2002 Fiscal Year Final Research Report Summary
A study of an association between childhood Helicobacter pylori infection and gastric mucosal damage
| Project/Area Number |
13670780
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Tohoku University |
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Principal Investigator |
KATO Seiichi Tohoku University Hospital Lecturer, 医学部附属病院, 講師 (90177452)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Helicobacter pylori / atrophy / gastric cancer / apoptosis / proliferation / gastritis / duodenal ucler / child |
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| Research Abstract |
Because our multicenter study demonstrated that ^<13>C-urea breath test and stool antigen test are reliable for the diagnosis of childhood Helicobacter pylori infection, H. pylori status was confirmed using these non-invasive tests and biopsy tests. Histology (n=196) showed that H. pylori induced mononuclear cell and neutrophil infiltration in both the antrum and corpus mucosa of the stomach and that mucosal atrophy frequently developed in the antrum (51.9%) and corpus (34.8%) of the infected children. Our data suggests that the high incidence of gastric cancer in Japan may be related to this early development of atophy. The serological study with serum pepsinogen I and II also showed a significant association between H. pylori and gastric inflammation.
Using immunohistochemistry, a total of 28 pediatric patients were studied on gastric atrophy. H. pylori induced proliferation (p<0.001) and apoptosis (p<0.001) of gastric epithelial cells compared with non-infected stomach. Furthermore, successful eradication of the bacteriurn decreased the epithelial proliferalion (p<0.01) and apoptosis (p<0.01). From these results, it is concluded that the increased epithelial proliferation and apoptosis induced by H. pylori play an important role in the development of atrophy in children.
Endoscopic gastrin test (n=32) demonstrated that H. pylori infection is associated with gastric hypersecretion and that peak acid output was higher in H. pylori-positive duodenal ulcer than in gastritis alone. We believe that gastric hypersecretion induced by H. pylori infection is important in the pathogenesis of H. pylori-associated duodenal ulcer in childhood.
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