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Aspirin inhibits cyclooxygenase (COX) enzymes, blocking prostaglandin synthesis. Prostaglandins normally protect the gastric mucosa by stimulating mucus and bicarbonate secretion, maintaining blood flow, and regulating acid production. This inhibition leads to reduced mucosal defenses, making the stomach lining vulnerable to acid and pepsin erosion.[1][2]
Acute: Erosions visible in 1-24 hours post-dose. Subacute (1-7 days): Ulcers and bleeding emerge. Chronic (>1 month): Risk of perforation or strictures rises 2-4 fold.[4][7]
Upper endoscopy confirms changes (e.g., Lanza score rates erosion severity). Fecal occult blood tests detect subclinical bleeding in 10-20% of users.[3]
Damage often heals within 1-2 weeks after stopping, but chronic use risks persistent ulcers. Proton pump inhibitors (PPIs) like omeprazole reduce risk by 70-90% by suppressing acid. Misoprostol or enteric-coated formulations offer partial protection.[7][9] Sources [1] PubMed: Aspirin and gastric mucosa [2] Nature Reviews: NSAID gastropathy [3] NEJM: Aspirin-induced gastric injury [4] Gastroenterology: Endoscopic findings [5] Lancet: Low-dose aspirin risks [6] Pharmacology Reviews: COX inhibition [7] Annals of Internal Medicine: Prevention strategies [8] American Journal of Gastroenterology: Risk factors [9] Cochrane: PPI co-therapy
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