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幽门螺杆菌引起的胃酸分泌变化与上消化道疾病

Helicobacter pylori-Induced Changes in Gastric Acid Secretion and Upper Gastrointestinal Disease.

作者信息

Smolka Adam J, Schubert Mitchell L

机构信息

Department of Medicine, Medical University of South Carolina, Charleston, SC, 29425, USA.

McGuire Veterans Administration Medical Center, Richmond, VA, 23249, USA.

出版信息

Curr Top Microbiol Immunol. 2017;400:227-252. doi: 10.1007/978-3-319-50520-6_10.

DOI:10.1007/978-3-319-50520-6_10
PMID:28124156
Abstract

Appropriate management of Helicobacter pylori infection of the human stomach is evolving and remains a significant clinical challenge. Acute infection results in hypochlorhydria, whereas chronic infection results in either hypo- or hyperchlorhydria, depending upon the anatomic site of infection. Acute hypochlorhydria facilitates survival of the bacterium and its infection of the stomach. Interestingly, most patients chronically infected with H. pylori manifest a pangastritis with reduced acid secretion due to bacterial virulence factors, inflammatory cytokines, and various degrees of gastric atrophy. While these patients are predisposed to develop gastric adenocarcinoma (~1%), there is increasing evidence from population studies that they are also protected from gastroesophageal reflux disease (GERD), Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC). Eradication of H. pylori, in these patients, may provoke GERD in predisposed individuals and may be a contributory factor for the rising incidence of refractory GERD, BE, and EAC observed in Westernized societies. Only ~10% of chronically infected patients, mainly the young, manifest an antral predominant gastritis with increased acid secretion due to a decrease in somatostatin and increase in gastrin secretion; these patients are predisposed to develop peptic ulcer disease. H. pylori-induced changes in acid secretion, in particular hypochlorhydria, may allow ingested microorganisms to survive transit through the stomach and colonize the distal intestine and colon. Such perturbation of gut microbiota, i.e. dysbiosis, may influence human health and disease.

摘要

人类胃部幽门螺杆菌感染的恰当管理方法正在不断演变,仍然是一项重大的临床挑战。急性感染会导致胃酸分泌过少,而慢性感染则会导致胃酸分泌过少或过多,这取决于感染的解剖部位。急性胃酸分泌过少有利于该细菌的存活及其在胃部的感染。有趣的是,大多数长期感染幽门螺杆菌的患者表现为全胃炎,由于细菌毒力因子、炎性细胞因子以及不同程度的胃萎缩,胃酸分泌减少。虽然这些患者易患胃腺癌(约1%),但越来越多的人群研究证据表明,他们也不易患胃食管反流病(GERD)、巴雷特食管(BE)和食管腺癌(EAC)。在这些患者中根除幽门螺杆菌,可能会在易感个体中引发GERD,并且可能是西方化社会中难治性GERD、BE和EAC发病率上升的一个促成因素。只有约10%的长期感染患者,主要是年轻人,表现为胃窦为主型胃炎,由于生长抑素分泌减少和胃泌素分泌增加,胃酸分泌增加;这些患者易患消化性溃疡病。幽门螺杆菌引起的胃酸分泌变化,尤其是胃酸分泌过少,可能会使摄入的微生物在通过胃部时存活下来,并在远端小肠和结肠定植。这种肠道微生物群的扰动,即生态失调,可能会影响人类健康和疾病。

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