Sakai N, Tatsuta M, Hirasawa R, Iishi H, Baba M, Yokota Y, Ikeda F
Department of Gastrointestinal Oncology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Japan.
Dig Dis Sci. 1998 Apr;43(4):766-72. doi: 10.1023/a:1018814014139.
Helicobacter pylori infection of the gastric mucosal surface was investigated in patients with hamartomatous fundic polyps or hyperplastic polyps and in patients without endoscopic evidence of disease (healthy subjects). Presence of H. pylori infection was determined by culture, histologic examination, and the endoscopic phenol red test. Adherence of H. pylori was evaluated with scanning electron microscopic examination of antral biopsy specimens. Both prevalence of H. pylori infection (P < 0.001) and H. pylori adherence (P < 0.05) were less in patients with hamartomatous fundic polyps than in healthy subjects and patients with hyperplastic polyps. However, the percentages of plasma cells in gastric mucosa that contained IgA and of gastric epithelial cells that expressed Lewis b did not differ significantly among the three groups. These findings suggest that defense mechanisms against the attachment of H. pylori other than IgA or Lewis b antigen are present in patients with hamartomarous fundic polyps.
对患有错构瘤性胃底息肉或增生性息肉的患者以及无内镜疾病证据的患者(健康受试者)的胃黏膜表面幽门螺杆菌感染情况进行了研究。通过培养、组织学检查和内镜酚红试验来确定幽门螺杆菌感染的存在。利用胃窦活检标本的扫描电子显微镜检查评估幽门螺杆菌的黏附情况。与健康受试者和增生性息肉患者相比,错构瘤性胃底息肉患者的幽门螺杆菌感染率(P < 0.001)和幽门螺杆菌黏附率(P < 0.05)均较低。然而,三组中胃黏膜中含IgA的浆细胞百分比以及表达Lewis b的胃上皮细胞百分比并无显著差异。这些发现表明,错构瘤性胃底息肉患者存在除IgA或Lewis b抗原之外的针对幽门螺杆菌黏附的防御机制。