Division of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai, Miyagi 980-8574, Japan.
J Gastroenterol. 2012 Feb;47(2):150-8. doi: 10.1007/s00535-011-0478-7. Epub 2011 Oct 27.
Low-dose aspirin is known to cause upper gastrointestinal complications. The mechanism by which the aspirin disrupts gastric mucosal integrity remains to be clarified. In this study we investigated the temporal association of gastric secretory parameters (acid and mucus) with aspirin-induced gastropathy.
In 42 long-term low-dose aspirin-takers and the same number of sex- and age-matched controls, pentagastrin-stimulated gastric juice was collected for 10 min during endoscopic examination. The collected gastric juice was divided and half was submitted to analysis for gastric acid (mEq/10 min) and the other half was analyzed for mucin (mg hexose/10 min) output. The grade of gastric mucosal injury was assessed endoscopically according to the modified Lanza score, and a score of more than 4 was defined as the presence of severe gastropathy.
While gastric acid secretion did not differ significantly between aspirin-takers and controls, gastric mucus secretion, in terms of mucin output, was significantly increased in aspirin-takers compared to controls (4.1 (SD 4.8) vs. 2.3 (1.4) mg hexose/10 min, P < 0.05). Consequently, the acid/mucin ratio was significantly decreased in aspirin-takers compared to controls (1.2 (1.0) vs. 1.7 (1.4), P < 0.05). In the subanalysis of 25 aspirin-takers without severe gastropathy, gastric mucus secretion was increased and the acid/mucus ratio was decreased compared with controls, but there was no such association in the remaining 17 aspirin-takers with severe gastropathy.
Overall, gastric mucus secretion is increased in aspirin-takers, suggesting a functional adaptive response to long-term administration of the drug. However, it is possible that the adaptive response is impaired in some aspirin takers, who might be susceptible to severe upper gastrointestinal complication.
已知小剂量阿司匹林可引起上消化道并发症。但阿司匹林破坏胃黏膜完整性的机制仍需阐明。本研究旨在探讨胃分泌参数（胃酸和黏液）与阿司匹林相关性胃病之间的时间关联。
在 42 例长期低剂量阿司匹林服用者和相同性别及年龄匹配的对照组中，在胃镜检查期间采集 10 分钟的五肽胃泌素刺激胃液。收集的胃液分为两部分，一半用于分析胃酸（mEq/10 分钟），另一半用于分析黏蛋白（mg 己糖/10 分钟）的分泌量。根据改良的 Lanza 评分评估胃黏膜损伤程度，评分>4 定义为严重胃病。
阿司匹林服用者和对照组之间的胃酸分泌无显著差异，但与对照组相比，阿司匹林服用者的胃黏液分泌（以黏蛋白分泌量表示）显著增加（4.1（SD 4.8）vs. 2.3（1.4）mg 己糖/10 分钟，P<0.05）。因此，与对照组相比，阿司匹林服用者的胃酸/黏液比值显著降低（1.2（1.0）vs. 1.7（1.4），P<0.05）。在无严重胃病的 25 例阿司匹林服用者的亚组分析中，与对照组相比，胃黏液分泌增加，胃酸/黏液比值降低，但在其余 17 例有严重胃病的阿司匹林服用者中，未发现这种关联。
总的来说，阿司匹林服用者的胃黏液分泌增加，提示长期服药后的一种功能性适应性反应。然而，在一些阿司匹林服用者中，这种适应性反应可能受损，他们可能更容易发生严重的上消化道并发症。
