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非麻醉性镇痛药引起的胃肠道不耐受和出血。

Gastrointestinal intolerance and bleeding with non-narcotic analgesics.

作者信息

Ivey K J

出版信息

Drugs. 1986;32 Suppl 4:71-89. doi: 10.2165/00003495-198600324-00007.

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.

摘要

阿司匹林和对乙酰氨基酚是最常用的轻度镇痛药,但它们对胃肠道的影响差异很大。其他非甾体抗炎药(NSAIDs),包括保泰松,其影响介于两者之间。阿司匹林与严重上消化道出血显著相关,而对乙酰氨基酚则不然。短期使用阿司匹林会导致红斑、糜烂,偶尔还会引发溃疡;对乙酰氨基酚则不会,而其他非甾体抗炎药会有不同程度的影响。在患有风湿性疾病的患者中,慢性胃溃疡与服用阿司匹林有关,在所有大量服用阿司匹林的人群中,从流行病学角度来看也是如此。仅有一项流行病学研究报道了对乙酰氨基酚摄入量与慢性胃溃疡之间存在矛盾的显著关联。大多数经常服用阿司匹林的人粪便潜血增加,但服用对乙酰氨基酚的人则不会。虽然显然没有对儿童进行正式研究,但在一些孤立的小型临床系列报道中,儿童在使用阿司匹林后确实会出现胃肠道出血和贫血。从病理生理学角度来看,阿司匹林会改变胃黏膜对氢离子的屏障,降低胃电位差;对乙酰氨基酚对这些参数没有影响。这种变化在超微结构上与使用阿司匹林后表面上皮细胞的损伤和微糜烂相关,但与使用对乙酰氨基酚后无关。阿司匹林和其他非甾体抗炎药会使胃黏膜产生保护性前列腺素的能力大幅降低;然而,对乙酰氨基酚也会减少前列腺素的生成。阿司匹林损伤的其他假定机制包括胃黏膜分泌减少、碳酸氢盐分泌减少以及细胞更新改变。由于阿司匹林和非甾体抗炎药对胃黏膜的损伤通常是“无症状的”,临床医生需要对这个问题有高度的怀疑和认识。对于容易出现胃损伤的患者,或有阿司匹林引起胃损伤病史的患者,当一个轻微的非炎症性问题需要使用镇痛药时,对乙酰氨基酚是首选药物。

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