Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) may damage any segment of the digestive tract. However, functional dyspepsia is the most common NSAID-related untoward effect as well as the major reason for discontinuing NSAID therapy. Chronic gastroduodenal ulcer, gastrointestinal bleeding or perforation are by far less frequent. There are well-established predisposing factors to these side effects, including past or active peptic ulcer, gastrointestinal bleeding, aging, and concomitant use of anticoagulants, platelet antiaggregants or systemic corticosteroids. These factors either require to combine an NSAID with a proton pump inhibitor or contraindicate NSAID use. The NSAID type, its dosage and the duration of treatment also influence the risk for developing a peptic ulcer. The relationships between NSAIDs and Helicobacter pylori (Hp) are complex. There is, however, evidence that testing Hp and, if positive, eradicating Hp do not provide any clear benefit in those patients who are already long-term NSAIDs users. Furthermore, it has been reported that NSAIDs may exacerbate chronic inflammatory bowel diseases (CIBD), precipitate their flares, and even induce them. Conversely, some studies suggest that these detrimental effects would not occur with conventional NSAIDs at low doses and short-term use of coxibs. Regarding corticosteroids, their ulcerogenic potential is uncertain, especially when given at low dosages. On the other hand, systemic corticosteroids may cause sigmoid diverticular abscess perforation. In this respect, they are more toxic than NSAIDs.

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