1998, pp 169-175

Histamine and Helicobacter pylori: are we closer to the answer?

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Abstract

The discovery of Helicobacter pylori initially diminished interest in gastric acid, but this proved temporary. It is now generally believed that the effect of the infection on acid secretion determines the disease outcome. Patients who respond to the infection with acid hypersecretion are likely to develop duodenal ulcer1, while those who develop hyposecretion are at risk of gastric cancer2. These changes in acid secretion are reversed by eradicating the infection. The effect of H. pylori on acid secretion is also relevant to therapy. Proton-pump inhibitors inhibit acid secretion to a greater extent in those who are infected3, while increasing gastritis in the corpus of the stomach4. Therefore it remains important to understand the factors which control acid secretion. The role of gastric mucosal histamine in the regulation of acid secretion was debated extensively until selective histamine H2-receptor antagonists revealed its crucial role. However, the matter has now become less clear once again. Firstly, in addition to H1 and H2 receptors it is now appreciated that various cells in the gastric mucosa carry histamine H3 receptors whose location and effects are still being defined5. Secondly, it is now appreciated that agonists of histamine receptors are produced not only by the enterochromaffin-like (ECL) cells present in gastric corpus mucosa, but also by mast cells which are more abundant in H. pylori infection6, and by H. pylori bacteria themselves in the form of Nα-methylhistamine7