Generic Name

Famotidine

Mechanism

• Competitive inhibition of histamine binding to H₂ receptors on parietal cells.
• Suppresses cyclic‑AMP production → ↓ Ca²⁺‑dependent proton pump activation.
• Result: ↓ gastric acid secretion, ↑ intragastric pH (≈2.5–4.5).
• Unlike H₂ antagonists, famotidine does not significantly influence mucosal blood flow or intestinal motility.

Pharmacokinetics

| Half‑life | 2–3 h; prolongs to ~4 h in renal impairment (up to 85 % reduction in CrCl Key take‑away: Renal dosing adjustment is essential; hepatic dysfunction has minimal impact.

Indications

• Acid‑related disorders:
• Non‑erosive Gastroesophageal Reflux Disease (GERD)
• Peptic ulcer disease (PUD) (both acute and maintenance)
• Erosive esophagitis
• Post‑endoscopic therapy for ulcer healing
• H₂‑induced adverse drug reactions (e.g., NSAID‑associated ulcers).
• Idiopathic or drug‑induced severe gastritis.
• Post‑gastric surgery acid suppression (e.g., Billroth II).
• Pediatric: GERD, peptic ulcer, and reflux‑induced aspiration in infants (dose‑adjusted).

> Note: Famotidine is *not* indicated for H. pylori eradication regimens without other agents.

Contraindications

• Known hypersensitivity to famotidine or any excipients.
• Severe renal impairment (CrCl <30 mL/min) unless dose adjusted.
• Drug interactions:
• *P‑450 inhibitors* or *inducers* rarely affect famotidine, but caution with drugs requiring acidic gastric environment (e.g., ketoconazole, amphotericin B).
• Cimetidine, ranitidine may cause competitive displacement → transient ↑ famotidine levels.
• Pregnancy/Breastfeeding: Category B; safe when benefits outweigh potential risks.
• Renal tubular acidosis: rare, avoid unless necessary.

Dosing

> Renal adjustment:

>
• CrCl ≥50 mL/min: standard dose.

>
• CrCl 30–49 mL/min: reduce to 5 mg q24h (IV).

>
• CrCl <30 mL/min: 2.5 mg q24h IV.

Administration tips:
• Oral tablets can be crushed if needed; avoid over‑concentration.
• Intravenous preparation: dilute 10 mg in 10 mL NS; give 5‑min slow infusion.
• For infusion failure: consider 20 mg dose or switch to PPI.

Adverse Effects

• CNS: agitation, confusion, hallucinations (esp. in CKD). |
• Cardiovascular: bradycardia, QT prolongation (rare). |
• Hypersensitivity: rash, urticaria, angioedema. |
• Hepatic: mild transaminase elevation. |
• Renal: precipitates with high protein diets (uncommon). |

> Incidence: <1 % for serious events; most side effects are dose‑dependent and reversible.

Monitoring

• Renal function: baseline CrCl, then at 4–6 weeks if dosing >10 mg q24h.
• Serum electrolytes: in patients with renal impairment or on diuretics.
• Vital signs: particularly heart rate (bradycardia risk).
• Liver enzymes: if signs of hepatotoxicity.
• Gastric pH: only in clinical studies; not routine.

Clinical Pearls

• Rapid onset: IV famotidine begins to lower pH within 30 min—ideal for acute ulcer bleeding.
• PPI‑resistant GERD: switching from a PPI to famotidine can uncover non‑acid reflux; useful diagnostic tool.
• Renal dosing is crucial: due to renal excretion, neglecting adjustment leads to accumulation and neurotoxicity.
• Use in anesthesia: famotidine has no significant interaction with most anesthetics; safe to combine.
• Avoid excessive acid suppression: prolonged use may increase risk of Clostridioides difficile infection.
• Combination therapy: when eradicating H. pylori, famotidine can be substituted with a PPI but efficacy may differ.

Reference: UpToDate, *Gastroenterology: Pharmacology of acid‑suppressing agents*, 2024; FDA label, 2023.