Effect of acid suppression therapy on development of gastric erosions after cure of Helicobacter pylori infection

2002 ◽  
Vol 16 ◽  
pp. 210-216 ◽  
Author(s):  
K. Miyake ◽  
T. Tsukui ◽  
S. Futagami ◽  
A. Tatsuguchi ◽  
K. Shinoki ◽  
...  
2006 ◽  
Vol 116 (4) ◽  
pp. 547-553 ◽  
Author(s):  
Nobuhiko Oridate ◽  
Hiroshi Takeda ◽  
Junji Yamamoto ◽  
Masahiro Asaka ◽  
Yasushi Mesuda ◽  
...  

2006 ◽  
Vol 57 (3) ◽  
pp. 262-267 ◽  
Author(s):  
Nobuhiko Oridate ◽  
Yasushi Mesuda ◽  
Noriko Nishizawa ◽  
Mika Mori ◽  
Yuji Nakamaru ◽  
...  

2020 ◽  
Vol 13 (10) ◽  
pp. 276
Author(s):  
Muhammad Miftahussurur ◽  
Boby Pratama Putra ◽  
Yoshio Yamaoka

Helicobacter pylori infection is a severe global health problem that is closely associated with acid-related diseases and gastric malignancies. Eradicating H. pylori is strongly recommended for lowering peptic ulcer recurrence and preventing gastric cancer. The current approved H. pylori eradication regimen combines a proton pump inhibitor (PPI) with two antibiotics. Unfortunately, this regimen failed to meet expectations mostly due to antibiotic resistance and insufficient gastric acid suppression. Vonoprazan, a novel potassium-competitive acid blocker, showed promising results as a PPI replacement. Vonoprazan inhibits gastric acid secretion by acting as a reversible competitive inhibitor against potassium ions and forming disulfide bonds with the cysteine molecule of H+/K+-ATPase. Vonoprazan has superior pharmacological characteristics over PPI, such as no requirement for acid activation, stability in acidic conditions, shorter optimum acid suppression period, and resistance to cytochrome P (CYP)2C19 polymorphism. Several comparative randomized controlled trials and meta-analyses revealed the superiority of vonoprazan in eradicating H. pylori, notably the resistant strains. The adverse effect caused by vonoprazan is long-term acid suppression that may induce elevated gastrin serum, hypochlorhydria, and malabsorption. All vonoprazan studies have only been conducted in Japan. Further studies outside Japan are necessary for universally conclusive results.


2013 ◽  
Vol 144 (5) ◽  
pp. S-53 ◽  
Author(s):  
Javier Molina-Infante ◽  
Marco Romano ◽  
Miguel Fernandez Bermejo ◽  
Alessandro Federico ◽  
Antonietta G. Gravina ◽  
...  

2002 ◽  
Vol 16 (9) ◽  
pp. 611-614 ◽  
Author(s):  
Colm A O’Morain ◽  
Asghar Qasim

There are several reasons for eradicating Helicobacter pylori in patients with chronic gastroesophageal reflux disease (GERD). Perhaps the most compelling is the evidence that chronic acid suppression therapy can lead to the development of atrophic gastritis, a premalignant condition, in patients with H pylori infection. Epidemiological data that suggest that H pylori is less prevalent in GERD patients than in control subjects may be susceptible to publication bias, and confounding social and environmental factors may also be involved. Although it has been thought that eradication of the organism might lead to increased esophageal acid exposure, this has not been demonstrated in practice. Studies that appeared to show that GERD could be provoked by antimicrobial therapy of duodenal ulcers also have methodological weaknesses. Underlying GERD symptoms might be unmasked after withdrawal of acid-suppression therapy, for reasons that are unrelated to H pylori. In fact, eradication of the organism has been shown to decrease heartburn in patients with peptic ulcer disease. When H pylori is successfully eradicated in patients with GERD, relapse rates are not increased, and the disease- free interval seems to be prolonged. Eradication of the organism is a wise policy in patients who face long term acid-suppression therapy for GERD.


Sign in / Sign up

Export Citation Format

Share Document