A 48-year-old woman with a history of NSAID use for chronic arthritis develops a duodenal ulcer. She is H. pylori-negative. What is the drug of choice for long-term management of this NSAID-induced peptic ulcer?

Explanation

## NSAID-Induced Peptic Ulcer Management **Key Point:** Proton pump inhibitors (PPIs) are the drug of choice for both healing and long-term prevention of NSAID-induced peptic ulcers. ### Pathophysiology of NSAID-Induced Ulcers 1. NSAIDs inhibit COX-1 and COX-2 enzymes 2. Reduced prostaglandin synthesis → decreased gastric mucus and bicarbonate secretion 3. Increased gastric acid exposure → ulcer formation 4. Risk is dose- and duration-dependent ### PPI as First-Line Therapy **High-Yield:** Omeprazole (or other PPIs: lansoprazole, pantoprazole) is superior to H₂-receptor antagonists for: - **Healing:** >90% ulcer healing at 4–8 weeks - **Prevention:** Reduces recurrence risk to <5% even with continued NSAID use - **Mechanism:** Profound acid suppression (pH >4) allows mucosal healing ### Dosing for NSAID-Induced Ulcer | Indication | Dose | Duration | |-----------|------|----------| | Acute healing | Omeprazole 20 mg OD | 4–8 weeks | | Long-term prophylaxis (if NSAID must continue) | Omeprazole 20 mg OD | Indefinite | **Clinical Pearl:** If the patient must continue NSAIDs (e.g., for severe arthritis), PPI prophylaxis is mandatory to prevent recurrence. Consider switching to a selective COX-2 inhibitor (celecoxib) + PPI if available. **Mnemonic:** **PUMP** = **P**roton pump inhibitor is **U**niversal for **M**anagement of **P**eptic ulcers (NSAID-induced) **Warning:** H₂-receptor antagonists (ranitidine, famotidine) are less effective for NSAID-induced ulcers than for H. pylori-associated ulcers. Sucralfate and antacids are adjunctive only and insufficient as monotherapy. [cite:Harrison 21e Ch 297]