[Helicobacter pylori and Arteriosclerosis]

Helicobacter pylori (H. pylori) infection-related diseases are known to include gastritis, gastric and duodenal ulcer, gastric cancer, gastric MALT lymphoma, idiopathic thrombocytopenic purpura, iron-deficient anemia, urticaria, reflux esophagitis, and some lifestyle-related diseases. It is indicated that homocysteine involved with arteriosclerosis induces lifestyle-related diseases. Homocysteine is decomposed to methionine and cysteine (useful substances) in the liver, through the involvement of vitamin B₁₂ (VB₁₂) and folic acid. However, deficiency of VB₁₂ and folic acid induces an increase in unmetabolized homocysteine stimulating active oxygen and promoting arteriosclerosis. VB₁₂ and folic acid are activated by the intrinsic factors of gastric parietal cells and gastric acid. The question of whether homocysteine, as a trigger of arteriosclerosis, was influenced by H. pylori infection was investigated. H. pylori infection induces atrophy of the gastric mucosa, and the function of parietal cells decreases with the atrophy to inactivate its intrinsic factor. The inactivation of the intrinsic factor causes a deficiency of VB₁₂ and folic acid to increase homocysteine's chances of triggering arteriosclerosis. The significance and usefulness of H. pylori eradication therapy was evaluated for its ability to prevent arteriosclerosis that induces lifestyle-related diseases. Persons with positive and negative results of H. pylori infection were divided into a group of those aged 65 years or more (early and late elderly) and a group of those under 65 years of age, and assessed for gastric juice. For twenty-five persons from each group who underwent gastrointestinal endoscopy, the degree of atrophy of the gastric mucosa was observed. Blood homocysteine was measured as a novel index of arteriosclerosis, as well as VB₁₂ and folic acid that affect the metabolism of homocysteine, and then activated by gastric acid and intrinsic factors. Their arterioscleroses, measured by pulse wave velocity (PWV), were investigated and compared. The levels of homocysteine were significantly high in the elderly persons and those with H. pylori infection. On the contrary, the levels of VB₁₂ and folic acid were low in these persons. The results of PWV showed a positive correlation with the levels of gastrin and homocysteine and an inverse correlation with the levels of VB₁₂ and folic acid. Persons with a negative result of H. pylori infection showed a lower degree of arteriosclerosis than those with a positive result who were of the same age group. Persons with a positive result of H. pylori infection tended to show an improvement from arteriosclerosis after eradication therapy without a significant difference. 1 ) It is suggested that severity of atrophy of the gastric mucosa are correlated with the severity of arteriosclerosis. 2 ) It is hypothesized that H. pylori infection may induce arteriosclerosis.