A. Courillonmallet et al., HELICOBACTER-PYLORI INFECTION - PHYSIOPATHOLOGICAL IMPLICATION OF N-ALPHA-METHYL HISTAMINE, Gastroenterology, 108(4), 1995, pp. 959-966
Background/Aims: In the gastric mucosa of Helicobacter pylori-infected
subjects, we previously detected N-alpha-methyl histamine (N-alpha-Me
HA), 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. Met
hods: Ten noninfected patients and 13 patients with intense colonizati
on were compared. N-alpha-MeHA content and its synthetic enzyme activi
ty, N-alpha-histamine methyltransferase, binding of [H-3]N-alpha-MeHA,
histamine and somatostatin contents, and histidine decarboxylase acti
vity were assayed in antral and fundic biopsy specimens and in culture
d H. pylori strains. Results: Gastric histamine and somatostatin conte
nts as well as histidine decarboxylase activity were decreased in infe
cted patients and were restored to normal after antimicrobial treatmen
t: Both N-alpha-MeHA and N-alpha-histamine methyltransferase activity
were present in the mucosa of infected patients and in cultured strain
s 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 characteri
zed as H-3 receptors. The amount of bound [H-3]N-alpha-MeHA seemed cor
related positively with somatostatin content and histidine decarboxyla
se activity and negatively with N-alpha-MeHA content and N-alpha-hista
mine methyltransferase activity. Conclusions: H. pylori is the main so
urce of gastric N-alpha-MeHA that may lower histidine decarboxylase ac
tivity and somatostatin content through H-3 receptors.