Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1986:32 Suppl 4:71-89.
doi: 10.2165/00003495-198600324-00007.

Gastrointestinal intolerance and bleeding with non-narcotic analgesics

Review

Gastrointestinal intolerance and bleeding with non-narcotic analgesics

K J Ivey. Drugs. 1986.

Abstract

Aspirin and paracetamol (acetaminophen) are the most commonly used minor analgesics, but their effects on the gastrointestinal tract differ widely. The effects of other nonsteroidal anti-inflammatory drugs (NSAIDs), including phenylbutazone, are intermediate. Aspirin is significantly associated with major upper gastrointestinal haemorrhage, whereas paracetamol is not. Short term use of aspirin produces erythema, erosions and occasionally ulcers; paracetamol does not, while other NSAIDs do so to varying degrees. Chronic gastric ulcer is linked to aspirin intake in patients with rheumatic disease, and epidemiologically in all heavy aspirin users. In only one epidemiological study was a paradoxical significant association reported between paracetamol intake and chronic gastric ulcer. Faecal occult blood loss is increased in most regular aspirin users but not in those taking paracetamol. Although formal studies in children have apparently not been made, in isolated small clinical series it has been reported that gastrointestinal bleeding and anaemia do occur in the paediatric age group after the use of aspirin. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference; paracetamol 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 paracetamol. Aspirin and other NSAIDs cause a dramatic reduction in the ability of gastric mucosa to generate protective prostaglandins; however, paracetamol also reduces prostaglandins. Other postulated mechanisms of aspirin damage include reduction in gastric mucosal secretion, reduction in bicarbonate output, and alteration of cell turnover. Because damage to gastric mucosa by aspirin and NSAIDs is often 'silent', the clinician needs a high level of suspicion and awareness regarding this problem. In patients prone to gastric damage, or in those with a past history of aspirin-induced gastric damage, paracetamol is the drug of choice when a minor, non-inflammatory problem requires an analgesic.

PubMed Disclaimer

Similar articles

Cited by

References

    1. J Clin Invest. 1968 Sep;47(9):2169-80 - PubMed
    1. Gastroenterology. 1969 Mar;56(3):439-49 - PubMed
    1. Am J Med. 1961 Aug;31:259-65 - PubMed
    1. Lancet. 1958 Nov 1;2(7053):925-8 - PubMed
    1. Clin Pharmacol Ther. 1965 Jan-Feb;6:25-30 - PubMed

MeSH terms

Substances

LinkOut - more resources