Cabral Mônica M D A, Oliveira Celso A, Mendes Cláudia M C, Guerra Juliana, Queiroz Dulciene M M, Rocha Gifone A, Rocha Andreia M C, Nogueira Ana M M F
Faculty of Medicine, Department of Pathology, Laboratory of Research in Bacteriology, University Hospital Federal University of Minas Gerais, Brazil.
Scand J Gastroenterol. 2007 May;42(5):545-54. doi: 10.1080/00365520601014034.
Helicobacter pylori infection causes hyperproliferation which is believed to predispose to the development of gastric carcinoma. The aim of this study was to analyze epithelial cell proliferation topographically in H. pylori gastritis in relationship to cagA status.
The proliferative index (PI: Ki-67-labeled nuclei/total number of foveolar nuclei) was determined in gastric mucosa biopsies taken at the antrum (lesser and greater curvatures), incisura, and corpus (greater curvature) from 78 patients with H. pylori gastritis and 20 H. pylori-negative patients. H. pylori and cagA status were determined by polymerase chain reaction (PCR) and serology.
PIs were significantly higher in H. pylori- and cagA-positive patients, in comparison with H. pylori- and cagA-negative patients, at all sites (p<or=0.002 and p<or=0.009) and in the antrum in comparison to the corpus, in both H. pylori-negative (p=0.04) and positive patients (p<10(-3)). At the antral lesser curvature, PIs were higher than in all the other sites, both in H. pylori- (p<or=0.002) and cagA-positive groups (p<or=0.02). The PI correlated directly and significantly with inflammation in infected patients (r=0.45, p<10(-3)) and in cagA-positive patients (r=0.41, p=0.005). The PI was significantly higher in the antrum of infected patients with atrophy (p=0.03) and intestinal metaplasia (p=0.05) than in those without atrophy and intestinal metaplasia, respectively.
We demonstrated that H. pylori infection and cagA-positive strains promote epithelial proliferation that was correlated with host inflammatory reaction and mostly at the antral lesser curvature, which is recognized as the area where most carcinomas arise.
幽门螺杆菌感染会导致细胞过度增殖，据信这易引发胃癌。本研究的目的是分析幽门螺杆菌胃炎中上皮细胞增殖的局部情况与cagA状态的关系。
测定了78例幽门螺杆菌胃炎患者和20例幽门螺杆菌阴性患者取自胃窦（小弯和大弯）、胃切迹和胃体（大弯）的胃黏膜活检标本的增殖指数（PI：Ki-67标记的细胞核/胃小凹细胞核总数）。通过聚合酶链反应（PCR）和血清学检测幽门螺杆菌及cagA状态。
与幽门螺杆菌和cagA阴性患者相比，幽门螺杆菌和cagA阳性患者在所有部位的PI均显著更高（p≤0.002和p≤0.009），且在胃窦中，幽门螺杆菌阴性患者（p = 0.04）和阳性患者（p＜10⁻³）的PI均高于胃体。在胃窦小弯处，幽门螺杆菌阳性组（p≤0.002）和cagA阳性组（p≤0.02）的PI均高于所有其他部位。在感染患者中，PI与炎症直接且显著相关（r = 0.45，p＜10⁻³），在cagA阳性患者中也是如此（r = 0.41，p = 0.005）。感染患者中伴有萎缩（p = 0.03）和肠化生（p = 0.05）者胃窦的PI分别显著高于无萎缩和肠化生者。
我们证明幽门螺杆菌感染和cagA阳性菌株会促进上皮增殖，这与宿主炎症反应相关，且主要发生在胃窦小弯处，而胃窦小弯被认为是大多数癌症的起源部位。
