Hitomi Ichikawa

Potent acid inhibition by vonoprazan in comparison with esomeprazole, with reference to CYP2C19 genotype.

Acid inhibitory effects of proton pump inhibitors (PPIs) are influenced by CYP2C19 genotype. In contrast, the potent acid inhibition of vonoprazan is not influenced by CYP2C19 genotype.

Twice‐daily dosing of esomeprazole effectively inhibits acid secretion in CYP2C19 rapid metabolisers compared with twice‐daily omeprazole, rabeprazole or lansoprazole

Twice‐daily dosing of proton pump inhibitors (PPIs) is used to treat Helicobacter pylori or acid‐related diseases, such as gastro‐oesophageal reflux disease (GERD) refractory to standard dose of a PPI. Genetic polymorphisms of CYP2C19 are involved to different extents in the metabolism of four kinds of PPIs (omeprazole, lansoprazole, rabeprazole and esomeprazole) available in Japan.

Efficacy of Tailored Helicobacter pylori Eradication Treatment Based on Clarithromycin Susceptibility and Maintenance of Acid Secretion

Insufficient acid inhibition during Helicobacter pylori eradication treatment and bacterial resistance to antibiotics often causes eradication failure. Four times daily dosing (q.i.d.) of a proton‐pump inhibitor (PPI) achieves potent acid inhibition, suggesting its potential usefulness as a regimen for eradicating H. pylori infection. Therefore, a tailored eradication regimen based on antibiotic susceptibility and maintenance of acid inhibition should have a high success rate. We investigated the efficacy of such treatment based on clarithromycin (CAM) susceptibility.

Sitafloxacin-based third-line rescue regimens for Helicobacter pylori infection in Japan.

Quinolone‐based regimens have been used as the rescue for eradication of Helicobacter pylori. Sitafloxacin is known to have low minimum inhibitory concentration for H. pylori. Here, we compared two sitafloxacin‐based eradication regimens as rescue for the eradication of H. pylori.

Rabeprazole 10 mg q.d.s. decreases 24‐h intragastric acidity significantly more than rabeprazole 20 mg b.d. or 40 mg o.m., overcoming CYP2C19 genotype

Standard dosing (i.e. once daily) of proton pump inhibitors (PPIs) cannot inhibit acid secretion for a full 24 h. Better therapeutic regimens using PPIs are required to sustain potent acid inhibition for the full 24 h in all patients with acid‐related diseases.

High Helicobacter pylori cure rate with sitafloxacin-based triple therapy.

Bacterial resistance of Helicobacter pylori to antibiotics is increasing and it often leads to failure of antibiotic treatment. A new sitafloxacin‐based triple therapy was developed to counter this situation; the fluoroquinolone sitafloxacin has a low minimum inhibitory concentration for H. pylori.

Rapid metabolizer genotype of CYP2C19 is a risk factor of being refractory to proton pump inhibitor therapy for reflux esophagitis.

Proton pump inhibitors (PPIs) are mainly metabolized by cytochrome P450 2C19 (CYP2C19) and used as the first‐line therapy for gastroesophageal reflux disease (GERD). However, while several studies have examined the influence of CYP2C19 polymorphism on GERD treatment with PPIs, most have had small sample sizes and were conducted in a single center. Here, we used meta‐analysis to investigate whether or not the CYP2C19 rapid metabolizer (RM) genotype is a risk factor for GERD patients being refractory to PPI therapy.

Effect of dosing schemes of amoxicillin on eradication rates of Helicobacter pylori with amoxicillin-based triple therapy

In standard regimens for Helicobacter pylori infection, amoxicillin is dosed twice daily, although the bactericidal effect of amoxicillin depends on the %time‐above‐MIC. We aimed to examine whether dosing schemes of amoxicillin influenced eradication rates of amoxicillin‐based regimens.

Gastroesophageal Reflux Disease in Time Covering Eradication for All Patients Infected with Helicobacter pylori in Japan.

Background: The prevalence of gastroesophageal reflux disease (GERD) has increased in Japan since the end of the 20th century due to changes in environmental factors, such as a decreased infection rate of Helicobacter pylori and increased ability of acid secretion in the Japanese population. In 2013, the Japanese health insurance system started to cover eradication treatment for all patients infected with H. pylori to prevent gastric cancer, suggesting we may soon be able to completely eradicate this infection in Japan. Re-clarification of the clinical characteristics of GERD in Japan is therefore required in time covering the eradication for all patients infected with H. pylori. Summary: In Japan, more than half of GERD patients exhibit non-erosive reflux disease, and a majority of erosive esophagitis (RE) cases have mild severity of GERD (Los Angeles classification of grades A and B). The prevalence of RE in H. pylori-positive patients is relatively low (4.1%) compared to the general Japanese population (7.6-10.6%). In multivariate analysis to evaluate a risk of RE development, a risk in H. pylori-positive patients is elevated in those with mild gastric mucosal atrophy (C-I and C-II according to the Kimura-Takemoto classification, OR 12.14, 95% CI 1.28-115.26, p = 0.03) or with hiatal hernia (OR 5.24, 95% CI 1.80-15.22, p < 0.01). Here, we provide a comprehensive review of GERD in Japan, including associations between GERD and H. pylori infection, low-dose-aspirin-induced GERD, and pharmacological treatment for GERD. Key Messages: The recent decrease in the rate of H. pylori infection and increase in the proportion of elderly persons might have increased the prevalence of GERD in Japan.

Influence of prostate stem cell antigen gene polymorphisms on susceptibility to Helicobacter pylori-associated diseases: a case-control study.

Patients with duodenal ulcer have a reduced risk of developing gastric cancer compared to those without. Recently, the prostate stem cell antigen (PSCA) rs2294008 C>T polymorphism was found to be associated with different pathogenesis of duodenal ulcer and gastric cancer developments. However, whether PSCA rs2294008 C>T polymorphism is associated with severity of gastric mucosal atrophy is unclear. We examined the influence of the PSCA rs2294008 C>T polymorphism on susceptibility to H. pylori‐related diseases and the relationships between PSCA polymorphism and gastric mucosal atrophy.