Abstract
Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid.
Highlights
Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease, gastric adenocarcinoma, or mucosa-associated lymphoid tissue (MALT) lymphoma
Inhibition of the gastric H+,K+-ATPase, the final step in the acid secretion pathway, by proton pump inhibitors (PPIs) was initially included in eradication regimens to aid in symptom relief in patients suffering from peptic ulcer disease
It was found that PPIs and antibiotics act synergistically in eradicating H. pylori and acid inhibitors have been included in successful eradication treatments ever since
Summary
Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease, gastric adenocarcinoma, or mucosa-associated lymphoid tissue (MALT) lymphoma. Amoxicillin resistance appears to be on the rise in Asia and Africa, so the antibiotic used for dual therapy should be based on geographical resistance rates[22,23] Support for this concept is found in eradication studies of high-dose dual therapy (HDDT), slow PPI metabolizers, and novel potent acid inhibitors. The t1/2 of dissociation is 4.7 and 7.5 hours for rabbit and hog proton pumps, respectively[33] Taken together, these parameters indicate that vonoprazan has the potential for rapid, reversible, and longlasting inhibition of acid secretion when compared to the PPIs. The unique properties of vonoprazan combined with its greater degree of acid inhibition as compared with the PPIs, should provide greater efficacy in H. pylori eradication. Specific to H. pylori, would be compounds targeted to essential acid acclimation proteins such as UreI or carbonic anhydrase
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