Helicobacter Pylori
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 21, 2005; 11(23): 3514-3517
Published online Jun 21, 2005. doi: 10.3748/wjg.v11.i23.3514
Direct measurement of gastric H+/K+-ATPase activities in patients with or without Helicobacter pylori-associated chronic gastritis
Duangporn Thong-Ngam, Pisit Tangkijvanich, Pichet Sampatanukul, Paungpayom Prichakas, Varocha Mahachai, Piyaratana Tosukowong
Duangporn Thong-Ngam, Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Pisit Tangkijvanich, Piyaratana Tosukowong, Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Pichet Sampatanukul, Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Paungpayom Prichakas, Department of Nuclear Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Varocha Mahachai, Department of Medicine, Chulalongkorn University Hospital, Bangkok 10330, Thailand
Author contributions: All authors contributed equally to the work.
Correspondence to: Duangporn Thong-Ngam, Department of Physiology, Chulalongkorn University Hospital, Bangkok 10330, Thailand. d.thong@mailcity.com
Received: December 11, 2003
Revised: December 12, 2003
Accepted: January 29, 2004
Published online: June 21, 2005
Abstract

AIM: The role of Helicobacter pylori (H pylori ) infection in gastric acid secretion of patients with chronic gastritis remains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens.

METHODS: Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured.

RESULTS: The mean gastric H+/K+-ATPase activity in H pylori-positive group (42 patients) was slightly higher than that in H pylori-negative group (29 patients) (169.65±52.9 and 161.38±43.85 nmol Pi/(mg·h), respectively, P = 0.301). After eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03±59.50 and 158.42±38.93 nmol Pi/(mg·h), respectively, P = 0.805). The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92±39.65 pg/mL vs 75.04± 42.57 pg/mL, P = 0.228). The gastrin levels fell significantly after the eradication of H pylori. (Before treatment 87.00±30.78 pg/mL, after treatment 64.73±18.96 pg/mL, P = 0.015).

CONCLUSION: Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.

Keywords: H pylori; Gastric acid secretion; Chronic gastritis