ArticleWorld journal of gastroenterology2005
Direct measurement of gastric H+/K+-ATPase activities in patients with or without Helicobacter pylori-associated chronic gastritis.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Pathogenesis of Helicobacter pylori infection.Clinical microbiology reviews · 2006Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe 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.
methodsEighty-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.
resultsThe 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).
conclusionGastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.
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