The prevalence of Helicobacter Pylori infection and the status of gastric acid secretion in patients with Barrett's esophagus in Japan
The prevalence of Helicobacter Pylori infection and the status of gastric acid secretion in patients with Barrett's esophagus in Japan
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DOI：
10.1111/j.1572-0241.2004.30313.x
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发表时间：
2004-07-01
影响因子：
9.8
通讯作者：
Shimosegawa, T
中科院分区：
文献类型：
--
作者：
Abe, Y;Ohara, S;Shimosegawa, T
结论：进入食管的反流液的酸度是胃食管反流病发病的关键因素。幽门螺杆菌（H. pylori）感染可影响胃酸分泌。我们报道了H.幽门螺杆菌感染通过减少日本患者的胃酸分泌来预防反流性食管炎，但这种微生物在Barrett食管中的作用尚不清楚。本研究的目的是调查H。pylori感染和胃酸分泌在日本患者的反流性食管炎与或不Barrett食管。方法：我们纳入了112例反流性食管炎患者进行了检查的H。pylori和胃酸分泌。根据Barrett食管的存在与否，将他们分为三组：无Barrett食管的反流性食管炎组（仅反流性食管炎）（80例患者）;短节段Barrett食管组（16例患者）;长节段Barrett食管组（LSBE）（16例患者）。年龄和性别匹配的对照组也被分配到80例反流性食管炎患者。H.通过组织学、快速尿素酶试验和血清IgG抗体确定幽门螺杆菌感染。采用内镜下胃泌素试验（EGT）评价胃酸分泌情况。反流性食管炎组pylori感染率（24.1%）显著低于对照组（71.2%）（比值比0.13，95%可信区间0.07-0.24; p < 0.0001）。H. Barrett食管组pylori感染率明显低于单纯反流性食管炎组（单纯反流性食管炎组：30.0%，SSBE组; 18.7%，LSBE组; 0%），尤其是LSBE组与单纯反流性食管炎组相比有显著性差异（P < 0.01）。各反流性食管炎患者组的EGT值显著高于对照组。Barrett食管患者的EGT值有高于单纯反流性食管炎患者的趋势，但差异无统计学意义。在H.在幽门螺杆菌阴性的受试者中，对照受试者与单纯反流性食管炎患者之间的EGT值无差异，但Barrett食管患者的EGT值显著高于对照受试者（p < 0.05）。另一方面，在H.幽门螺杆菌阳性者中，单纯反流性食管炎患者的EGT值显著高于对照组（p < 0.01）。pylori感染可能在Barrett食管的发展中起保护作用，特别是在日本LSBE的发展中。胃酸分泌过多除了与H.幽门感染
OBJECTIVES: The acidity of the refluxate into the esophagus is a key factor for the pathogenesis of gastroesophageal reflux disease. Helicobacter pylori (H. pylori) infection can influence gastric acid secretion. We have reported that H. pylori infection prevents reflux esophagitis by decreasing gastric acid secretion in Japanese patients, but the role of this organism in Barrett's esophagus is unclear. The aim of this study was to investigate the prevalence of H. pylori infection and gastric acid secretion in Japanese patients with reflux esophagitis with or without Barrett's esophagus.METHODS: We enrolled 112 reflux esophagitis patients who were examined for the status of H. pylori and acid secretion in this study. They were divided into three groups, according to the presence or absence of Barrett's esophagus as follows: reflux esophagitis group without Barrett's esophagus (reflux esophagitis alone) (80 patients); short-segment Barrett's esophagus group (16 patients); and long-segment Barrett's esophagus group (LSBE) (16 patients). Age- and sex-matched control subjects were also assigned to the 80 patients with reflux esophagitis alone. The prevalence of H. pylori infection was determined by histology, rapid urease tests, and serum IgG antibodies. Gastric acid secretion was evaluated by the endoscopic gastrin test (EGT).RESULTS: The overall prevalence of H. pylori infection in the reflux esophagitis patient group (24.1%) was significantly lower than the control group (71.2%) (odds ratio 0.13, 95% confidence interval 0.07-0.24; p < 0.0001). The prevalence of H. pylori infection in the patients with Barrett's esophagus tended to be lower than that in the patients with reflux esophagitis alone (reflux esophagitis alone; 30.0%, SSBE; 18.7%, LSBE; 0%), especially in the patients with LSBE compared with the reflux esophagitis alone group (p < 0.01). The EGT value of the respective reflux esophagitis patient group was significantly higher than the control group. The EGT value in the patients with Barrett's esophagus tended to be higher than that in the patients with reflux esophagitis alone, but the difference was not statistically significant. When examined in H. pylori-negative subjects, no difference was found in the EGT value between the control subjects and the patients with reflux esophagitis alone, but it was significantly higher in patients with Barrett's esophagus than the control subjects (p < 0.05). On the other hand, when examined in the H. pylori-positive subjects, the EGT value was significantly higher in the patients with reflux esophagitis alone than in the control subjects (p < 0.01).CONCLUSIONS: H. pylori infection may play a protective role in the development of Barrett's esophagus, especially in the development of LSBE in Japan. Gastric acid hypersecretion may be concerned with the development of Barrett's esophagus in addition to the absence of H. pylori infection.