Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Kurume, Fukuoka, Japan; Division of GI Endoscopy, Digestive Disease Center, Kurume University Hospital, Kurume, Fukuoka, Japan.
J Gastroenterol Hepatol. 2013 Sep;28(9):1444-9. doi: 10.1111/jgh.12221.
Bleeding from esophageal and gastric varices is a fatal event in patients with liver cirrhosis and portal hypertension. However, the effects of Helicobacter pylori (H. pylori) infection on esophagogastric variceal bleeding are not known. The present study was aimed to elucidate the role of H. pylori infection in esophagogastric variceal bleeding.
The subjects were 196 cirrhotic patients who were admitted to the Kurume University Hospital to treat their esophagogastric varices consisted of 95 with acute bleeding and 101 with nonbleeding but high risk of bleeding. For the diagnosis of H. pylori infection, a (13) C-urea breath test was used, and serum pepsinogen (PG) I and II levels and the PG I/II ratio were also measured.
Esophagogastric variceal bleeding was seen in 34.9% (n = 30) of the H. pylori-infected patients (n = 86) and in 59.1% (n = 65) of the noninfected patients (n = 110) (P < 0.0007). There was no significant difference in the infection rate between the bleeding sites of the esophagus and the stomach. The serum PG I and II levels and the PG I/II ratio were 65.6 ng/dL, 14.7 ng/dL, and 4.4, respectively, for the bleeding patients (n = 95), and 43.7 ng/dL, 17.7 ng/dL, and 3.1 for the nonbleeding patients (n = 101). Thus, the nonbleeding patients had significantly higher rate of H. pylori infection and lower acid secretion than bleeding patients (0.001). In addition, multivariate logistic regression analysis showed a significant negative association between H. pylori infection and esophagogastric variceal bleeding.
These results suggest that H. pylori infection has a protective effect against esophagogastric variceal bleeding through the induction of gastric mucosal atrophy and concomitant hypoacidity.
食管胃静脉曲张出血是肝硬化和门静脉高压患者的致命事件。然而，幽门螺杆菌（H. pylori）感染对食管胃静脉曲张出血的影响尚不清楚。本研究旨在阐明 H. pylori 感染在食管胃静脉曲张出血中的作用。
研究对象为 196 例因食管胃静脉曲张就诊于久留米大学医院的肝硬化患者，其中 95 例为急性出血，101 例为无出血但高出血风险。采用（13）C-尿素呼气试验诊断 H. pylori 感染，同时检测血清胃蛋白酶原（PG）I 和 II 水平及其比值。
H. pylori 感染患者（n=86）中食管胃静脉曲张出血发生率为 34.9%（n=30），非感染患者（n=110）中出血发生率为 59.1%（n=65）（P<0.0007）。食管和胃出血部位的感染率无显著差异。出血患者（n=95）的血清 PG I 和 II 水平及其比值分别为 65.6ng/dL、14.7ng/dL 和 4.4，非出血患者（n=101）分别为 43.7ng/dL、17.7ng/dL 和 3.1。因此，非出血患者的 H. pylori 感染率显著高于出血患者，胃酸分泌也显著低于出血患者（0.001）。此外，多变量逻辑回归分析显示 H. pylori 感染与食管胃静脉曲张出血呈显著负相关。
这些结果表明，H. pylori 感染通过诱导胃黏膜萎缩和伴随的低酸度对食管胃静脉曲张出血具有保护作用。
