Interactions of proton pump inhibitors and Helicobacter pylori in vivo

Martínek, Jan

doi:10.1007/978-3-0348-8795-3_8

Cited by 3 publications

(3 citation statements)

References 53 publications

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“…However, if this was the major mechanism for the apparent reduction in acid suppressing efficacy of omeprazole after cure of H. pylori , the intragastric acidity after the administration of a reversible PPA such as pumaprazole should not be affected by H. pylori status. This is because PPAs, which bind reversibly to the proton pump, are not activated in the acidic milieu of the parietal cell 35 . However, as has already been discussed ( Table 1), pumaprazole and omeprazole produced a similar intragastric pH both before and after cure of H. pylori infection 26 .…”

Section: Potential Mechanisms For the Effect Of H Pylori On The Effimentioning

confidence: 76%

“…The exact mechanism(s) underlying the effect of H. pylori on the efficacy of acid inhibitory agents are unclear. In general, the observed phenomenon could be related to the pharmacokinetic properties of a drug, changes induced by H. pylori ‐related gastritis or a direct product of H. pylori metabolism, such as ammonia 35 . Furthermore, it is not known whether acid inhibitory agents are truly more effective in H. pylori ‐positive patients or whether the combined effects of omeprazole and H. pylori result in a higher pH being achieved.…”

Section: Potential Mechanisms For the Effect Of H Pylori On The Effimentioning

confidence: 99%

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Review article: the clinical influence of Helicobacter pylori in effective acid suppression—implications for the treatment of gastro‐oesophageal reflux disease

Martínek

Kuzela²,

Špičák

et al. 2000

Aliment Pharmacol Ther

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The relationship between gastro‐oesophageal reflux disease (GERD) and Helicobacter pylori is unclear. Recent data indicate that H. pylori probably exerts a protective effect against GERD. In recent years, the interaction between H. pylori, proton pump inhibitors and GERD has been widely studied. Currently available proton pump inhibitors produce significantly higher intragastric pH in H. pylori‐positive patients than in those who are H. pylori negative, and this phenomenon may be clinically relevant. The mechanisms responsible for this difference in efficacy are not fully understood, although there are two major theories. Ammonia, produced by H. pylori, is able to neutralize gastric acid, and thus apparently increase the effect of acid suppressive agents (the ‘ammonia theory’). The other theory is that decrease in acid output is due to the development of corpus gastritis during treatment with a proton pump inhibitor (the ‘gastritis theory’). Treatment strategies to overcome this lowered sensitivity to acid suppression are to increase the frequency/dose of a proton pump inhibitor or to add an H2‐receptor antagonist in the evening—but both have pharmaco‐economic implications. An agent that could provide adequate pH control regardless of H. pylori status would be highly beneficial in the treatment of GERD, and may also lower treatment costs.

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Section: Potential Mechanisms For the Effect Of H Pylori On The Effimentioning

confidence: 76%

Section: Potential Mechanisms For the Effect Of H Pylori On The Effimentioning

confidence: 99%

Review article: the clinical influence of Helicobacter pylori in effective acid suppression—implications for the treatment of gastro‐oesophageal reflux disease

Martínek

Kuzela²,

Špičák

et al. 2000

Aliment Pharmacol Ther

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“…One major reason is the speed of metabolism via the cytochrome P 450 isoenzyme 2C19: it has been shown that slow metabolizers exert more profound inhibition of acid secretion than rapid metabolizers; this effect on acid inhibition is paralleled by differences in healing rates of oesophagitis [1], [34]. Another factor influencing the intragastric pH is the Helicobacter pylori (H. p.) status [5]: acid inhibition leads to higher pH levels in individuals infected with H.p. irrespective of drugs employed for acid suppression but most pronounced in patients with PPI of therapy.…”

Section: Proton Pump Inhibitorsmentioning

confidence: 99%

Medical Therapy of Gastro-Oesophageal Reflux Disease

Koop

2006

Gastroesophageal Reflux Disease

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Medikament�se Therapie der gastro�sophagealen Refluxkrankheit

Koop

2005

Chirurg

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Acid-suppressant drugs predominate in the treatment of gastroesophageal reflux disease. Proton pump inhibitors (PPI) are the first-line choice in both reflux esophagitis and nonerosive reflux disease (NERD). H(2)-blockers play a minor role and should not be used in erosive esophagitis. Other drugs such as mucosa-protective compounds, prokinetics, and antacids do not play a role, either alone oder in combination with acid suppressants. Proton pump inhibitors should also be used in maintenance therapy which is not associated with significant risks. There is a general trend toward on-demand treatment (already established in NERD). In cases refractory to therapy, the choice of drug should be critically analyzed (in case H(2)-blockers are used), and increasing the PPI dose is recommended; persistent symptoms should lead to reevaluation of the diagnosis. Asymptomatic Barrett's esophagus represents no indication for treatment, which in symptomatic patients is carried out in the normal fashion.

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Interactions of proton pump inhibitors and Helicobacter pylori in vivo

Cited by 3 publications

References 53 publications

Review article: the clinical influence of Helicobacter pylori in effective acid suppression—implications for the treatment of gastro‐oesophageal reflux disease

Review article: the clinical influence of Helicobacter pylori in effective acid suppression—implications for the treatment of gastro‐oesophageal reflux disease

Medical Therapy of Gastro-Oesophageal Reflux Disease

Medikament�se Therapie der gastro�sophagealen Refluxkrankheit

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