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NSAID gastropathy

Etiology: 1) non-steroidal anti inflammatory agents (NSAIDs) 2) risk factors a) history of peptic ulcer b) high-dose NSAID use c) simultaneous use of multiple NSAIDs d) age > 60 years e) concomitant use of glucocorticoids f) anticoagulation g) tobacco use h) alcohol use i) protein malnutrition j) female sex k) concomitant cardiac disease l) concomitant H pylori infection* * controversial Epidemiology: 1) 5-10% of duodenal ulcers 2) 20-40% as gastric ulcers Pathology: -> occult blood loss & iron deficiency anemia Clinical manifestations: 1) dyspepsia a) NOT predictive of NSAID gastropathy b) many patients have no antecedent dyspepsia 2) peptic ulcer disease (20%)* 3) acute upper GI hemorrhage or perforation (1-2%) * 20% of patients taking NSAIDs long-term will have endoscopic evidence of gastric or duodenal ulceration Management: 1) proton-pump inhibitors (standard dose) 1st line [1] a) prevention of peptic ulcers in patients using NSAIDs [3] b) can heal gastric (& probably duodenal) ulcers even while NSAID therapy is continued [2,4,5] c) more effective than H2-receptor antagonists 2) H2-receptor antagonists a) may decrease incidence of duodenal ulcers b) not effective for prevention of gastric ulcers* 3) misoprostol a) 200-400 mg PO QID b) can heal as well as prevent ulcers in most patients taking NSAIDs c) ONLY agent with proven benefit in patients with rheumatoid arthritis 4) treat concurrent H. pylori infection 5) sucralfate of NO benefit [2] 6) stopping NSAID may be indicated 7) a COX-2 inhibitor may be useful 8) if stopping anti-inflammatory agent is not an option, the most effective strategy to prevent recurrence is use of celecoxib plus twice daily proton pump inhibitor [1,5] 9) restarting low-dose aspirin 3-5 days after upper GI bleed reduces 30-day mortality 10-fold in patients with cardiovascular disease, while increasing rebleeding rates only 2-fold [1] * one study found famotidine effective in prevention of both duodenal & gastric ulcers in patients on long-term NSAID therapy

Related

dyspepsia (indigestion) non-steroidal anti-inflammatory agent (NSAID)

General

gastritis adverse drug reaction (ADR)

References

  1. Medical Knowledge Self Assessment Program (MKSAP) 11, 15, 16, 17. American College of Physicians, Philadelphia 1998, 2009, 2012, 2015
  2. UCLA Intensive Course in Geriatric Medicine & Board Review, Marina Del Ray, CA, Sept 12-15, 2001
  3. Scheiman JM et al, Prevention of ulcers by esomeprazole in at-risk patients using non-selective NSAIDs and COX-2 inhibitors Am J Gastroenterol 2006; 1-1:701 PMID: 16494585
  4. Luo J-C et al. Randomised clinical trial: Rabeprazole plus aspirin is not inferior to rabeprazole plus clopidogrel for the healing of aspirin-related peptic ulcer. Aliment Pharmacol Ther 2011 Sep; 34:519 PMID: 21726257
  5. Lanza FL, Chan FK, Quigley EM; Practice Parameters Committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. 2009 Mar;104(3):728-38 PMID: 19240698