HELICOBACTER-PYLORI INFECTION - PHYSIOPATHOLOGICAL IMPLICATION OF N-ALPHA-METHYL HISTAMINE

Background/Aims: In the gastric mucosa of Helicobacter pylori-infected subjects, we previously detected N-alpha-methyl histamine (N-alpha-MeHA), a minor catabolite of histamine and a potent agonist of histamine H-3 receptors. The origin of N-alpha-MeHA and its effects on gastric histamine and somatostatin in infected subjects were investigated. Methods: Ten noninfected patients and 13 patients with intense colonization were compared. N-alpha-MeHA content and its synthetic enzyme activity, N-alpha-histamine methyltransferase, binding of [H-3]N-alpha-MeHA, histamine and somatostatin contents, and histidine decarboxylase activity were assayed in antral and fundic biopsy specimens and in cultured H. pylori strains. Results: Gastric histamine and somatostatin contents as well as histidine decarboxylase activity were decreased in infected patients and were restored to normal after antimicrobial treatment: Both N-alpha-MeHA and N-alpha-histamine methyltransferase activity were present in the mucosa of infected patients and in cultured strains and were very low in noninfected patients or after eradication of H. pylori. [H-3]N-alpha-MeHA bound to gastric mucosa but not to cultured strains. The [H-3]N-alpha-MeHA specific binding sites were characterized as H-3 receptors. The amount of bound [H-3]N-alpha-MeHA seemed correlated positively with somatostatin content and histidine decarboxylase activity and negatively with N-alpha-MeHA content and N-alpha-histamine methyltransferase activity. Conclusions: H. pylori is the main source of gastric N-alpha-MeHA that may lower histidine decarboxylase activity and somatostatin content through H-3 receptors.