(fa MOE ti deen)
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Generic: 20 mg (50 mL); 20 mg/2 mL (2 mL); 40 mg/4 mL (4 mL); 200 mg/20 mL (20 mL); 500 mg/50 mL (50 mL [DSC])
Solution, Intravenous [preservative free]:
Generic: 20 mg/2 mL (2 mL)
Suspension Reconstituted, Oral:
Pepcid: 40 mg/5 mL (50 mL) [contains methylparaben sodium, propylparaben sodium, sodium benzoate; cherry banana mint flavor]
Generic: 40 mg/5 mL (50 mL)
Acid Reducer: 10 mg
Acid Reducer Maximum Strength: 20 mg
Heartburn Relief: 10 mg
Heartburn Relief Max St: 20 mg
Pepcid: 20 mg [DSC] [scored]
Pepcid: 20 mg [contains corn starch]
Pepcid: 40 mg [DSC]
Pepcid: 40 mg [contains corn starch]
Generic: 10 mg, 20 mg, 40 mg
Brand Names: U.S.
- Acid Reducer Maximum Strength [OTC]
- Acid Reducer [OTC]
- Heartburn Relief Max St [OTC]
- Heartburn Relief [OTC]
- Histamine H2 Antagonist
Competitive inhibition of histamine at H2 receptors of the gastric parietal cells, which inhibits gastric acid secretion
Oral: Incompletely absorbed
Infants: 0 to 3 months of age: 1.4 ± 0.4 L/kg to 1.8 ± 0.3 L/kg; >3 to 12 months: 2.3 ± 0.7 L/kg
Children <11 years of age: 2.07 ± 1.49 L/kg
Children and Adolescents 11 to 15 years of age: 1.5 ± 0.4 L/kg
Adults: 1.3 ± 0.2 L/kg
30% to 35%; minimal first-pass metabolism; forms one metabolite (S-oxide)
Urine (25% to 30% [oral], 65% to 70% [IV] as unchanged drug)
Infants: 0 to 3 months of age: 0.13 to 0.21 ± 0.06 L/hour/kg; >3 to 12 months: 0.49 ± 0.17 L/hour/kg
Children <11 years of age: 0.54 ± 0.34 L/hour/kg
Children and Adolescents 11 to 15 years of age: 0.48 ± 0.14 L/hour/kg
Adults: 0.39 ± 0.14 L/hour/kg
Onset of Action
Antisecretory effect: Oral: Within 1 hour; Peak effect: Antisecretory effect: Oral: Within 1 to 3 hours (dose-dependent); IV: Within 30 minutes
Time to Peak
Serum: Oral: ~1 to 3 hours; orally disintegrating tablet: 2.5 hours
Duration of Action
Antisecretory effect: IV, Oral: 10 to 12 hours
Infants: 0 to 3 months of age: 8.1 ± 3.5 hours to 10.5 ± 5.4 hours; >3 to 12 months: 4.5 ± 1.1 hours
Children <11 years of age: 3.38 ± 2.6 hours
Children and Adolescents 11 to 15 years of age: 2.3 ± 0.4 hours
Adults: 2.5 to 3.5 hours; prolonged with renal impairment; Oliguria: >20 hours; Anuria: 24 hours
15% to 20%
Use: Labeled Indications
Duodenal ulcer: Short-term treatment of active duodenal ulcer and maintenance therapy after healing of active ulcer.
Gastric ulcer: Short-term treatment of active benign gastric ulcer.
Gastroesophageal reflux disease: Short-term treatment of gastroesophageal reflux disease (GERD) and esophagitis due to GERD, including erosive or ulcerative disease diagnosed by endoscopy.
Pathological hypersecretory conditions: Treatment of pathological hypersecretory conditions (eg, Zollinger-Ellison syndrome, multiple endocrine adenomas).
Heartburn (OTC only): Relief of heartburn, acid indigestion, and sour stomach.
Off Label Uses
Gastritis (symptomatic relief)
A multicenter, prospective, single-arm, open-label study in patients with chronic symptomatic gastritis were treated with famotidine for 4 weeks. In a subgroup analysis, famotidine significantly attenuated epigastralgia, epigastric fullness, heartburn, and abdominal symptom-related quality of life impairment in all patients with chronic symptomatic gastritis, functional dyspepsia without organic disease, and functional disease defined by Rome III criteria [Kinoshita 2012]. Additional trials may be necessary to further define the role of famotidine for the symptomatic relief of gastritis.
Reducing gastrointestinal risks of NSAIDs and antiplatelet therapies
The American College of Gastroenterology supports the use of H2 receptor antagonists for the prevention of gastrointestinal complications associated with NSAID use and antiplatelet therapy; however, preference is given towards proton pump inhibitors. These recommendations are based on systematic reviews and a meta-analysis, respectively.
Refractory urticaria, treatment:
A joint guideline published by the American Academy of Allergy, Asthma, & Immunology and the Joint Council of Allergy, Asthma, & Immunology recommend the addition of an H2 receptor antagonist to a second generation H1 receptor antagonist for patients with acute or chronic urticaria.
Stress ulcer prophylaxis in critically-ill patients
Data from a prospective, randomized, crossover study of continuous infusion or bolus administration of famotidine in patients who were critically ill supports the use of either continuous or bolus administration famotidine to increase gastric pH above 4; however, the use of continuous infusion resulted in a sustained gastric pH above 4 necessary to prevent stress ulcer [Baghaie 1995]. A meta-analysis found no difference between proton pump inhibitors and histamine-2 receptor antagonists in terms of stress-related upper gastrointestinal bleeding prophylaxis, pneumonia, and mortality in intensive care units [Lin 2010].
The American Society of Health-System Pharmacists (ASHP) recommends and supports the use of histamine H2 receptor antagonists for stress ulcer prophylaxis in critically-ill patients, although there was limited data on the use of proton pump inhibitors for stress ulcer prophylaxis at the time of publication [ASHP 1999].
Based on the Surviving Sepsis Campaign International Guidelines for the Management of Severe Sepsis and Septic Shock, stress ulcer prophylaxis using a histamine H2-receptor antagonist or a proton pump inhibitor is recommended in sepsis or septic shock patients who have GI bleeding risk factors.
Hypersensitivity to famotidine, other H2 antagonists, or any component of the formulation
OTC labeling: When used for self-medication (OTC), do not use if trouble or pain when swallowing food, vomiting with blood, or bloody or black stools; allergic to other acid reducers; renal impairment; coadministration with other acid reducers.
IV: 20 mg every 12 hours
Oral: Acute therapy: 40 mg once daily at bedtime (or 20 mg twice daily) for 4 to 8 weeks; maintenance therapy: 20 mg once daily at bedtime
IV: 20 mg every 12 hours
Oral: Acute therapy: 40 mg/day at bedtime
Esophagitis and accompanying symptoms due to GERD:
IV: 20 mg every 12 hours
Oral: 20 mg or 40 mg twice daily for up to 12 weeks
Treatment of GERD (short-term):
IV: 20 mg every 12 hours
Oral: 20 mg twice daily for 6 weeks
Heartburn: OTC labeling: Oral: 10 to 20 mg every 12 hours (maximum dose: 40 mg/day)
Pathological hypersecretory conditions:
Oral: Initial: 20 mg every 6 hours (higher initial dose may be required); may adjust dose based on patient response up to 160 mg every 6 hours has been used). Note: Proton pump inhibitors (PPIs) are preferred for hypersecretory conditions.
Reducing gastrointestinal risks of NSAIDs and antiplatelet therapies (off-label use): Oral: 40 mg twice daily (Abraham 2010; Lanza 2009)
Refractory urticaria, treatment (off-label use): Oral: 20 mg twice daily (Bernstein 2014)
Stress ulcer prophylaxis in critically-ill patients (off-label use): Oral, IV, or nasogastric (NG) tube: 20 mg twice daily (ASHP 1999; Baghaie 1995); Note: Intended for patients with associated risk factors (eg, coagulopathy, mechanical ventilation for >48 hours, sepsis/septic shock); discontinue use once risk factors have resolved (Rhodes 2017).
Refer to adult dosing.
Treatment of GERD (short-term):
Infants 1 to <3 months: 0.5 mg/kg/dose once daily for up to 8 weeks; if not effective, may increase to 1 mg/kg once daily (Orenstein 2003)
Infants ≥3 months to < 1 year: 0.5 mg/kg/dose twice daily for up to 8 weeks; if not effective, may increase to 1 mg/kg twice daily (Orenstein 2003)
Children ≥1 year to Adolescents ≤16 years: 0.5 mg/kg/dose twice daily (maximum dose: 40 mg twice daily); doses up to 1 mg/kg/dose twice daily have been used
Heartburn: OTC labeling: Oral: Children ≥12 years and Adolescents: Refer to adult dosing.
Pathological hypersecretory conditions: Oral: Adolescents ≥17 years: Refer to adult dosing.
Peptic ulcer: Children ≥1 year to Adolescents ≤16 years:
Oral: 0.5 mg/kg/day at bedtime or divided twice daily (maximum dose: 40 mg/day); doses up to 1 mg/kg/day have been used
IV: 0.25 mg/kg every 12 hours (maximum dose: 40 mg/day); doses up to 0.5 mg/kg every 12 hours have been used
Dosing: Renal Impairment
CrCl ≥50 mL/minute: No dosage adjustment necessary.
CrCl <50 mL/minute: Administer 50% of dose or increase the dosing interval to every 36 to 48 hours.
Pediatric: There are no specific dosage adjustments provided in the manufacturer's labeling; however, decreased doses or extended dosing intervals are recommended in patients with moderate to severe renal impairment; some have suggested the following (Aronoff 2007): Note: Renally adjusted dose recommendations are based on doses of 0.5 to 1 mg/kg/day divided every 12 hours.
GFR 30 to 50 mL/minute/1.73 m2: 0.5 mg/kg/dose every 24 hours
GFR 10 to 29 mL/minute/1.73 m2: 0.25 mg/kg/dose every 24 hours
GFR <10 mL/minute/1.73 m2: 0.125 mg/kg/dose every 24 hours
Intermittent hemodialysis: 0.125 mg/kg/dose every 24 hours
Peritoneal dialysis (PD): 0.125 mg/kg/dose every 24 hours
Continuous renal replacement therapy (CRRT): 0.5 mg/kg/dose every 24 hours
Dosing: Hepatic Impairment
There are no dosage adjustments provided in the manufacturer's labeling.
Solution for injection:
IV push: Dilute 2 mL (20 mg) with NS (or another compatible solution) to a total of 5 to 10 mL. May also administer undiluted (Lipsy 1995).
Infusion: Dilute 2 mL (20 mg) with 100 mL of D5W or another compatible solution.
Note: A famotidine suspension (8 mg/mL) is commercially available.
8 mg/mL Oral Suspension
An 8 mg/mL oral suspension may be made with tablets. Crush seventy 40 mg tablets in a mortar and reduce to a fine powder. Add small portions of sterile water and mix to a uniform paste. Mix while adding a 1:1 mixture of Ora-Plus and Ora-Sweet in incremental proportions to almost 350 mL; transfer to a calibrated bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 350 mL. Label "shake well." Stable for 95 days at room temperature.Dentinger PJ, Swenson CF, Anaizi NH. Stability of famotidine in an extemporaneously compounded oral liquid. Am J Health Syst Pharm. 2000;57(14):1340-1342.10918924
IV push: Inject over at least 2 minutes.
Solution for infusion: Administer over 15 to 30 minutes.
Oral: May administer with antacids.
Suspension: Shake vigorously before use.
Tablet (OTC): Do not chew. To prevent symptoms, administer 10 to 60 minutes before eating food or drinking beverages known to cause heartburn.
Powder for oral suspension: Prior to reconstitution, store at 25°C (77°F). Reconstituted oral suspension is stable for 30 days at room temperature; do not freeze.
Tablet: Store at room temperature. Protect from moisture.
Solution for injection: Prior to use, store at 2°C to 8°C (36°F to 46°F). If solution freezes, allow to solubilize at room temperature. Protect from light.
IV push: Following preparation, solutions for IV push should be used immediately, or may be stored in refrigerator and used within 48 hours.
Infusion: Following dilution in D5W, D10W, NS or LR, may be stored for up to 48 hours under refrigeration; however, solutions for infusion have been found to be physically and chemically stable for 7 days at room temperature (maintains at least 90% of initial potency).
Solution for injection, premixed bags: Store at 25°C (77°F); avoid excessive heat.
Acalabrutinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Acalabrutinib. Management: To minimize the potential for a significant interaction, separate administration of these agents by giving acalabrutinib 2 hours before ingestion of a histamine-2 receptor antagonist. Consider therapy modification
Atazanavir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Atazanavir. Management: Specific dose limitations and administration guidelines exist; consult full interaction monograph or atazanavir prescribing information. Consider therapy modification
Bosutinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Bosutinib. Management: Administer histamine H2 receptor antagonists more than 2 hours before or after bosutinib. Consider therapy modification
BuPROPion: May increase the serum concentration of OCT2 Substrates. Monitor therapy
Cefditoren: Histamine H2 Receptor 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. Consider therapy modification
Cefpodoxime: Histamine H2 Receptor Antagonists may decrease the absorption of Cefpodoxime. Separate oral doses by at least 2 hours. Monitor therapy
Cefuroxime: Histamine H2 Receptor Antagonists may decrease the absorption of Cefuroxime. Separate oral doses by at least 2 hours. Avoid combination
Cysteamine (Systemic): Histamine H2 Receptor Antagonists may diminish the therapeutic effect of Cysteamine (Systemic). Monitor therapy
Dabrafenib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Dabrafenib. Monitor therapy
Dasatinib: Histamine H2 Receptor Antagonists may decrease the absorption of Dasatinib. Management: Antacids (taken 2 hours before or after dasatinib administration) can be used in place of H2-antagonists if some acid-reducing therapy is needed. Avoid combination
Delavirdine: Histamine H2 Receptor 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. Avoid combination
Dexmethylphenidate: Histamine H2 Receptor 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. Monitor therapy
Erlotinib: Histamine H2 Receptor 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. Consider therapy modification
Fosamprenavir: Histamine H2 Receptor 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. Monitor therapy
Gefitinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Gefitinib. Management: Administer gefitinib at least 6 hours before or after administration of a histamine H2-antagonist, and closely monitor clinical response to gefitinib. Consider therapy modification
Indinavir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Indinavir. Monitor therapy
Iron Salts: Histamine H2 Receptor Antagonists may decrease the absorption of Iron Salts. Exceptions: Ferric Carboxymaltose; Ferric Citrate; Ferric Gluconate; Ferric Hydroxide Polymaltose Complex; Ferric Pyrophosphate Citrate; Ferumoxytol; Iron Dextran Complex; Iron Isomaltoside; Iron Sucrose. Monitor therapy
Itraconazole: Histamine H2 Receptor Antagonists may decrease the serum concentration of Itraconazole. Management: When this combination is used, the itraconazole should be administered with a non-diet cola beverage (8 ounces). Itraconazole oral suspension may be less sensitive to this interaction. Monitor patient response to itraconazole closely. Consider therapy modification
Ketoconazole (Systemic): Histamine H2 Receptor 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. Consider therapy modification
Ledipasvir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Ledipasvir. Consider therapy modification
Mesalamine: Histamine H2 Receptor 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. Consider therapy modification
Methylphenidate: Histamine H2 Receptor 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. Monitor therapy
MiFEPRIStone: May enhance the QTc-prolonging effect of QTc-Prolonging Agents (Indeterminate Risk and Risk Modifying). Management: Though the drugs listed here have uncertain QT-prolonging effects, they all have some possible association with QT prolongation and should generally be avoided when possible. Consider therapy modification
Multivitamins/Minerals (with ADEK, Folate, Iron): Histamine H2 Receptor Antagonists may decrease the serum concentration of Multivitamins/Minerals (with ADEK, Folate, Iron). Specifically, the absorption of iron may be impaired by H2-antagonists. Monitor therapy
Nelfinavir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Nelfinavir. Concentrations of the active M8 metabolite may also be reduced. Monitor therapy
Neratinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Neratinib. Specifically, histamine H2 receptor antagonists may reduce neratinib absorption. Avoid combination
Nilotinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Nilotinib. Management: The nilotinib dose should be given 10 hours after or 2 hours before the H2 receptor antagonist in order to minimize the risk of a significant interaction. Consider therapy modification
PAZOPanib: Histamine H2 Receptor Antagonists may decrease the serum concentration of PAZOPanib. Management: Avoid the use of histamine H2-antagonists in combination with pazopanib. Strategies to minimize the expected interaction between these agents (eg, dose separation) have not been investigated. Avoid combination
Posaconazole: Histamine H2 Receptor Antagonists may decrease the serum concentration of Posaconazole. Management: Avoid concurrent use of oral suspension with H2-antagonists whenever possible. Monitor patients closely for decreased antifungal effects if this combination is used. Delayed-release posaconazole tablets may be less likely to interact. Consider therapy modification
QTc-Prolonging Agents (Highest Risk): QTc-Prolonging Agents (Indeterminate Risk and Risk Modifying) may enhance the QTc-prolonging effect of QTc-Prolonging Agents (Highest Risk). Management: Avoid such combinations when possible. Use should be accompanied by close monitoring for evidence of QT prolongation or other alterations of cardiac rhythm. Consider therapy modification
QTc-Prolonging Agents (Moderate Risk): QTc-Prolonging Agents (Indeterminate Risk and Risk Modifying) may enhance the QTc-prolonging effect of QTc-Prolonging Agents (Moderate Risk). Monitor therapy
Rilpivirine: Histamine H2 Receptor Antagonists may decrease the serum concentration of Rilpivirine. Management: Administer histamine H2 receptor antagonists at least 12 hours before or 4 hours after rilpivirine. Consider therapy modification
Risedronate: Histamine H2 Receptor Antagonists may increase the serum concentration of Risedronate. This applies specifically to delayed-release risedronate. Avoid combination
Saquinavir: Histamine H2 Receptor Antagonists may increase the serum concentration of Saquinavir. Monitor therapy
Secretin: Histamine H2 Receptor Antagonists may diminish the diagnostic effect of Secretin. Specifically, use of H2-Antagonists may cause a hyperresponse in gastrin secretion in response to secretin stimulation testing, falsely suggesting gastrinoma. Management: Avoid concomitant use of histamine H2-antagonists (H2RAs) and secretin. Discontinue H2RAs at least 2 days prior to secretin administration. Consider therapy modification
Varenicline: Histamine H2 Receptor Antagonists may increase the serum concentration of Varenicline. Management: Monitor for increased varenicline adverse effects with concomitant use of cimetidine or other H2-antagonists, particularly in patients with severe renal impairment. International product labeling recommendations vary. Consult appropriate labeling. Monitor therapy
Velpatasvir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Velpatasvir. Monitor therapy
Central nervous system: Agitation (<1 year of age: ≤14%)
Gastrointestinal: Vomiting (<1 year of age: ≤14%)
1% to 10%:
Central nervous system: Headache (5%), dizziness (1%)
Gastrointestinal: Diarrhea (2%), constipation (1%), necrotizing enterocolitis (very low birth weight neonates; Guillet 2006)
<1% (Limited to important or life-threatening): Abdominal distress, acne vulgaris, agranulocytosis, alopecia, anaphylaxis, angioedema, anorexia, anxiety, arthralgia, atrioventricular block, bronchospasm, cardiac arrhythmia, cholestatic jaundice, confusion, conjunctival injection, decreased libido, depression, drowsiness, dysgeusia, facial edema, fatigue, fever, flushing, hallucination, hepatitis, hypersensitivity reaction, increased liver enzymes, injection site reaction, insomnia, interstitial pneumonitis, leukopenia, muscle cramps, nausea, palpitations, pancytopenia, paresthesia, prolonged Q-T interval on ECG, pruritus, rhabdomyolysis, seizure, skin rash, Stevens-Johnson syndrome, thrombocytopenia, tinnitus, torsades de pointes, toxic epidermal necrolysis, urticaria, weakness, xeroderma, xerostomia
Concerns related to adverse effects.
• ECG changes: Prolonged QT interval has been reported in patients with renal dysfunction. The FDA has received reports of torsades de pointes occurring with famotidine (Poluzzi 2009).
• Vitamin B12 deficiency: Prolonged treatment (≥2 years) may lead to vitamin B12 malabsorption and subsequent vitamin B12 deficiency. The magnitude of the deficiency is dose-related and the association is stronger in females and those younger in age (<30 years); prevalence is decreased after discontinuation of therapy (Lam 2013).
• Gastric malignancy: Relief of symptoms does not preclude the presence of a gastric malignancy.
• Renal impairment: Use with caution in patients with moderate to severe renal impairment (CrCl <50 mL/minute); dosage adjustment recommended.
Concurrent drug therapy issues:
• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.
• Pediatric: Use of gastric acid inhibitors, including proton pump inhibitors and H2 blockers, has been associated with an increased risk for development of acute gastroenteritis and community-acquired pneumonia in pediatric patients (Canani 2006).
Dosage form specific issues:
• Benzyl alcohol and derivatives: Some dosage forms may contain benzyl alcohol and/or sodium benzoate/benzoic acid; benzoic acid (benzoate) is a metabolite of benzyl alcohol; large amounts of benzyl alcohol (≥99 mg/kg/day) have been associated with a potentially fatal toxicity (“gasping syndrome”) in neonates; the “gasping syndrome” consists of metabolic acidosis, respiratory distress, gasping respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension, and cardiovascular collapse (AAP ["Inactive" 1997]; CDC 1982); some data suggests that benzoate displaces bilirubin from protein binding sites (Ahlfors 2001); avoid or use dosage forms containing benzyl alcohol and/or benzyl alcohol derivative with caution in neonates. See manufacturer’s labeling.
• OTC labeling: When used for self-medication (OTC), notify health care provider before use if any of the following are present: Frequent chest pain; frequent wheezing particularly with heartburn; nausea/vomiting; unexplained weight loss; stomach pain; heartburn >3 months; heartburn with light-headedness, sweating, or dizziness; chest pain or shoulder pain with shortness of breath; sweating; pain that spreads to arms, neck, or shoulders; light-headedness. Discontinue use and notify health care provider if heartburn continues or worsens, or if use is required >14 days.
CBC, gastric pH, occult blood with GI bleeding
Pregnancy Risk Factor
Adverse events have not been observed in animal reproduction studies. Famotidine crosses the placenta (Dicke 1988). An increased risk of congenital malformations or adverse events in the newborn has generally not been observed following maternal use of famotidine 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. Although if needed, famotidine is not the agent of choice (Cappell 2003; Richter 2003; Richter 2005). Histamine H2 antagonists may be used for aspiration prophylaxis prior to cesarean delivery (ASA 2007).
• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
• Patient may experience headache (HCAHPS).
• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for health care professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients.
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