A study of an association between childhood Helicobacter pylori infection and gastric mucosal damage

由于我们的多中心研究表明，^<13 b> c -尿素呼气试验和粪便抗原试验是诊断儿童幽门螺杆菌感染的可靠方法，因此使用这些非侵入性检查和活检检查来确认幽门螺杆菌状态。组织学（n=196）显示幽门螺杆菌诱导胃窦和胃体粘膜单核细胞和中性粒细胞浸润，胃窦（51.9%）和胃体（34.8%）常发生粘膜萎缩。我们的数据表明，日本胃癌的高发病率可能与这种早期病变有关。血清胃蛋白酶原I和II的血清学研究也显示幽门螺杆菌与胃炎症有显著相关性。采用免疫组织化学方法对28例小儿胃萎缩患者进行了研究。与未感染的胃相比，幽门螺杆菌诱导胃上皮细胞增殖（p<0.001）和凋亡（p<0.001）。此外，成功根除细菌可降低上皮细胞增殖（p<0.01）和细胞凋亡（p<0.01）。由此可见，幽门螺杆菌诱导的上皮细胞增殖和凋亡的增加在儿童萎缩的发展中起重要作用。内镜胃泌素试验（n=32）显示幽门螺杆菌感染与胃分泌过多有关，幽门螺杆菌阳性十二指肠溃疡的酸输出峰值高于单独胃炎。我们认为幽门螺杆菌感染引起的胃高分泌在儿童期幽门螺杆菌相关十二指肠溃疡的发病机制中起重要作用。

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.