Eradication of Helicobacter pylori by a potassium-competitive acid blocker alone?

Helicobacter pylori (H. pylori), the dominating cause of gastric cancer, most often infects children initiating inflammation in the antral part and spreads orally to the oxyntic mucosa. Traditionally, eradication of H. pylori has been based upon a combination of antibiotics together with a proton pump inhibitor (PPI) to reduce gastric destruction of the antibiotics. Recently it has been shown that the more efficient inhibitors of acid secretion, the potassium-competitive acid blockers (PCABs) in combination with amoxicillin alone gave highly sufficient H. pylori eradication.

To further elucidate the importance of gastric acidity we studied the literature for the connection between gastric acidity and the presence of H. pylori.

It is well-known that H. pylori is dependent of some acidity in the surroundings to neutralize NH₃ produced by its urease, explaining the loss of H. pylori in total oxyntic atrophy. With adequate dosing PCABs can induce almost complete anacidity for 24-h which probably is necessary for H. pylori eradication. Even a short period with hypergastrinemia may induce mutations in the target cell of gastrin, the enterochromaffin-like (ECL) cell which may contribute to the relatively short interval between H. pylori eradication and gastric cancer in the users of profound acid inhibitors.

The use of PCABs alone dosed sufficiently seems promising for H. pylori eradication, but a combination with a gastrin antagonist would be preferable.