Gastrointestinal effects of antipyretic analgesics

Abstract

Aspirin and paracetamol (acetaminophen) are the most commonly used minor analgesics, but their effects on the gastrointestinal tract differ widely. Aspirin is significantly associated with major upper gastrointestinal hemorrhage, whereas acetaminophen is not. Short-term use of aspirin produces erythema, erosions, and occasionally ulcers; acetaminophen use does not. Chronic gastric ulcer is linked to aspirin intake in patients with rheumatic disease, and epidemiologically in all heavy aspirin users; paradoxically, in only one epidemiologic study was a significant association found between acetaminophen intake and chronic gastric ulcer. Fecal occult blood loss is increased in most regular aspirin users but not in those taking acetaminophen. Although studies in children have not apparently been made, in isolated small clinical series it has been shown that gastrointestinal bleeding and anemia do occur in the pediatric age group following the use of aspirin. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference; acetaminophen has no effect on these parameters. Such changes correlate ultrastructurally with damage in surface epithelial cells and microerosions after the use of aspirin, but not after the use of acetaminophen. Aspirin causes a dramatic reduction in the ability of gastric mucosa to generate protective prostaglandins; however, acetaminophen also reduces prostaglandins. Other postulated mechanisms of aspirin damage include reduction in gastric mucosal secretion, bicarbonate output, and alteration of cell turnover. Because aspirin damage to gastric mucosa is often "silent," the clinician needs a high level of suspicion and awareness. In patients prone to gastric damage, or in those with a past history of aspirin-induced gastric damage, acetaminophen is the drug of choice when a minor, noninflammatory problem requires an analgesic.