Drugs Used for Peptic Ulcer Disease (PUD)

Overview

Peptic ulcer disease (PUD) encompasses ulceration of the gastric or duodenal mucosa due to an imbalance between aggressive factors (gastric acid, pepsin, Helicobacter pylori, bile, and nonsteroidal anti-inflammatory drugs [NSAIDs]) and mucosal defenses (mucus-bicarbonate barrier, prostaglandins, mucosal blood flow, epithelial restitution). Pharmacologic therapy aims to relieve symptoms, promote healing, prevent complications (bleeding, perforation, obstruction), eradicate H. pylori when present, and prevent recurrence. Drug classes include antacids, histamine H2-receptor antagonists (H2RAs), proton pump inhibitors (PPIs), mucosal protective agents (sucralfate, bismuth), prostaglandin analogs (misoprostol), and antibiotics for H. pylori eradication. Choice depends on etiology (H. pylori vs NSAID/stress-related), severity, risk factors, and local antibiotic resistance patterns [1–4].

Pathophysiology: Targets for Pharmacotherapy

Aggressive factors

• Gastric acid and pepsin: Acid secretion is driven by parietal cell H+/K+-ATPase (the proton pump), stimulated by acetylcholine (M3), histamine (H2), and gastrin receptors. Acid and pepsin damage mucosa when protective barriers fail [1,2].
• H. pylori: Spiral gram-negative bacterium that colonizes mucus, produces urease (ammonia buffer), cytotoxins, and induces inflammation, weakening defenses and increasing gastrin and acid secretion (particularly in duodenal ulcers) [1–3].
• NSAIDs: Systemic prostaglandin inhibition (COX-1 > COX-2) reduces mucus and bicarbonate secretion, impairs mucosal blood flow and epithelial repair, and topical injury occurs in the stomach/duodenum [1–4].

Defensive factors

• Mucus-bicarbonate layer and surface phospholipids.
• Prostaglandins (especially PGE2, PGI2) that stimulate mucus/bicarbonate, maintain blood flow, and limit acid secretion.
• Rapid epithelial restitution and adequate blood flow remove back-diffused H+ [1–3].

Therapeutic Goals and Principles

• Rapid symptom control and ulcer healing: potent acid suppression (PPIs > H2RAs) accelerates healing in gastric and duodenal ulcers.
• Eradicate H. pylori when present to cure infection, heal ulcers, and prevent relapse and complications.
• Prevent NSAID-induced ulcers: minimize NSAID use, use COX-2 selective agents when appropriate, and co-prescribe gastroprotection (PPI or misoprostol) in high-risk patients.
• Prevent stress-related mucosal bleeding in high-risk critically ill patients with appropriate prophylaxis.
• Prevent recurrence: eradicate H. pylori or maintain protective therapy in selected cases (e.g., refractory hypersecretory states) [1–4].

Classification of Drugs

• Antacids: neutralize gastric acid (aluminum, magnesium, calcium, sodium salts).
• H2-receptor antagonists: cimetidine, ranitidine, famotidine, nizatidine.
• Proton pump inhibitors: omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole, rabeprazole.
• Cytoprotective agents: sucralfate, bismuth compounds.
• Prostaglandin analog: misoprostol.
• Antibiotics for H. pylori: amoxicillin, clarithromycin, metronidazole, tinidazole, tetracycline, levofloxacin, rifabutin; plus bismuth in quadruple therapy [1–4].

Antacids

Mechanism and agents

Antacids are weak bases that react with gastric hydrochloric acid to form salts and water, raising intragastric pH, reducing pepsin activity, and providing rapid symptom relief. They do not significantly alter nocturnal acid secretion or promote ulcer healing when used alone, but can contribute to symptom control and as-needed relief [1,2].

• Sodium bicarbonate: fast onset, short duration; systemic absorption can cause metabolic alkalosis.
• Calcium carbonate: fast onset; may cause acid rebound and hypercalcemia/constipation.
• Magnesium hydroxide: rapid and potent; causes osmotic diarrhea.
• Aluminum hydroxide: slower; causes constipation, binds phosphate (risk of hypophosphatemia).
  Combination Al/Mg preparations balance bowel effects; alginate formulations can form a “raft” barrier in reflux [1–4].

Pharmacokinetics

Neutralization occurs in the lumen; systemic absorption varies (notably sodium bicarbonate, calcium). Magnesium and aluminum salts are minimally absorbed but can accumulate in renal insufficiency. Duration of effect ~1–2 hours; food prolongs action [1,2].

Adverse effects and interactions

• GI: constipation (Al, Ca), diarrhea (Mg).
• Electrolyte disturbances in renal impairment; milk-alkali syndrome with excessive calcium carbonate plus dairy.
• Drug interactions: chelation or adsorption reduces absorption of tetracyclines, fluoroquinolones, iron, and some azoles; separate by 2–4 hours. Alkalinization of urine may alter excretion of weak acids/bases [1–4].

Therapeutic use and dosing

Symptomatic relief of dyspepsia and heartburn; adjunctive therapy in PUD. Typical dosing: 5–15 mL or 1–3 tablets after meals and at bedtime or as needed. Avoid excessive sodium load in heart failure/renal disease; monitor in chronic use [1–3].

H2-Receptor Antagonists

Mechanism

H2RAs competitively block H2 receptors on parietal cells, reducing basal and meal-stimulated acid secretion—most effective for nocturnal acid output. They also reduce pepsin concentration secondarily. Potency order (per mg): famotidine > nizatidine ≈ ranitidine > cimetidine [1,2].

Agents and dosing (typical adult)

• Cimetidine: 400 mg twice daily or 800 mg at bedtime for ulcers.
• Ranitidine: 150 mg twice daily or 300 mg at bedtime.
• Famotidine: 20 mg twice daily or 40 mg at bedtime.
• Nizatidine: 150 mg twice daily or 300 mg at bedtime.
  Dose adjustment in renal insufficiency is required for all H2RAs. For maintenance, lower once-daily bedtime dosing can be used [1–4].

Clinical efficacy and uses

H2RAs heal duodenal ulcers in 6–8 weeks and gastric ulcers in 8–12 weeks, relieve symptoms, and reduce rebleeding risk when used intravenously in upper GI bleeding (though PPIs are favored). They are also used for GERD and dyspepsia; tolerance can develop with continued use [1–3].

Adverse effects

Generally well tolerated: headache, dizziness, diarrhea/constipation. Rare: confusion (especially elderly, renal/hepatic impairment), bradycardia/hypotension (IV), elevated creatinine (cimetidine via tubular secretion inhibition). Endocrine effects notable with cimetidine (gynecomastia, galactorrhea, decreased libido) due to antiandrogenic activity and increased prolactin [1–3].

Drug interactions

• Cimetidine inhibits CYP1A2, 2C9, 2D6, and 3A4, increasing levels of warfarin, phenytoin, theophylline, lidocaine, etc. Famotidine, ranitidine, and nizatidine have fewer CYP interactions.
• All H2RAs can reduce absorption of drugs requiring acidic pH (e.g., ketoconazole).
• Additive CNS effects with anticholinergics/benzodiazepines in susceptible patients [1–4].

Proton Pump Inhibitors (PPIs)

Mechanism

PPIs are prodrugs that require activation in the acidic environment of the parietal cell secretory canaliculus. The activated sulfenamide forms covalent disulfide bonds with cysteines of the H+/K+-ATPase, irreversibly inactivating the pump. Acid secretion resumes only after synthesis of new pumps, providing profound and long-lasting suppression of both basal and stimulated acid secretion [1,2].

Agents and dosing (typical adult)

• Omeprazole: 20–40 mg once daily (BID for H. pylori regimens).
• Esomeprazole: 20–40 mg once daily (BID for H. pylori).
• Lansoprazole: 15–30 mg once daily (BID for H. pylori).
• Dexlansoprazole: 30–60 mg once daily.
• Pantoprazole: 40 mg once daily (BID for H. pylori).
• Rabeprazole: 20 mg once daily (BID for H. pylori).
  Take 30–60 minutes before breakfast; for BID regimens, before breakfast and dinner. IV formulations exist (e.g., pantoprazole, esomeprazole) for acute upper GI bleeding or when oral administration is not possible [1–4].

Pharmacokinetics

Enteric-coated formulations protect from degradation; absorbed in small intestine; highly protein-bound; short plasma half-life (~1–2 hours) but prolonged effect due to irreversible pump binding. Metabolized mainly by CYP2C19 and CYP3A4. Genetic polymorphisms in CYP2C19 alter exposure; Asian populations have higher prevalence of poor metabolizers, increasing efficacy and adverse effects [1,2].

Clinical efficacy and uses

• Duodenal and gastric ulcer healing: faster and higher rates than H2RAs; promote hemostasis and reduce rebleeding when used IV in bleeding ulcers (following endoscopic therapy).
• H. pylori eradication: essential component of triple/quadruple regimens (BID dosing).
• NSAID-associated ulcers: effective for treatment and prophylaxis during NSAID or antiplatelet therapy.
• Hypersecretory states (Zollinger–Ellison syndrome) and GERD.
• Stress ulcer prophylaxis in high-risk ICU patients [1–3].

Adverse effects

Common: headache, nausea, abdominal pain, diarrhea/constipation, rash. Generally safe, but long-term/high-dose use has been associated with:

• Vitamin and mineral malabsorption: B12 deficiency, iron malabsorption, hypomagnesemia (rare but can be serious).
• Bone effects: small increased risk of fractures with chronic use (possibly via calcium absorption changes).
• Infections: increased risk of enteric infections including Clostridioides difficile and possibly community-acquired pneumonia, likely from gastric acid suppression.
• Renal: rare interstitial nephritis; observational links to chronic kidney disease.
• Gastric histology: hypergastrinemia, ECL cell hyperplasia, fundic gland polyps (benign).
• Rebound acid hypersecretion upon abrupt withdrawal after prolonged therapy [1–3].
  Causality for some associations remains debated; use the lowest effective dose for the shortest duration consistent with indications [1–3].

Drug interactions

• Reduced bioavailability of drugs needing acidic pH (e.g., ketoconazole, itraconazole).
• Omeprazole and esomeprazole inhibit CYP2C19, potentially reducing activation of clopidogrel; consider pantoprazole if antiplatelet effect is critical.
• Monitoring magnesium with long-term therapy; caution with digoxin (increased absorption may occur with hypomagnesemia) [1–3].

Cytoprotective and Mucosal Defense Agents

Sucralfate

• Mechanism: A sulfated polysaccharide complexed with aluminum hydroxide that, in acidic pH, polymerizes and binds to ulcer bases and epithelial cells, forming a protective barrier, concentrating growth factors, and inhibiting pepsin and bile salt diffusion. Does not significantly alter gastric pH [1,2].
• Dosing: 1 g four times daily (before meals and at bedtime) or 2 g twice daily for 4–8 weeks. Requires acidic environment; avoid concurrent antacids/PPIs/H2RAs if possible around dosing.
• Adverse effects: constipation (aluminum), dry mouth, nausea; aluminum accumulation in renal impairment.
• Interactions: Binds many drugs (fluoroquinolones, tetracyclines, digoxin, phenytoin); separate by ≥2 hours.
• Uses: Promotes ulcer healing; sometimes used in stress ulcer prophylaxis, though PPIs/H2RAs are more common [1–3].

Bismuth compounds

• Agents: Bismuth subsalicylate, bismuth subcitrate.
• Mechanism: Coats ulcer craters, has direct antimicrobial activity against H. pylori and binds enterotoxins; reduces stool liquidity.
• Dosing in H. pylori regimens: bismuth subsalicylate 524–525 mg four times daily or bismuth subcitrate 120–300 mg four times daily (formulations vary) as part of quadruple therapy.
• Adverse effects: black tongue and stools, constipation; salicylate toxicity if overused; avoid in aspirin/salicylate allergy and caution in renal insufficiency and with anticoagulants [1–3].

Misoprostol (PGE1 analog)

• Mechanism: Prostaglandin analog that stimulates mucus and bicarbonate secretion, enhances mucosal blood flow, and directly inhibits acid secretion via EP3 receptors on parietal cells.
• Indication: Prevention of NSAID-induced gastric ulcers in high-risk patients; less effective for duodenal ulcers.
• Dosing: 200 micrograms four times daily with food (lower doses reduce adverse effects but may be less effective).
• Adverse effects: diarrhea (dose-related), abdominal cramping; uterine contractions—contraindicated in pregnancy (abortifacient) and requires contraception in women of childbearing potential.
• Limitations: Frequent dosing and GI side effects limit adherence; PPIs are often preferred for NSAID ulcer prevention due to tolerability [1–4].

Helicobacter pylori Eradication Therapy

Rationale and principles

H. pylori infection accounts for most duodenal and many gastric ulcers. Eradication cures infection, heals ulcers, and greatly reduces recurrence and complications. Effective regimens combine a PPI plus two or more antibiotics, often with bismuth. Regimen choice is guided by macrolide resistance prevalence, individual antibiotic exposure history, allergies, and tolerability. Duration of 10–14 days improves eradication compared with shorter courses [1–3].

Recommended regimens (typical adult dosing)

Bismuth quadruple therapy (preferred where clarithromycin resistance is high or prior macrolide exposure):

• PPI (standard dose) twice daily + bismuth subsalicylate 525 mg four times daily + tetracycline 500 mg four times daily + metronidazole 500 mg three or four times daily for 10–14 days.
  Advantages: Efficacy despite macrolide resistance; option for penicillin allergy (if tetracycline tolerable) [1–3].

Clarithromycin triple therapy (only if local clarithromycin resistance is low and no prior macrolide exposure):

• PPI twice daily + clarithromycin 500 mg twice daily + amoxicillin 1000 mg twice daily (or metronidazole 500 mg twice daily if penicillin allergy) for 14 days.
  Declining efficacy in many regions due to macrolide resistance [1–3].

Concomitant (non-bismuth quadruple) therapy:

• PPI twice daily + amoxicillin 1000 mg twice daily + clarithromycin 500 mg twice daily + metronidazole (or tinidazole) 500 mg twice daily for 10–14 days.
  Useful alternative in areas of moderate resistance [1–3].

Levofloxacin triple therapy (salvage):

• PPI twice daily + levofloxacin 500 mg once daily + amoxicillin 1000 mg twice daily for 10–14 days.
  Avoid if high fluoroquinolone resistance or contraindications [1–3].

Rifabutin triple therapy (salvage):

• PPI twice daily + amoxicillin 1000 mg twice daily + rifabutin 150 mg twice daily for 10–14 days.
  Consider for multiple prior failures, mindful of myelotoxicity risk [1,2].

Notes:

• Substitute tinidazole for metronidazole when preferred/tolerated.
• In penicillin allergy, bismuth quadruple therapy is the main option; consider allergy testing if multiple failures.
• Dosing may vary with specific PPI; use standard or double-dose PPI (e.g., omeprazole 20 mg BID or 40 mg BID depending on regimen) [1–3].

Antibiotics used: mechanisms, adverse effects, interactions

• Amoxicillin: Beta-lactam inhibiting cell wall synthesis; well tolerated; diarrhea, rash; adjust in renal impairment; low resistance in H. pylori [1–3].
• Clarithromycin: Macrolide inhibiting 50S ribosome; dysgeusia, QT prolongation, CYP3A4 inhibition leading to interactions (e.g., statins, warfarin); resistance common reduces efficacy [1–3].
• Metronidazole/tinidazole: Nitroimidazoles causing DNA strand breakage; nausea, metallic taste, disulfiram-like reaction with alcohol (avoid alcohol during therapy and 48–72 hours after); interactions with warfarin (INR elevation) [1–3].
• Tetracycline: 30S inhibitor; photosensitivity, GI upset; avoid in pregnancy/children; chelation with divalent/trivalent cations (separate from antacids, iron) [1–3].
• Levofloxacin: Fluoroquinolone inhibiting DNA gyrase/topoisomerase IV; tendinopathy, QT prolongation, dysglycemia, CNS effects; significant resistance concerns [1,2].
• Rifabutin: Inhibits bacterial RNA polymerase; myelotoxicity (neutropenia), uveitis (especially with inhibitors of its metabolism), orange discoloration of body fluids; potent inducer of CYP enzymes (fewer interactions than rifampin but still relevant) [1,2].

Confirmation of eradication and management of failure

Confirm eradication at least 4 weeks after antibiotics and after 1–2 weeks off PPIs (or using H2RA/antacids for bridge) using urea breath test, stool antigen test, or biopsy-based tests when indicated. If eradication fails, select a regimen using different antibiotics (e.g., bismuth quadruple after clarithromycin triple failure) and consider susceptibility testing when available [1–3].

NSAID-Associated Ulcers

Prevention strategies

• Avoid NSAIDs if possible; use the lowest effective dose; consider COX-2 selective inhibitors in patients with low cardiovascular risk.
• Co-therapy with PPI (once daily) effectively prevents gastric and duodenal ulcers and bleeding in high-risk patients (history of ulcer, age >65, concomitant anticoagulants, steroids, or high-dose NSAIDs).
• Misoprostol 200 micrograms four times daily prevents NSAID-induced gastric ulcers but is limited by diarrhea and cramping. H2RAs prevent duodenal more than gastric ulcers and are less effective than PPIs for NSAID-related gastric ulcers [1–4].

Treatment of established NSAID ulcers

• Discontinue NSAID if feasible and treat with PPI for 8 weeks; if NSAID must continue, a PPI should be continued (often maintenance while NSAID persists).
• Test and treat H. pylori if positive, because coinfection with H. pylori and NSAID use increases risk of complications [1–3].

Stress-Related Mucosal Disease (SRMD) and Prophylaxis

Indications

Critically ill patients (e.g., mechanical ventilation >48 hours, coagulopathy, severe burns, traumatic brain injury, sepsis with multi-organ failure) have increased risk for stress-related mucosal bleeding. Pharmacologic prophylaxis is indicated in high-risk patients only [1–3].

Drugs and approach

• PPIs (IV or oral) or H2RAs reduce clinically significant bleeding.
• Sucralfate is less effective and can occlude feeding tubes.
• Weigh risks: acid suppression may increase nosocomial pneumonia and C. difficile risk; reassess daily and discontinue prophylaxis when risk factors resolve [1–3].

Special Populations and Clinical Considerations

Pregnancy and lactation

• Antacids (avoid sodium bicarbonate for systemic alkalosis/edema risk) are first-line for dyspepsia.
• H2RAs (e.g., ranitidine historically, famotidine) and most PPIs (particularly omeprazole, lansoprazole, pantoprazole) have reassuring safety profiles; use when needed.
• Misoprostol is contraindicated (abortifacient).
• For H. pylori, deferring eradication until after pregnancy is often appropriate unless complications occur; avoid tetracycline, levofloxacin, and clarithromycin when risks outweigh benefits. Amoxicillin-based regimens may be considered postpartum [1–3].

Pediatrics

• H. pylori eradication when there is endoscopically confirmed ulcer disease; regimens tailored to weight and local resistance; PPIs and amoxicillin are commonly used; avoid tetracyclines (<8 years) and fluoroquinolones [1,2].
• Use acid suppression judiciously to avoid overuse.

Geriatrics

• Increased susceptibility to adverse effects (CNS effects with H2RAs, infections with PPIs, electrolyte disturbances with antacids).
• Polypharmacy increases interaction risk (cimetidine CYP inhibition, PPIs affecting clopidogrel). Tailor dosing to renal function [1–3].

Renal and hepatic impairment

• H2RAs require dose reduction in renal insufficiency; risk of CNS effects.
• Aluminum/magnesium antacids accumulate in renal failure—avoid or monitor closely.
• PPIs: no standard dose adjustment, but hepatic impairment may increase exposure; monitor for adverse effects [1–3].

Drug interaction summary

• Antacids and sucralfate: chelation/adsorption—separate from other drugs.
• Cimetidine: significant CYP inhibition; avoid when interacting drugs are critical.
• PPIs: reduced absorption of pH-dependent drugs; omeprazole/esomeprazole with clopidogrel; monitor magnesium with long-term use.
• Clarithromycin, metronidazole, levofloxacin: notable CYP/QT/warfarin interactions—review carefully during H. pylori therapy [1–4].

Comparative Efficacy and Choosing Therapy

Acid suppression: PPIs vs H2RAs vs antacids

• PPIs provide the most potent and sustained acid suppression and are first-line for ulcer healing, bleeding prevention in high-risk states, and as part of H. pylori regimens.
• H2RAs are effective for nocturnal acid suppression and ulcer healing but less potent; tachyphylaxis can occur with continuous use.
• Antacids are for rapid, short-lived symptom relief; not adequate for healing as monotherapy [1–3].

Cytoprotective agents

• Sucralfate can promote healing but is less convenient due to dosing frequency and interactions; consider when acid suppression must be minimized.
• Misoprostol is specifically valuable for NSAID ulcer prevention but limited by GI side effects and contraindication in pregnancy.
• Bismuth is central to quadruple therapy for H. pylori and provides symptomatic relief in dyspepsia/diarrhea [1–4].

H. pylori eradication approach

• In regions with high clarithromycin resistance, use bismuth quadruple or concomitant therapy first-line.
• Prior antibiotic exposure guides selection (avoid repeating macrolides if previously used).
• Ensure adequate PPI dosing and full 10–14 day duration to maximize eradication.
• Confirm eradication and plan salvage using non-cross-resistant regimens if needed [1–3].

Practical Prescribing and Stewardship

Duration and follow-up

• Uncomplicated duodenal ulcers: 4 weeks PPI; gastric ulcers: 8 weeks PPI; extend if large or complicated.
• NSAID ulcers: treat 8 weeks; continue PPI if NSAID persists.
• H. pylori: full course 10–14 days; confirm eradication after an appropriate interval off PPIs [1–3].

Deprescribing PPIs

• Review indication periodically; for healed, uncomplicated disease without ongoing risk, attempt step-down (dose reduction) or discontinuation.
• To minimize rebound, taper dose or use alternate-day dosing temporarily; consider H2RA or antacids for transient symptoms [1–3].

Improving adherence

• Educate on timing (PPI before meals), avoidance of alcohol with nitroimidazoles, completion of antibiotic courses, and spacing of interacting agents (antacids/sucralfate).
• Use combination packs where available to simplify H. pylori therapy [1–3].

Selected Drug Profiles

Cimetidine

• Strength: Ulcer healing; OTC options for dyspepsia.
• Limitations: CYP inhibition, endocrine effects, CNS effects in elderly/renally impaired; requires renal dose adjustment [1–3].

Famotidine

• Strength: Potent H2RA with minimal CYP interactions; better safety profile than cimetidine.
• Limitations: Tolerance with continuous use; renal dose adjustment [1–3].

Omeprazole/Esomeprazole

• Strength: Potent PPIs; extensive clinical experience; BID dosing in H. pylori regimens.
• Limitations: CYP2C19 inhibition (clopidogrel interaction); potential long-term adverse associations [1–3].

Pantoprazole

• Strength: Lower potential for CYP2C19-mediated interactions; IV formulation widely used.
• Limitations: Class-related risks apply [1–3].

Sucralfate

• Strength: Non-systemic cytoprotection; option when avoiding acid suppression.
• Limitations: QID dosing, drug binding, requires acidic environment, constipation [1,2].

Misoprostol

• Strength: Proven NSAID ulcer prevention.
• Limitations: Diarrhea, cramping; contraindicated in pregnancy; adherence challenges [1–4].

Bismuth

• Strength: Key component of quadruple therapy; symptomatic benefit in dyspepsia/diarrhea.
• Limitations: Black stools/tongue; salicylate-related cautions for subsalicylate [1–3].

Clinical Scenarios

H. pylori-positive duodenal ulcer

• Preferred: 14-day bismuth quadruple or concomitant therapy, depending on local resistance and availability.
• Follow-up: Confirm eradication; no maintenance therapy typically needed after cure [1–3].

Chronic NSAID user with prior GI bleed

• If NSAID essential: switch to COX-2 selective agent plus daily PPI; avoid additional risk factors; test and eradicate H. pylori if present; misoprostol is an alternative if PPIs are contraindicated or not tolerated [1–4].

Upper GI bleed due to peptic ulcer

• After endoscopic hemostasis: high-dose IV PPI (e.g., 80 mg bolus then 8 mg/h infusion for 72 hours, or equivalent intermittent dosing) to maintain intragastric pH >6, reduce rebleeding; then oral PPI for 6–8 weeks. Evaluate and treat H. pylori when appropriate [1–3].

Refractory or recurrent ulcers

• Assess adherence, smoking, ongoing NSAIDs, gastrinoma/hypersecretory state, and H. pylori persistence. Optimize PPI dosing, consider nocturnal H2RA add-on for nocturnal acid breakthrough in selected cases, and evaluate for other causes (Crohn’s, CMV) if nonhealing [1–3].

Key Takeaways

• PPIs are first-line for ulcer healing and critical components of H. pylori therapy and NSAID ulcer prevention.
• H. pylori eradication cures infection and prevents recurrence; choose regimens mindful of resistance and prior antibiotic exposure.
• Misoprostol prevents NSAID ulcers but is limited by tolerability and contraindication in pregnancy; PPIs are commonly preferred for prevention during chronic NSAID therapy.
• Antacids provide rapid symptom relief; H2RAs are useful for nocturnal acid suppression and symptom control but are less potent than PPIs.
• Avoid unnecessary long-term acid suppression; review indications and deprescribe when appropriate; monitor for potential long-term adverse effects and interactions [1–4].

Suggested Adult Dosing Summary (Typical)

• PPI for ulcer healing: omeprazole 20–40 mg daily (4 weeks duodenal, 8 weeks gastric); alternatives as class equivalents.
• H. pylori bismuth quadruple (14 days): PPI BID + bismuth subsalicylate 525 mg QID + tetracycline 500 mg QID + metronidazole 500 mg TID–QID.
• H. pylori clarithromycin triple (14 days, only if low resistance): PPI BID + clarithromycin 500 mg BID + amoxicillin 1000 mg BID (or metronidazole 500 mg BID if penicillin allergy).
• NSAID prophylaxis: PPI once daily; or misoprostol 200 micrograms QID if tolerated.
• Sucralfate: 1 g QID on empty stomach [1–3].

References

1. Brunton LL, Hilal-Dandan R, Knollmann BC, editors. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 14th ed. New York: McGraw-Hill Education; 2022.
2. Katzung BG, Kruidering-Hall M, Trevor AJ. Basic & Clinical Pharmacology. 15th ed. New York: McGraw-Hill Education; 2021.
3. Tripathi KD. Essentials of Medical Pharmacology. 8th ed. New Delhi: Jaypee Brothers Medical Publishers; 2018.
4. Ritter JM, Flower RJ, Henderson G, Loke YK, MacEwan DJ, Rang HP, et al. Rang & Dale’s Pharmacology. 9th ed. London: Elsevier; 2019.