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 <scp>CYP</scp>2<scp>C</scp>19 genotype

Sugimoto, Mitsushige; Shirai, Naohito; Nishino, Masafumi; Kodaira, Chise; Uotani, Takahiro; Yamade, Mihoko; Sahara, Shu; Ichikawa, Hitomi; Sugimoto, Ken; Miyajima, Hiroaki; Furuta, Takahisa

doi:10.1111/apt.12014

Cited by 56 publications

(62 citation statements)

References 40 publications

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“…PPI dose, PPI treatment schedule, 12,13 and schedule of meals. 14 We therefore conducted a meta-analysis to clarify whether or not having a CYP2C19 RM genotype increases the risk of GERD patients being refractory to PPI therapy.…”

Section: Discussionmentioning

confidence: 99%

“…[7][8][9][10][11] In the GERD management guidelines, an 8-week course of a PPI is recommended for symptom relief and healing of erosive esophagitis. 1 However, given that the efficacy of acid inhibition with a PPI relates to cytochrome P450 2C19 (CYP2C19) activity, PPI dose, PPI treatment schedule 12,13 , and meal time, 14 GERD patients are often refractory to PPI therapy. In addition, approximately 25% of patients with RE and 50% with NERD are refractory to therapy with a standard dose of a PPI.…”

Section: Introductionmentioning

confidence: 99%

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

Ichikawa

Sugimoto

et al. 2016

J of Gastro and Hepatol

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Ichikawa

Sugimoto

et al. 2016

J of Gastro and Hepatol

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“…This result was similar to that of a previous report investigating PPI q.i.d. treatment [4,12,13,14]. As plasma PPI levels prior to and 3 h after dosing were often below detectable levels in EMs, adequate PPI levels were unable to be maintained during the interval between doses in EMs when a PPI was administered only once a day [4,5,10,11].…”

Section: Discussionmentioning

confidence: 99%

“…were sustained for the full 24-h period, although that with esomeprazole 40 mg o.i.d. was not [13]. Third, in this study, esomeprazole was administrated after meal or without meal.…”

Section: Discussionmentioning

confidence: 99%

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Potent Gastric Acid Inhibition Over 24 Hours by 4-Times Daily Dosing of Esomeprazole 20 mg

et al. 2015

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Background: When administered at a standard dose, proton pump inhibitors (PPIs) do not always provide sufficient acid inhibition for all subjects, particularly in extensive metabolizers (EMs) of CYP2C19. Whether esomeprazole at a dose of 20 mg four times daily dosing (q.i.d.) can attain sufficient acid inhibition throughout 24 h in EMs remains unclear. We therefore investigated the efficacy of esomeprazole q.i.d. for acid inhibition. Methods: In a randomized cross-over design, 30 Helicobacter pylori-negative healthy young Japanese volunteers received esomeprazole at a dose of 20 mg two times a day (b.i.d.) or q.i.d. for 7 days. A pH monitoring was conducted before the trial as a control and on day 7 of both regimens. Results: Median pH values in the q.i.d. regimen were significantly higher than those with the b.i.d. regimen in EMs (b.i.d.: 5.3, q.i.d.: 6.6, p = 0.022), intermediate metabolizer (IM) (b.i.d.: 5.5, q.i.d.: 6.8, p = 0.005) and poor metabolizer (PM) (b.i.d.: 6.2, q.i.d.: 7.0, p = 0.047), respectively. Median pH with the b.i.d. regimen differed significantly by CYP2C19 genotypes (p = 0.004), but not the q.i.d. regimen (p = 0.384). Conclusion: Esomeprazole q.i.d. achieved potent acid inhibition in all Helicobacter pylori-negative subjects, irrespective of CYP2C19 genotype, which might be one of the rescue regimens for patients' refractory to PPI treatment.

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Prevention of gastric mucosal injury induced by anti‐platelet drugs by famotidine

Uotani

Sugimoto

Nishino

et al. 2014

The Journal of Clinical Pharma

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Anti-platelet drug-induced gastric mucosal injury correlates with intragastric pH. Our aim was to investigate prophylaxis effects of famotidine, one of the representative histamine-2 receptor antagonists (H2RA), on gastric mucosal injury induced by dual therapy with low-dose aspirin and clopidogrel in relation to Helicobacter pylori (H. pylori) infection and CYP2C19 genotypes. This study was conducted for 20 healthy Japanese volunteers (10 H. pyloripositive and 10-negative subjects) with 100 mg aspirin plus 75 mg clopidogrel (AC) once-daily dosing and AC plus 20 mg famotidine twice-daily dosing (ACH). Mucosal injury was endoscopically assessed on day 3 and 7 and 24-hour intragastric pH and antiplatelet-function test was performed on day 7. Median pH in ACH was similar between CYP2C19 extensive metabolizer (EM) and intermediate metabolizer (IM)/poor metabolizer (PM) and was significantly higher in H. pylori-positive than negative subjects (P < .05). Mucosal injury with ACH significantly decreased in both day 3 and 7 compared with AC, irrespective with H. pylori and CYP2C19 genotypes (P < .05). Although antiplatelet effect of clopidogrel in EM was significantly higher than that in IM/PM, the additional famotidine did not affect the effect. Anti-platelet drug-induced gastric injury was alleviated by famotidine without attenuation of anti-platelet functions irrespective of H. pylori and CYP2C19 genotypes.

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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

Cited by 56 publications

References 40 publications

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

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

Potent Gastric Acid Inhibition Over 24 Hours by 4-Times Daily Dosing of Esomeprazole 20 mg

Prevention of gastric mucosal injury induced by anti‐platelet drugs by famotidine

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