A CRITICAL ANALYSIS, WITH APPROPRIATE CONTROLS, OF GASTRIC-ACID AND PEPSIN-SECRETION IN CLINICAL ESOPHAGITIS
A CRITICAL ANALYSIS, WITH APPROPRIATE CONTROLS, OF GASTRIC-ACID AND PEPSIN-SECRETION IN CLINICAL ESOPHAGITIS
复制标题
DOI：
10.1016/0016-5085(91)90062-p
复制
发表时间：
1991-11-01
期刊：
影响因子：
29.4
通讯作者：
HIRSCHOWITZ, BI
中科院分区：
文献类型：
--
作者：
HIRSCHOWITZ, BI
由于食管炎是一种假定的“酸消化性”疾病，因此在155例经内镜检查确诊（1-4级）的食管炎患者和508例无食管炎的对照患者中研究了空腹胃内容物（体积、酸和胃蛋白酶浓度）以及基础和五肽胃泌素刺激的酸和胃蛋白酶排出量。食管炎患者的基础胃蛋白酶、最大胃酸和胃蛋白酶排出量低于无食管炎患者。在进一步的分析中，患者被细分为三个类别，十二指肠溃疡，非溃疡性食管炎以外的疾病，和胃手术后，因为这些类别影响胃分泌独立于食管疾病和给定的排名顺序。每个类别都按性别细分，因为男性比女性分泌更多。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物参数无关。食管裂孔疝在50%的食管炎患者中存在，而在无食管炎的对照组中为15%（P< 0.01）;然而，这并不独立影响胃液分泌结果。还测量了62例患者的下食管括约肌压力，其中31例有食管炎，31例无食管炎。低于10 mm Hg（括约肌功能不全），10例患者中有9例发生食管炎，但仅占食管炎患者的<30%，而11例基础酸排出量<0.1 mEq/h和下食管括约肌压力>10 mm Hg的患者中无一例发生食管炎。由于胃液成分、基础胃酸或刺激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，因此胃液量或成分本身以外的因素必须对食管炎的易感性负责。
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< 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 <30% of the patients with esophagitis, whereas none of 11 patients with basal acid output of <0.1 mEq/h and lower esophageal sphincter pressure of >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.