Handa Y, Saitoh T, Kawaguchi M, Misaka R, Ohno H, Tsai C R, Tani Y, Tsurui M, Yoshida H, Morita S, Midorikawa S, Sanji T
Fourth Department of Internal Medicine, Tokyo Medical College, Japan.
J Gastroenterol. 1996 Nov;31 Suppl 9:29-32.
The major purpose of this study was to evaluate the association of Helicobacter pylori and diffuse type gastric cancer (DGC) clinicopathologically (study 1). The second aim was to investigate genetic differences of H. pylori in patients with DGC and intestinal type cancer (IGC) (study 2). The prevalence of H. pylori and the types of histopathological changes were evaluated in resected early gastric cancer (DGC; 25 patients, IGC; 25 patients). Genetic differences of H. pylori in DGC patients (n = 19) and IGC patients (n = 22) were analyzed by polymerase chain reaction (PCR) methods in terms of restriction fragment length polymorphism patterns of the ureB gene and cagA gene positive rates. All patients had evidence of H. pylori infection in the resected stomach, but the positive rate for H. pylori in the area surrounding cancer was 52% (in DGC; 56%, IGC; 48%). But in 40.0% of DGC cases (10/25), mucosal atrophy and intestinal metaplasia were rarely seen in the area surrounding cancer and the positive rate of H. pylori was 80.0% (8/10), in contrast, in 60.0% of IGC cases (15/25), atrophy and metaplasia were progressed and positive rate of H. pylori was 26.7% (4/15) in the area. UreB gene products from 89.5% of DGC cases (17/19) were unable to be digested by Spe I. 31.8% of products from IGC cases (7/22) were also unable to be digested by Spe I, but the positive rate of cagA gene in this group was higher than other groups. The high prevalence of H. pylori infection in DGC patients suggests that H. pylori plays a role in the pathogenesis of DGC, but in the stomach with DGC, it is considered atrophy and intestinal metaplasia are not so implicated in H. pylori, compared with IGC. A genetic specificity of H. pylori in DGC and IGC was indicated by the results, suggesting that H. pylori may play different roles in the pathogenesis of DGC and IGC.
本研究的主要目的是从临床病理学角度评估幽门螺杆菌与弥漫型胃癌（DGC）之间的关联（研究1）。第二个目的是调查DGC患者和肠型胃癌（IGC）患者中幽门螺杆菌的基因差异（研究2）。对切除的早期胃癌患者（DGC；25例，IGC；25例）的幽门螺杆菌感染率及组织病理学变化类型进行评估。采用聚合酶链反应（PCR）方法，从ureB基因的限制性片段长度多态性模式和cagA基因阳性率方面，分析DGC患者（n = 19）和IGC患者（n = 22）中幽门螺杆菌的基因差异。所有患者切除的胃组织均有幽门螺杆菌感染证据，但癌周区域幽门螺杆菌阳性率为52%（DGC为56%，IGC为48%）。然而，在40.0%的DGC病例（10/25）中，癌周区域很少见到黏膜萎缩和肠化生，幽门螺杆菌阳性率为80.0%（8/10）；相比之下，在60.0%的IGC病例（15/25）中，萎缩和化生进展，该区域幽门螺杆菌阳性率为26.7%（4/15）。89.5%的DGC病例（17/19）的UreB基因产物不能被Spe I消化。IGC病例中有31.8%（7/22）的产物也不能被Spe I消化，但该组中cagA基因的阳性率高于其他组。DGC患者中幽门螺杆菌感染率较高，提示幽门螺杆菌在DGC发病机制中起作用，但在伴有DGC的胃中，与IGC相比，萎缩和肠化生与幽门螺杆菌的关系不那么密切。结果表明DGC和IGC中幽门螺杆菌存在基因特异性，提示幽门螺杆菌在DGC和IGC发病机制中可能发挥不同作用。
