis for Stress Ulcer,” Crit Care Med, 1988, 16(3):229-32.
Ohsawa T, Masuhara K, and Hirata W, “Reversal of Ranitidine-Induced Hypergastrinemia by Cimetidine,” Ann Pharmacother, 1994, 28(11):1303.
Richter JE, “Gastroesophageal Reflux Disease During Pregnancy,” Gastroenterol Clin North Am, 2003, 32(1):235-61.
Roberts CJ, “Clinical Pharmacokinetics of Ranitidine,” Clin Pharmacokinet, 1984, 9(3):211-21.
Romaguera C, Grimalt F, and Vilaplana J, “Epidemic of Occupational Contact Dermatitis From Ranitidine,” Contact Dermatitis, 1988, 18(3):177-8.
Souza Lima MA, “Hepatitis Associated With Ranitidine,” Ann Intern Med, 1984, 101(2):207-8.
Todd P, Norris P, Hawk JL, et al, “Ranitidine-Induced Photosensitivity,” Clin Exp Dermatol, 1995, 20(2):146-8.
International Brand Names
Lexi-Comp.com
Last full review/revision March 2012
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