Balan K K, Jones A T, Roberts N B, Pearson J P, Critchley M, Jenkins S A
Department of Nuclear Medicine, Royal Liverpool University Hospital, United Kingdom.
Am J Gastroenterol. 1996 Jul;91(7):1400-6.
To investigate the prevalence of Helicobacter pylori infection in 50 cirrhotic patients with biopsy-proven cirrhosis with and without portal hypertensive gastropathy and to study whether or not the effects of H. pylori colonization of the stomach on gastric acid and pepsin secretion, serum gastrin and pepsinogen I levels, gastric mucus, and gastric emptying contributed to the development of portal hypertensive gastropathy in cirrhotics.
All patients underwent an upper GI endoscopy followed by determination of basal and pentagastrin and insulin-stimulated gastric acid and pepsin secretion and serum gastrin and pepsinogen I levels. The gastric biopsies were stained to detect H. pylori infection, portal hypertensive gastropathy, and gastritis. The amount of gastric mucus was estimated by a microanalytical technique. The rate of gastric emptying was assessed by the radionuclide method using a semi-solid meal.
Thirty-three (66%) patients had endoscopic evidence of portal hypertensive gastropathy, 10 with the severe (20%) and 23 with mild form (46%). Twenty (40%) patients had histological evidence of H. pylori infection. Eleven out of 33 (33%) patients with endoscopic portal hypertensive gastropathy had microscopic evidence of H. pylori infection. Eighteen out of 20 (90%) patients with chronic active gastritis had concomitant H. pylori colonization. In contrast, the gastric mucosa was histologically normal in 21 of the 30 patients (70%) not infected with H. pylori. Marked hypochlorhydria and reduced pepsin secretion associated with a tendency to hypergastrinemia were observed in cirrhotic patients colonized with H. pylori compared with those without. However, there was no significant difference in serum pepsinogen I concentrations, the ratio of polymeric to degraded gastric mucus, or the rate of gastric emptying between cirrhotics with and without H. pylori colonization of the stomach. Furthermore, these parameters were not significantly different in patients with portal hypertensive gastropathy with and without H. pylori infection.
These observations suggest that H. pylori infection is unlikely to be involved in the pathogenesis of portal hypertensive gastropathy.
调查50例经活检证实为肝硬化且伴有或不伴有门脉高压性胃病的患者中幽门螺杆菌（Helicobacter pylori，H. pylori）感染的患病率，并研究胃内H. pylori定植对胃酸和胃蛋白酶分泌、血清胃泌素和胃蛋白酶原I水平、胃黏液及胃排空的影响是否会导致肝硬化患者门脉高压性胃病的发生。
所有患者均接受上消化道内镜检查，随后测定基础胃酸分泌量、五肽胃泌素刺激及胰岛素刺激后的胃酸和胃蛋白酶分泌量以及血清胃泌素和胃蛋白酶原I水平。对胃活检组织进行染色以检测H. pylori感染、门脉高压性胃病及胃炎。采用微量分析技术估算胃黏液量。使用放射性核素法，通过进食半固体餐评估胃排空率。
33例（66%）患者有门脉高压性胃病的内镜证据，其中10例为重度（20%），23例为轻度（46%）。20例（40%）患者有H. pylori感染的组织学证据。33例有内镜门脉高压性胃病的患者中，11例（33%）有H. pylori感染的微观证据。20例慢性活动性胃炎患者中，18例（90%）伴有H. pylori定植。相比之下，30例未感染H. pylori的患者中，21例（70%）胃黏膜组织学正常。与未感染H. pylori的肝硬化患者相比，感染H. pylori的肝硬化患者出现明显胃酸过少及胃蛋白酶分泌减少，并伴有高胃泌素血症倾向。然而，胃内有或无H. pylori定植的肝硬化患者血清胃蛋白酶原I浓度、聚合型与降解型胃黏液的比例或胃排空率均无显著差异。此外，有或无H. pylori感染的门脉高压性胃病患者的这些参数也无显著差异。
这些观察结果表明，H. pylori感染不太可能参与门脉高压性胃病的发病机制。
