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 and AimHelicobacter pylori eradication clearly decreases peptic ulcer recurrence rates. H. pylori eradication is achieved in 70–90% of cases, but treatment failures due to poor patient compliance and resistant organisms do occur. Lactobacillus gasseri can suppress both clarithromycin-susceptible and -resistant strains of H. pylori in vitro. The aim of this study was to determine the effect of pretreatment with L. gasseri- containing yogurt on H. pylori eradication. We conducted a randomized, controlled clinical trial in patients with H. pylori infection.MethodsA total of 229 patients were randomized into either a 1-week triple therapy of rabeprazole (10 mg bid), amoxicillin (750 mg bid), and clarithromycin (200 mg bid) or triple therapy plus L. gasseri-containing yogurt. In the yogurt-plus-triple therapy groups, yogurt containing L. gasseri OLL2716 (112 g) was given twice daily for 4 weeks (3 weeks pretreatment and also 1 week during eradication therapy). Clarithromycin resistance was determined by the detection of a mutation in 23S rRNA using nested polymerase chain reaction and the direct sequencing of DNA from pretreatment feces. H. pylori eradication was diagnosed based on the urea breath test and a stool antigen test after 8 weeks of eradication.ResultsThe status of H. pylori susceptibility to clarithromycin was successively determined in 188 out of 229 samples. The rate of infection with clarithromycin-resistant strains of H. pylori was 27.1%. Overall eradication (intention to treat/per protocol) was 69.3/74.5% for the triple-only group, and 82.6/85.6% for the yogurt-plus-triple group (P = 0.018/P = 0.041). Eradication of primary clarithromycin-resistant strains tended to be higher for yogurt-plus-triple therapy than triple-only therapy (38.5 vs 28.0%, respectively, P = 0.458).ConclusionThis study confirmed that the major cause of treatment failure is resistance to clarithromycin. A 4-week treatment with L. gasseri-containing yogurt improves the efficacy of triple therapy in patients with H. pylori infection.
These findings indicate that IL-1B polymorphisms enhance IL-1beta production in the antrum; however, other factors might regulate the production of IL-1beta in the corpus of the stomach, regardless of IL-1B polymorphisms, and high IL-1beta production may be associated with the grade of gastric atrophy in the corpus mucosa in patients with H. pylori infection.
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