The prevalence of GERD in the Japanese was 17.9% and the prevalence rates of NERD and erosive esophagitis were 10.9% and 8.6%, respectively. The majority of symptomatic patients did not have endoscopically proven esophagitis. Hiatal hernia is the only important predictor of the presence of GERD symptoms.
The therapeutic ef®cacy of drugs that suppress gastric acid secretion in the healing of peptic ulcers and gastrooesophageal re¯ux disease (GERD) depends on the potency of acid suppression.1, 2 The proton pump inhibitors, which cause potent and long-lasting inhibition of the terminal step in gastric acid secretion, are considered to be the most effective medical treatment for the management of patients with acid-related diseases.3, 4 However, interindividual variations in the suppressive effect of proton pump inhibitors on gastric acid secretion have been reported. 5±7 Helicobacter pylori infection is reported to affect the acid suppressing effect of proton pump inhibitors and is regarded as one of the factors that cause interindividual variations in their effect.
8±12Recently, it has also been found that CYP2C19, which is one of the isoenzymes of cytochrome P450 (CYP) in the liver and has important roles in the catabolism of proton pump inhibitors, has two genetically determined phenotypes: extensive metabolizers (EMs) and poor metabolizers (PMs).13±17 Variation in phenotype affects the acid suppressing effects of omeprazole by changing its rate of catabolism.18 These two phenotypes of CYP2C19 can be determined by measuring urinary 4¢-hydroxymephenytoin excretion or urinary S/R enantiomeric ratio after a single dose of racemic SUMMARY Background: CYP2C19 has an important role in the catabolism of several proton pump inhibitors. However, the relative contribution of CYP2C19-mediated metabolism varies among the different proton pump inhibitors. Aim: To determine the effect of CYP2C19 genotype status on intragastric pH during dosing with lansoprazole or rabeprazole. Subjects and methods: The subjects were 20 male volunteers without Helicobacter pylori infection. Their CYP2C19 genotype status was determined by a polymerase chain reaction-restriction fragment length polymorphism method. Twenty-four-hour monitoring of intragastric acidity was performed three times: once
Background:
Nocturnal gastric acid breakthrough is defined as night‐time periods when gastrin pH falls below 4.0 for greater than 1h during administration of a proton pump inhibitor. This phenomenon is a serious problem for patients who require strict control of their gastric acid secretions.
Aim:
To investigate the prevalence of nocturnal gastric acid breakthrough in Japanese subjects during administration of rabeprazole, and to clarify the relationship between Helicobacter pylori infection and nocturnal gastric acid breakthrough.
Methods:
Thirty‐one normal male volunteers were examined by ambulatory 24 h gastric pH monitoring four times: without medication, after a morning or an evening dose of 20 mg rabeprazole, and after administration of an H2‐receptor antagonist at bedtime, in addition to the morning dose of rabeprazole. H. pylori infection was determined by the 13C‐urea breath test and an assay for serum anti‐H. pylori antibody.
Result:
Nocturnal gastric acid breakthrough was observed in 12 patients (39%) after the morning dose of 20 mg rabeprazole. In all cases, nocturnal gastric acid breakthrough was inhibited completely by administration of the H2‐receptor antagonist at bedtime. Only one patient with nocturnal gastric acid breakthrough had H. pylori infection.
Conclusion:
The absence of H. pylori infection appears to be closely related to the occurrence of nocturnal gastric acid breakthrough during dosing with a proton pump inhibitor.
Since endoscopic treatment has been evaluated and become established as treatment for early gastric cancer, metachronous recurrence has become a major problem. In this report, predictive factors for recurrence were studied using the Kaplan-Meier method and Cox's proportional hazards regression model in 76 patients who received endoscopic treatment. There were 48 men and 28 women age 69.6 +/- 8.3 years (mean +/- standard deviation), 5 of whom had synchronous multiple lesions and 71 who had a single lesion found during the initial endoscopic treatment. In all patients, periodic follow-ups were performed by endoscopy for more than 2 years after treatment. Helicobacter pylori infection was assessed in 55 of the 76 patients, and proved positive in 43 and negative in 12. Metachronous recurrence was detected significantly more frequently in patients whose synchronous multiple lesions were found during the initial treatment. In addition, age affected the recurrence positively. However, gender and H. pylori infection had no significant relationship with metachronous recurrence.
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