Minor effects of Helicobacter pylori on gastric secretion and dose of lansoprazole during long-term treatment in ZE and non-ZE acid hypersecretors
B. I. Hirschowitz,
J. Simmons,
J. Mohnen,
B. I. Hirschowitz
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, Birmingham, AL, USA
Search for more papers by this authorJ. Simmons
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, Birmingham, AL, USA
Search for more papers by this authorJ. Mohnen
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, Birmingham, AL, USA
Search for more papers by this authorB. I. Hirschowitz,
J. Simmons,
J. Mohnen,
B. I. Hirschowitz
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, Birmingham, AL, USA
Search for more papers by this authorJ. Simmons
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, Birmingham, AL, USA
Search for more papers by this authorJ. Mohnen
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, Birmingham, AL, USA
Search for more papers by this author
Dr B. I. Hirschowitz, Division of Gastroenterology, University of Alabama at Birmingham, UAB Station, Birmingham, AL 35294-0007, USA. E-mail: [email protected]
Abstract
Background:
Helicobacter pylori infection may increase or decrease acid secretion and may augment proton pump inhibitor efficacy. Pepsin effects have not been reported. In Zollinger–Ellison syndrome (ZE) specifically, H. pylori has been reported to decrease acid.
Aim:
To examine H. pylori effects on secretion and dose of medication in hypersecretors (basal acid output > 15 mmol/h) undergoing long-term treatment with individually optimized lansoprazole doses.
Methods:
Sixty-five patients (47 ZE and 18 non-ZE), treated for > 3 months to 10 years, were tested every 6 months with endoscopy, gastric analysis and serum gastrin.
Results:
Forty-three per cent were H. pylori-positive. Acid, pepsin and gastrin were not different between H. pylori-positive and H. pylori-negative patients before or during long-term lansoprazole treatment. Initially, H. pylori-positive patients required less lansoprazole than H. pylori-negative patients (68 ± 6 vs. 96 ± 8 mg/day), but after 3 years the doses converged (83 vs. 86 mg/day). The disappearance of H. pylori in 15 patients caused no significant changes in acid, pepsin, gastrin or lansoprazole dose in the following 4 years.
Conclusions:
H. pylori had no significant initial or long-term physiological or potential clinical effects on acid or pepsin secretion or gastrin in these acid hypersecretors.
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