Therapy of NSAIDs-induced gastropathy.

R La Corte, M Caselli, M Ruina, G Bajocchi, V Alvisi, F Trotta
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Abstract

NSAID-induced gastropathy is the most frequent side effect due to NSAID use. The resulting clinical event is usually of little significance and only in a small percentage of cases results in serious side effects. Nevertheless, the large worldwide use of NSAIDs makes, even a rare side effect, numerically consistent. The pathogenesis of NSAID-induced gastropathy is related to two main mechanisms: an initial topical effect which is pH dependent and a systemic effect which is, more slowly developing, and mainly correlated to the inhibition of prostaglandin synthesis. The therapy of NSAID-gastropathy is almost completely identified with the therapy of NSAID ulceration because of its frequent relation to the development of potentially serious complications. In the case of symptomatic ulcer development the first therapeutic step is NSAID suspension and, in such a case all "antiulcer" drugs are efficient. When the NSAID can not be discontinued, omeprazole seems to be the most efficient drug; H2 blockers can promote ulcer healing but at a slower rate; sucralfate shows an efficacy similar to H2 blockers; misoprostol is useful in the prevention of NSAID-gastropathy. However, it is not so efficient in the treatment of established lesions and shows poor efficacy in the reduction of dyspeptic symptoms. For each one of these drugs it is necessary to obtain further data.

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非甾体抗炎药诱发胃病的治疗。
非甾体抗炎药引起的胃病是使用非甾体抗炎药最常见的副作用。由此产生的临床事件通常意义不大,只有一小部分病例会导致严重的副作用。尽管如此,非甾体抗炎药在世界范围内的大量使用使得即使是罕见的副作用,在数字上也是一致的。非甾体抗炎药诱发胃病的发病机制主要有两种机制:一种是依赖于pH值的初始局部效应,另一种是发展较慢的全身效应,主要与抑制前列腺素合成有关。非甾体抗炎药-胃病的治疗几乎完全等同于非甾体抗炎药溃疡的治疗,因为它经常与潜在严重并发症的发展有关。在症状性溃疡发展的情况下,第一步治疗是停用非甾体抗炎药,在这种情况下,所有“抗溃疡”药物都是有效的。当非甾体抗炎药不能停药时,奥美拉唑似乎是最有效的药物;H2阻滞剂能促进溃疡愈合,但速度较慢;硫糖铝表现出与H2阻滞剂相似的疗效;米索前列醇在预防非甾体抗炎药胃病方面是有用的。然而,它在治疗已建立的病变方面效果不佳,在减轻消化不良症状方面效果不佳。对于每一种药物,都需要获得进一步的数据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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NSAID gastropathy: state of the art. Epidemiological aspects of NSAID gastropathy. Therapy of NSAIDs-induced gastropathy. Endoscopic aspects of gastroduodenal mucosa due to NSAIDs. Histopathological aspects of mucosal injury related to non-steroidal anti-inflammatory drugs.
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