Tolerance to H2 receptor antagonist correlates well with the decline in efficacy against gastroesophageal reflux in patients with gastroesophageal reflux disease

Background and Aim:  The attenuated antisecretory activity of H2 receptor antagonists (H2RA) during continuous administration is known as the tolerance phenomenon. The authors recently clarified that presence or absence of Helicobacter pylori infection influences the occurrence of the tolerance phenomenon. The aim of this study was to clarify whether tolerance to H2RA is correlated with attenuation of the inhibitory effect against gastroesophageal acid reflux in patients with gastroesophageal reflux disease (GERD).

[1]  Y. Kinoshita,et al.  Helicobacter pylori infection prevents the occurrence of the tolerance phenomenon of histamine H2 receptor antagonists , 2004, Alimentary pharmacology & therapeutics.

[2]  Y. Kinoshita,et al.  Tolerance to famotidine and ranitidine treatment after 14 days of administration in healthy subjects without Helicobacter pylori infection , 2003, Journal of gastroenterology and hepatology.

[3]  Y. Kinoshita,et al.  Influence of lansoprazole, famotidine, roxatidine and rebamipide administration on the urea breath test for the diagnosis of Helicobacter pylori infection , 2003, Journal of gastroenterology and hepatology.

[4]  S. Ishihara,et al.  Influence of Helicobacter pylori infection on the prevalence of reflux esophagitis in Japanese patients , 2001, Journal of gastroenterology and hepatology.

[5]  Y. Kinoshita,et al.  Predominant nocturnal acid reflux in patients with Los Angeles grade C and D reflux esophagitis , 2001, Journal of gastroenterology and hepatology.

[6]  T. Koike,et al.  Helicobacter pylori infection prevents erosive reflux oesophagitis by decreasing gastric acid secretion , 2001, Gut.

[7]  N. Ishimura,et al.  Efficacy of ecabet sodium for Helicobacter pylori eradication triple therapy in comparison with a lansoprazole‐based regimen , 2001, Alimentary pharmacology & therapeutics.

[8]  S. Ishihara,et al.  CYP2C19 genotype status and intragastric pH during dosing with lansoprazole or rabeprazole , 2000, Alimentary pharmacology & therapeutics.

[9]  Y. Kinoshita,et al.  Helicobacter pylori infection influences nocturnal gastric acid breakthrough , 2000, Alimentary pharmacology & therapeutics.

[10]  Smout,et al.  Helicobacter pylori eradication increases nocturnal acid breakthrough , 2000, Alimentary pharmacology & therapeutics.

[11]  Adachi,et al.  Efficacy of sucralfate for Helicobacter pylori eradication triple therapy in comparison with a lansoprazole‐based regimen , 2000, Alimentary pharmacology & therapeutics.

[12]  Jansen,et al.  Standard‐dose lansoprazole is more effective than high‐dose ranitidine in achieving endoscopic healing and symptom relief in patients with moderately severe reflux oesophagitis , 1999, Alimentary pharmacology & therapeutics.

[13]  O. Kawamura,et al.  Helicobacter pylori infection correlates with severity of reflux esophagitis: with manometry findings , 1999, Journal of Gastroenterology.

[14]  P. Malfertheiner,et al.  Gastric Helicobacter pylori infection accelerates healing of reflux esophagitis during treatment with the proton pump inhibitor pantoprazole. , 1999, Gastroenterology.

[15]  J. Hüsler,et al.  Effect of repeated injection and continuous infusion of omeprazole and ranitidine on intragastric pH over 72 hoursFigure 1 , 1999, American Journal of Gastroenterology.

[16]  N. Arebi,et al.  How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology. , 1997, Gastroenterology.

[17]  A. Sandvik,et al.  Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound , 1997, Alimentary pharmacology & therapeutics.

[18]  T. Chiba,et al.  Helicobacter pylori independent chronological change in gastric acid secretion in the Japanese , 1997, Gut.

[19]  F. Halter,et al.  Comparison of acid inhibition by either oral high‐dose ranitidine or omeprazole , 1994, Alimentary pharmacology & therapeutics.

[20]  R. Berlin,et al.  Nocturnal therapy with famotidine for 1 year is effective in preventing relapse of gastric ulcer , 1991, Alimentary pharmacology & therapeutics.

[21]  G. Porro,et al.  A controlled study of 20 mg famotidine nocte vs. 150 mg ranitidine nocte for the prevention of duodenal ulcer relapse , 1991, Alimentary pharmacology & therapeutics.

[22]  J. Dent,et al.  The usefulness of a structured questionnaire in the assessment of symptomatic gastroesophageal reflux disease. , 1998, Scandinavian journal of gastroenterology.

[23]  H. Festen Prevention of duodenal ulcer relapse by long-term treatment with omeprazole. , 1994, Scandinavian journal of gastroenterology. Supplement.

[24]  C. Wilder-Smith,et al.  Loss of acid suppression during dosing with H2-receptor antagonists. , 1990, Alimentary pharmacology & therapeutics.

[25]  R. Pounder,et al.  Tolerance during 8 days of high-dose H2-blockade: placebo-controlled studies of 24-hour acidity and gastrin. , 1990, Alimentary pharmacology & therapeutics.

[26]  R. Pounder,et al.  Tolerance during 29 days of conventional dosing with cimetidine, nizatidine, famotidine or ranitidine. , 1990, Alimentary pharmacology & therapeutics.