Drug-induced gastrointestinal disorders

• Autores: Caroline L. Sharratt, Anthony J. Norman, Christopher J. Hawkey
• Localización: Medicine, ISSN-e 1357-3039, Vol. 43, Nº. 4, 2015, págs. 223-229
• Idioma: inglés
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• Resumen

  • Adverse drug effects on the gastrointestinal (GI) tract can occur as a predictable result of a drug's mode of action, by direct injury, through compromising GI defences, or as a consequence of changes in colonic bacterial flora. Non-steroidal anti-inflammatory drugs (NSAIDs) are the most common cause of gastroduodenal injury, owing to inhibition of prostaglandin synthesis, and increase the risk of serious GI complications between twofold and fourfold. Low doses of aspirin are associated with an increased risk of upper GI haemorrhage. COX-2 inhibitors largely spare the GI mucosa from injury. Advancing technology for investigating the small bowel now allows identification of subtle changes to the small bowel mucosa (such as ulceration and erosions) secondary to drugs. This can lead to occult iron deficiency anaemia, hypoalbuminaemia and protein-losing enteropathy. Drug-induced colitis is an important problem, with antibiotics the most common drug cause. Drugs can also exacerbate pre-existing inflammatory bowel disease. Strategies to minimize the adverse GI effects of drugs include drug avoidance or minimization, using lowest doses for the shortest time, selective COX-2 inhibitors for high-GI/low-cardiovascular risk patients, and upper GI mucosal protection by co-prescription of proton pump inhibitors with GI irritants.