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胃黏膜分泌增加可缓解非甾体抗炎药引起的腹痛。

Increased gastric mucus secretion alleviates non-steroidal anti-inflammatory drug-induced abdominal pain.

机构信息

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.

出版信息

Tohoku J Exp Med. 2013 Sep;231(1):29-36. doi: 10.1620/tjem.231.29.

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) can cause dyspeptic symptoms, including abdominal pain. Gastric mucus is important as the first line of defense against luminal irritants. In the present study, we investigated whether gastric mucus secretion could influence the severity of gastric mucosal injuries or NSAID-induced dyspeptic symptoms. Fifteen Helicobacter pylori-negative, healthy males were administered two types of NSAIDs, a non-selective cyclooxygenase inhibitor, naproxen (300 mg, twice a day), or a cyclooxygenase-2-selective inhibitor, etodolac (200 mg, twice a day), for 1 week in a crossover study, with an interval of ≥ 4 weeks. Study participants underwent endoscopic examinations before and after treatment. Pentagastrin-stimulated gastric secretions were collected for 10 min during endoscopic examinations, and were analyzed for gastric acid levels (mEq/10 min) and mucus output (mg hexose/10 min). The grade of gastric mucosal injury was assessed endoscopically. Among 29 subjects who completed the crossover study, 11 individuals reported abdominal pain following the administration of naproxen or etodolac for 1 week, as judged by elevated pain scores, while 18 individuals did not report abdominal pain. The occurrence of symptoms was not associated with the type of NSAIDs administered or the occurrence of erosive injury visualized by endoscopy. Gastric mucus secretion was significantly increased in subjects without drug-induced abdominal pain (P < 0.05), whereas it was significantly reduced in those with drug-induced abdominal pain (P < 0.05). In conclusion, the occurrence of NSAID-induced abdominal pain is associated with reduced levels of gastric mucus secretion rather than the occurrence of endoscopic mucosal injury.

摘要

非甾体抗炎药(NSAIDs)可引起消化不良症状,包括腹痛。胃粘液是防止腔道刺激物的第一道防线,具有重要作用。在本研究中,我们研究了胃粘液分泌是否会影响胃粘膜损伤的严重程度或 NSAID 引起的消化不良症状。15 名 H.pylori 阴性健康男性进行了交叉研究,在 4 周以上的间隔内,分别服用两种 NSAIDs,一种是非选择性环氧化酶抑制剂萘普生(300mg,每日两次),或一种环氧化酶-2 选择性抑制剂依托度酸(200mg,每日两次),持续 1 周。研究参与者在治疗前后进行了内镜检查。在胃镜检查期间,收集 10 分钟的五肽胃泌素刺激胃分泌物,用于分析胃酸水平(mEq/10min)和粘液分泌量(mg 己糖/10min)。根据内镜检查评估胃粘膜损伤的程度。在完成交叉研究的 29 名受试者中,11 名在服用萘普生或依托度酸 1 周后报告腹痛,通过升高的疼痛评分判断,而 18 名没有报告腹痛。症状的发生与给予的 NSAIDs 类型或内镜下可见的侵蚀性损伤无关。在没有药物引起腹痛的受试者中,胃粘液分泌明显增加(P<0.05),而在有药物引起腹痛的受试者中,胃粘液分泌明显减少(P<0.05)。总之,NSAID 引起的腹痛发生与胃粘液分泌减少有关,而不是内镜下粘膜损伤的发生。

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