Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria.
Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria.
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发表时间：
1988-09
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通讯作者：
D. Y. Graham;Alpert Lc;Smith Jl;Yoshimura Hh
中科院分区：
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作者：
D. Y. Graham;Alpert Lc;Smith Jl;Yoshimura Hh
在许多情况下，有描述在接受重复胃分泌研究的受试者中出现流行性胃酸缺乏，通常作为研究方案的一部分。我们观察了一名 37 岁健康男性的病例，他每周接受一次胃分析，以及内窥镜检查和胃活检，作为研究胃对阿司匹林适应的研究方案的一部分。在服用阿司匹林的第2周中期，他出现了严重的恶心和上腹不适。停止服用阿司匹林，但按照方案继续进行胃分析、内窥镜检查和活检。与急性发病前一周相比，生化分析显示基础胃酸短暂增加7.4倍，胃蛋白酶分泌增加3.6倍，DNA丢失增加8.8倍，粘液分泌增加5.6倍，胃出血增加12倍。感染第2周期间基础酸分泌为零，胃蛋白酶分泌为对照的三分之一。出现症状时的内窥镜检查显示胃体和胃窦糜烂，以及大量粘膜出血和胃窦急性溃疡。 7天后胃镜检查显示，胃粘膜几乎完全恢复，仅在先前溃疡的部位看到浅层糜烂。服用阿司匹林前和服用阿司匹林前 2 周期间胃活检结果正常。急性疾病时进行的胃活检（与基础酸分泌增加有关）显示胃窦有明显的急性炎症，有许多幽门弯曲杆菌。当时，胃体活检中既没有发现急性炎症，也没有发现幽门螺杆菌。 1周后获得的活组织检查（零基础酸）显示胃体和胃窦均存在急性炎症。一周后，胃体活检显示轻度局灶性急性炎症，中度慢性炎症，偶见淋巴滤泡；胃窦呈慢性炎症。 2年后获得的胃窦活检显示持续性慢性胃炎，伴有明显的淋巴滤泡和散在的急性炎症细胞灶；幽门螺杆菌仍然存在，但不太明显。我们认为，急性（流行性）胃炎综合征通常是医源性幽门螺杆菌感染。我们的病例表明，在幽门螺杆菌感染的急性期，基础酸和胃蛋白酶分泌增加发生在基础酸过少之前。
On a number of occasions, there have been descriptions of epidemic achlorhydria in subjects undergoing repeated gastric secretory studies, typically as part of research protocols. We observed a case in a 37-yr-old healthy man undergoing weekly gastric analyses, along with endoscopy and gastric biopsy, as part of a research protocol studying gastric adaptation to aspirin. In the middle of the 2nd wk of aspirin administration, he developed severe nausea and epigastric discomfort. Aspirin administration was discontinued, but, as per protocol, gastric analyses, endoscopies, and biopsies were continued. Compared to the week preceding the acute illness, biochemical analyses showed a transient 7.4-fold increase in basal gastric acid, 3.6-fold increase in pepsin secretion, 8.8-fold increase in DNA loss, 5.6-fold increase in mucus secretion, and 12-fold increase in gastric bleeding. Basal acid secretion was zero, and pepsin secretion was one-third of control during the 2nd wk of the infection. Endoscopy at the time of symptoms showed erosions in the gastric body and antrum, as well as numerous mucosal hemorrhages and an acute ulcer in the antrum. Endoscopy 7 days later revealed that the gastric mucosa had almost completely recovered, with only a shallow erosion seen at the site of the previous ulcer. Gastric biopsies were normal before and during the first 2 wk of aspirin ingestion. Gastric biopsies taken at the time of the acute illness (associated with increased basal acid secretion) showed marked acute inflammation of the antrum with many Campylobacter pylori bacilli. At that time, neither acute inflammation nor C. pylori were found in biopsies from the body of the stomach. Biopsies obtained 1 wk later (zero basal acid) showed acute inflammation of both the gastric body and antrum. One week later, biopsies from the gastric body showed mild focal acute inflammation, moderate chronic inflammation, and an occasional lymphoid follicle; the gastric antrum showed chronic inflammation. Antral biopsies obtained 2 yr later showed persistent chronic gastritis with prominent lymphoid follicles and scattered foci of acute inflammatory cells; C. pylori bacilli were still present, but were less apparent. We believe that the syndrome of acute (epidemic) gastritis is often iatrogenic C. pylori infection. Our case shows that increased basal acid and pepsin secretion occur before onset of basal acid hypochlorhydria in the acute phase of C. pylori infection.