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Gastrointestinal side effects of drugs

2003; Taylor & Francis; Volume: 2; Issue: 4 Linguagem: Inglês

10.1517/14740338.2.4.421

1744-764X

Richard Makins, Anne Ballinger,

Inflammatory mediators and NSAID effects

Drugs can have adverse effects on any part of the gastrointestinal (GI) tract from mouth to colon. It is essential that a detailed and accurate drug history is taken in patients presenting with GI complaints. Many drug-induced effects will regress or heal on cessation of treatment. NSAIDs are usually associated with gastric and duodenal ulcers but are also recognised to cause lichen planus in the mouth, oesophageal inflammation and strictures, and small bowel and colonic ulcers and strictures. A newer class of anti-inflammatory drugs, the cyclooxygenase-2 (COX-2)-selective inhibitors, have been developed and have a more favourable GI safety profile than standard NSAIDs. Acute diarrhoea, relapse of inflammatory bowel disease (IBD), microscopic colitis and acute pancreatitis are also induced by ingestion of standard NSAIDs. The calcium antagonists, phenytoin and cyclosporin, induce gum hyperplasia, particularly in patients with poor oral hygiene. Alendronate, a bisphosphonate, has been associated with development of oesophageal ulcers, and specific recommendations are now given to reduce this complication. Of the many different forms of colitis associated with drug ingestion, the most frequent is pseudomembranous colitis. This is a complication of antibiotics and is caused by the toxin produced by Clostridium difficile. Many drugs have been associated with the development of acute pancreatitis, although a definite cause and effect relationship has been shown for only a few drugs. These include didanosine, furosomide, corticosteroids, azathioprine and sodium valproate.