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对临床食管炎中胃酸和胃蛋白酶分泌进行的一项带有适当对照的批判性分析。

A critical analysis, with appropriate controls, of gastric acid and pepsin secretion in clinical esophagitis.

作者信息

Hirschowitz B I

机构信息

Division of Gastroenterology, University of Alabama, Birmingham.

出版信息

Gastroenterology. 1991 Nov;101(5):1149-58. doi: 10.1016/0016-5085(91)90062-p.

Abstract

Because esophagitis is a presumed "acid-peptic" disease, fasting gastric contents (volume and acid and pepsin concentrations) and basal and pentagastrin-stimulated acid and pepsin outputs were studied in 155 patients with endoscopically defined (and graded 1-4) esophagitis and 508 control patients without esophagitis. Basal pepsin and maximal acid and pepsin outputs were lower in the patients with esophagitis than in those without esophagitis. In further analysis, the patients were subdivided into three categories, duodenal ulcer, nonulcer with no disease other than esophagitis, and postgastric surgery, because these categories affect gastric secretion independently of esophageal disease and in the rank order given. Each category was subdivided by sex, because men secreted more than women. Within each category there was no systematic difference in fasting, basal, or maximal gastric acid or pepsin secretion between patients with and patients without esophagitis. Severity of esophagitis was not related to any secretion parameters. Hiatal hernia was present in 50% of patients with esophagitis vs. 15% of controls without the condition (P less than 0.01); however, this did not independently influence the gastric secretion findings. Lower esophageal sphincter pressure was also measured in 62 of the patients, 31 with and 31 without esophagitis. Below 10 mm Hg (incompetent sphincter), 9 of 10 patients had esophagitis but accounted for only less than 30% of the patients with esophagitis, whereas none of 11 patients with basal acid output of less than 0.1 mEq/h and lower esophageal sphincter pressure of greater than 10 mm Hg had esophagitis. Because neither the composition of gastric juice nor basal or stimulated gastric acid or pepsin output could be correlated to the presence or severity of esophagitis, factors other than amount or composition of gastric juice per se must be responsible for susceptibility to esophagitis.

摘要

由于食管炎被认为是一种“酸-消化性”疾病,我们对155例经内镜确诊(并分为1-4级)的食管炎患者和508例无食管炎的对照患者进行了空腹胃内容物(容量、酸和胃蛋白酶浓度)以及基础和五肽胃泌素刺激后的酸和胃蛋白酶分泌量的研究。食管炎患者的基础胃蛋白酶以及最大酸和胃蛋白酶分泌量低于无食管炎患者。在进一步分析中,患者被分为三类:十二指肠溃疡、除食管炎外无其他疾病的非溃疡患者以及胃手术后患者,因为这些类别独立于食管疾病影响胃分泌,且按给定顺序排列。每个类别又按性别细分,因为男性分泌量多于女性。在每个类别中,有食管炎和无食管炎的患者在空腹、基础或最大胃酸或胃蛋白酶分泌方面没有系统性差异。食管炎的严重程度与任何分泌参数均无关联。50%的食管炎患者存在食管裂孔疝,而无该疾病的对照患者中这一比例为15%(P<0.01);然而,这并未独立影响胃分泌结果。我们还对62例患者测量了食管下括约肌压力,其中31例有食管炎,31例无食管炎。低于10 mmHg(括约肌功能不全)时,10例患者中有9例患有食管炎,但仅占食管炎患者的不到30%,而基础酸分泌量低于0.1 mEq/h且食管下括约肌压力大于10 mmHg的11例患者中无一例患有食管炎。由于胃液成分、基础或刺激后的胃酸或胃蛋白酶分泌量均与食管炎的存在或严重程度无关,因此除胃液本身的量或成分之外的其他因素必定是导致食管炎易感性的原因。

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