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甲硝唑可减轻非甾体抗炎药所致肠病中的肠道炎症和失血。

Metronidazole reduces intestinal inflammation and blood loss in non-steroidal anti-inflammatory drug induced enteropathy.

作者信息

Bjarnason I, Hayllar J, Smethurst P, Price A, Gumpel M J

机构信息

Division of Clinical Biochemistry, King's College School of Medicine, London.

出版信息

Gut. 1992 Sep;33(9):1204-8. doi: 10.1136/gut.33.9.1204.

Abstract

This study assessed the effect of metronidazole on the gastroduodenal mucosa, intestinal permeability, blood loss, and inflammation in patients on non-steroidal anti-inflammatory drugs (NSAIDs). Thirteen patients were studied before and after 2-12 weeks' treatment with metronidazole 800 mg/day, while maintaining an unchanged NSAID intake. Intestinal inflammation, as assessed by the faecal excretion of indium-111 labelled neutrophils, and blood loss, assessed with chromium-51 labelled red cells, were significantly reduced after treatment (mean (SD) 111In excretion 4.7 (4.7)% v 1.5 (1.3)% (N < 1.0%), p < 0.001, 51Cr red cells loss 2.6 (1.6) ml/day v 0.9 (0.5) ml/day (N < 1.0 ml/day), p < 0.01). Intestinal permeability assessed as the 5 hour urinary excretion ratio of 51CrEDTA/L-rhamnose did not change significantly (0.133 (0.046) v 0.154 (0.064), p > 0.1) and there were no significant changes in the endoscopic or microscopic appearances of the gastroduodenal mucosa. These results suggest that the neutrophil is the main damaging effector cell in NSAID induced enteropathy. The main neutrophil chemo-attractant in this enteropathy may be a metronidazole sensitive microbe.

摘要

本研究评估了甲硝唑对使用非甾体抗炎药(NSAIDs)患者的胃十二指肠黏膜、肠道通透性、失血及炎症的影响。13例患者在维持NSAIDs摄入量不变的情况下,接受每日800mg甲硝唑治疗2 - 12周,分别于治疗前后进行研究。治疗后,通过铟 - 111标记中性粒细胞的粪便排泄评估的肠道炎症以及用铬 - 51标记红细胞评估的失血情况均显著降低(平均(标准差)铟 - 111排泄量4.7(4.7)%对1.5(1.3)%(N < 1.0%),p < 0.001;铬 - 51红细胞损失量2.6(1.6)ml/天对0.9(0.5)ml/天(N < 1.0 ml/天),p < 0.01)。以51CrEDTA/L - 鼠李糖5小时尿排泄率评估的肠道通透性无显著变化(0.133(0.046)对0.154(0.064),p > 0.1),胃十二指肠黏膜的内镜及显微镜下表现也无显著改变。这些结果表明,中性粒细胞是NSAID诱导的肠病中的主要损伤效应细胞。该肠病中主要的中性粒细胞趋化因子可能是一种对甲硝唑敏感的微生物。

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