Treatment Guideline Chart
Peptic ulcer disease is the presence of ulceration in the stomach and proximal duodenum commonly and in the lower esophagus, distal duodenum or jejunum infrequently. It is characterized by mucosal damage secondary to pepsin and gastric acid secretion.
It is the principal cause of upper gastrointestinal hemorrhage.
Appropriate therapy depends on the cause of peptic ulcer disease.

Peptic%20ulcer%20disease Treatment

Principles of Therapy

  • The most appropriate therapy for peptic ulcer disease (PUD) depends on the cause
  • Treatment of both gastric and duodenal ulcers involves suppression of acid secretion, eradication of H pylori (if present) and avoidance of nonsteroidal anti-inflammatory drugs (NSAIDs)
    • Antisecretory therapy speeds up the healing process and allows faster relief of symptoms
    • Eradication of H pylori in high-risk patients has been shown to greatly lower the risk of subsequent ulceration and prevent recurrent bleeding in patients with bleeding peptic ulcer
  • It is important to suppress nocturnal acid secretion in patients with duodenal ulcers
  • Maintenance antisecretory therapy may be recommended in patients at high risk for ulceration (ie history of ulcer complications, have frequent recurrences) and for H pylori infection unresponsive to repeat treatment



  • Neutralize gastric acid and lower pepsin activity
  • Effective in relieving symptoms of PUD, promoting healing of ulcers and reducing recurrence
  • Used only for short-term relief of symptoms
  • May be absorbable (eg Sodium bicarbonate, Calcium bicarbonate) or non-absorbable (eg Aluminum or Magnesium hydroxide)
    • Absorbable antacids may provide fast and complete neutralization but may cause alkalosis and should be used only for 1-2 days
    • Non-absorbable antacids are preferred due to lesser systemic side effects

Bismuth subcitrate 

  • Has high affinity for damaged tissue
  • Coats the base of the ulcer crater that provides protection against gastric acid, pepsin and bile
  • Treatment efficacy is comparable with histamine2-receptor antagonists (H2RAs) and other ulcer healing agents

Histamine2-Receptor Antagonists (H2RAs) 

  • Eg Cimetidine, Famotidine, Lafutidine, Nizatidine, Ranitidine, Roxatidine
  • Decrease gastric secretion by blocking histamine action at the H2-receptors in the parietal cells of the stomach
  • All H2RAs are equally effective in healing duodenal ulcers
    • Healing rates were 70-80% after 4 weeks of therapy and 87-95% after 8 weeks
  • Double doses of H2RAs are effective in decreasing the risk of NSAID-induced gastric ulcer
    • H2RAs given with NSAIDs may be a cost-effective way of preventing ulcer bleeding secondary to NSAID use; however, no clinical data is available that proves that this strategy prevents ulcer complication
    • No study has evaluated the efficacy of H2RAs in chronic NSAID users
    • Less effective than proton pump inhibitors (PPIs)
  • H2RAs are generally well tolerated but can cause mild central nervous system effects due to their ability to cross the blood-brain barrier and react with central nervous system (CNS) histamine receptors
    • Cimetidine and Ranitidine both interact with hepatic cytochrome P-450 mixed oxidase system, hence can alter the metabolism of different drugs

Potassium-Competitive Acid Blockers (PCABs) 

  • Eg Revaprazan, Vonoprazan
  • Reversibly inhibit the activity of H+/K+-ATPase by competing for potassium on the luminal side of the parietal cell
  • Full effect is achieved with the first dose due to its rapid onset of action and with similar effect seen on repeated doses
  • Similar efficacy in terms of ulcer healing and prevention of NSAID-induced ulcers and comparable safety profile to PPIs
  • Studies have shown that Vonoprazan may also be effective for the eradication of H pylori in combination with antibiotics

Prostaglandin Analogues

  • Eg Misoprostol
  • Protect the gastroduodenal mucosa by promoting the secretion of bicarbonate and mucus, and by augmenting mucosal blood flow and cell restoration in the gastric mucosa
  • Also has antisecretory effect when given in high doses
    • Useful in healing ulcers and preventing ulcer recurrence
  • Primarily recommended for prevention of NSAID-induced gastroduodenal ulceration
  • Needs frequent dosing and associated with more side effects than H2RAs, hence, generally not used for the treatment of PUD
  • Major drawback is the incidence of diarrhea and its abortifacient property, hence, not for use by pregnant women and women of childbearing age

Proton Pump Inhibitors (PPIs) 

  • Eg Esomeprazole, Lansoprazole, Omeprazole, Pantoprazole, Rabeprazole
  • Most potent inhibitor of gastric acid secretion
  • Irreversibly inhibit the activity of H+/K+-ATPase pump of the gastric parietal cells
  • Have similar safety profile as with H2RAs but PPIs heal peptic ulcers faster than H2RAs
    • Has 80-100% healing rate after 4 weeks of therapy in patients with duodenal ulcer and 8 weeks for patients with gastric ulcer
    • Co-medication with PPIs is better than with H2RAs in preventing an ulcer bleed in patients on antiplatelet therapy
  • Extensively used in combination with NSAIDs to prevent NSAID-induced peptic ulcer
    • Associated with significant risk reduction for upper GI bleeding in patient who uses NSAIDs
    • Main agent for prophylaxis and treatment of NSAID-related upper GI injury
  • Recent studies suggest that PPIs in combination with COX-2 inhibitors is associated with the highest risk reduction for recurrent complication of ulcer
  • In high-risk patients with a non-variceal peptic ulcer bleed, high-dose intravenous (IV) or oral PPIs may be given after endoscopic hemostasis is achieved to decrease rebleeding and possible need for surgery
    • Oral PPIs are recommended to be given for 6-8 weeks after endoscopic treatment of bleeding peptic ulcer for mucosal healing
  • May also be used in patients with gastric outlet obstruction to heal any active ulcers


  • Has been used to treat PUD and has healing rates same as with antacids and H2RAs
  • Protects the gastroduodenal mucosa by adhering to the base of the ulcer, adsorbing bile acids, inactivating pepsin, and stimulating bicarbonate and mucus secretion; however, has no effect on gastric acid secretion
  • May also be used in preventing duodenal ulcer relapse
  • Has an excellent safety profile and is generally well tolerated
  • Treatment duration for PUD is 4 weeks
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