Helicobacter pylori胃炎の成立に関する問題点とThe Updated Sydney System

Unresolved Pathomorphological Problems Concerning The Genesis of Helicobacter pylori Gastritis

要旨　The Updated Sydney Systemが提唱したvisual analogue scaleの基準に従って，胃生検280症例530検体の評価を実践した．Hpの陽性率は70％であり，各組織学的要素との関係は既に報告されている結果と大略一致した．しかし，Hp陽性にもかかわらず好中球浸潤の認められない標本が全陽性検体の18％に認められ，このような標本の特徴とHp感染が成立困難な憩室の所見を総合的に考察すると，Hpの感染様式をfloating infectionとsticking infectionに大別する必要がある．活動性の炎症所見を呈するHp胃炎はsticking infectionの成立を必要としており，floating infectionからsticking infectionに移行する過程でHp以外の因子の関与が考えられる．

　According to the visual analogous scales mentioned in The Updated Sydney System, we examined 530 biopsy specimens from 280 cases with benign non-neoplastic lesions. Grading of Helicobacter pylori (Hp) colonization, neutrophil infiltration, mononuclear cell infiltration, intestinal metaplasia and glandular atrophy was carried out with the use of H・E, pH 2.5-AB-PAS and modified Giemsa staining. 70% of the total number of cases were positive for Hp.

　The results of grading of Hp colonization and other histopathologic components were not so different from those obtained in previous reports. However, 63 Hp-positive specimens without neutrophil activity were noteworthy. In 50 specimens of this kind, style of Hp colonization was distinctly characteristics; Hp proliferation limited to the surface mucous layer and there was no sticking infection on foveola epithelial cells. In addition, gastric diverticulum free of Hp infection was presented in this paper as a significant observation suggestive of the pathogenesis of Hp gastritis. Recently, Shimizu et al reported that the surface mucous gel layer of the human stomach was a very important area for Hp colonization and the normal structure of the surface mucous gel layer was destroyed by Hp proliferation, which resulted in the collapse of the defence system for peptic and other attacks. Considering our morphological findings and the investigations by Shimizu et al, the conclusions of the present report are summarized as follows: (1) The morphology of gastric diverticulum free from Hp infection is suggestive of a significant etiologic role of non-Hp factors producing Hp gastritis. (2) Two types of Hp colonization should be distinguished. One is the floating infection in the surface mucous gel layer and another is the sticking infection on foveola epithelial cells. (3) Sticking infection on foveola epithelial cells is a necessary condition for Hp active gastritis. The pathological process from floating to sticking infection of Hp should be investigated.