Azuma T, Ito S, Sato F, Yamazaki Y, Miyaji H, Ito Y, Suto H, Kuriyama M, Kato T, Kohli Y
Second Department of Internal Medicine, Fukui Medical School, Japan.
Cancer. 1998 Mar 15;82(6):1013-8. doi: 10.1002/(sici)1097-0142(19980315)82:6<1013::aid-cncr2>3.0.co;2-f.
It has been suggested that immunogenetic factors for susceptibility or resistance to disease caused by Helicobacter pylori exist in the host. To examine host genetic factors that increase the risk of gastric adenocarcinoma among H. pylori-infected persons, the HLA-DQA1 locus was examined in patients with gastric adenocarcinoma.
Eighty-two gastric adenocarcinoma patients and 167 unrelated controls were examined for H. pylori infection and HLA-DQA1 genotyping. In addition, serum pepsinogen A (PGA) and pepsinogen C (PGC) values and the PGA/PGC ratio, which have been characterized as markers of gastric mucosal atrophy, also were analyzed.
Of the 167 controls, 121 were H. pylori positive (+) and 46 were H. pylori negative (-). All H. pylori (-) individuals had normal endoscopic and histologic findings. Among the 121 H. pylori (+) controls, 36 had superficial gastritis and 85 had atrophic gastritis. The allele frequency of DQA10102 was significantly lower in the H. pylori (+) atrophic gastritis group than in the H. pylori (+) superficial gastritis and H. pylori (-) normal control groups. In addition, the allele frequency of DQA10102 also was significantly lower in the H. pylori (+) intestinal type gastric adenocarcinoma group than in the H. pylori (-) normal control, H. pylori (+) superficial gastritis, and H. pylori (-) diffuse type gastric adenocarcinoma groups. Serum PGA and PGC values and the PGA/PGC ratio did not differ significantly among HLA-DQA1 genotypes; however, the PGA/PGC ratio was significantly lower in the H. pylori (+) atrophic gastritis and H. pylori (+) intestinal type gastric adenocarcinoma groups than in the H. pylori (-) normal control and H. pylori (+) superficial gastritis groups.
The DQA10102 allele may contribute to resistance against H. pylori-associated gastric atrophy and its association with intestinal type gastric adenocarcinoma, whereas the absence of DQA10102 may be a host genetic risk factor for H. pylori-associated atrophic gastritis and intestinal type gastric adenocarcinoma.
有研究表明，宿主中存在针对幽门螺杆菌所致疾病易感性或抗性的免疫遗传因素。为了研究在幽门螺杆菌感染者中增加胃腺癌风险的宿主遗传因素，对胃腺癌患者的HLA - DQA1基因座进行了检测。
对82例胃腺癌患者和167名无关对照者进行了幽门螺杆菌感染检测和HLA - DQA1基因分型。此外，还分析了血清胃蛋白酶原A（PGA）和胃蛋白酶原C（PGC）值以及PGA/PGC比值，这些已被视为胃黏膜萎缩的标志物。
在167名对照者中，121人幽门螺杆菌阳性（+），46人幽门螺杆菌阴性（-）。所有幽门螺杆菌（-）个体的内镜和组织学检查结果均正常。在121名幽门螺杆菌（+）对照者中，36人患有浅表性胃炎，85人患有萎缩性胃炎。DQA10102等位基因频率在幽门螺杆菌（+）萎缩性胃炎组中显著低于幽门螺杆菌（+）浅表性胃炎组和幽门螺杆菌（-）正常对照组。此外，DQA10102等位基因频率在幽门螺杆菌（+）肠型胃腺癌组中也显著低于幽门螺杆菌（-）正常对照组、幽门螺杆菌（+）浅表性胃炎组和幽门螺杆菌（-）弥漫型胃腺癌组。血清PGA和PGC值以及PGA/PGC比值在HLA - DQA1基因型之间无显著差异；然而，幽门螺杆菌（+）萎缩性胃炎组和幽门螺杆菌（+）肠型胃腺癌组的PGA/PGC比值显著低于幽门螺杆菌（-）正常对照组和幽门螺杆菌（+）浅表性胃炎组。
DQA10102等位基因可能有助于抵抗幽门螺杆菌相关的胃萎缩及其与肠型胃腺癌的关联，而缺乏DQA10102可能是幽门螺杆菌相关萎缩性胃炎和肠型胃腺癌的宿主遗传风险因素。
