Sheu Bor-Shyang, Yang Hsiao-Bai, Sheu Shew-Meei, Huang Ay-Huey, Wu Jiunn-Jong
Department of Internal Medicine, Medical College, National Cheng Kung University, Tainan 70428, Taiwan.
Clin Cancer Res. 2003 Nov 1;9(14):5245-51.
This study was conducted to determine whether relatives of gastric cancer patients (GCF) showed greater gastric cycloxygenase-2 (COX-2) expression or a greater incidence of precancerous lesions after Helicobacter pylori infection and whether H. pylori eradication could reduce COX-2 expression.
Three hundred subjects were enrolled in this study: half were relatives of 50 H. pylori-infected gastric cancer patients, and half were relatives of 50 H. pylori-infected duodenal ulcer (DU) patients (controls). Each relative underwent endoscopy to detect H. pylori infection and related gastric histology. One hundred and twenty GCFs were found to have H. pylori infection. After H. pylori eradication, 90 of the 120 GCFs were followed up with annual endoscopy examinations over the next 2 years. Gastric COX-2 intensity in all of the specimens collected from these patients was immunochemically stained and graded from 0 to 4.
H. pylori infection, gastric atrophy, and intestinal metaplasia (IM) were more prevalent in GCFs than in relatives of H. pylori-infected patients with DUs (P < 0.05). H. pylori-infected GCFs also showed a greater COX-2 intensity than H. pylori-infected relatives of patients with DUs (89.1% versus 62.7%, P < 0.001; relative risk: 4.9; 95% confidence interval: approximately 2.34-10.29). Among the H. pylori-infected GCFs, COX-2 intensity correlated with atrophy and IM (P < 0.001). After H. pylori eradication, gastric COX-2 expression disappeared only in those relatives without IM (P < 0.001).
GCFs are more likely to show greater gastric COX-2 expression and a higher incidence of precancerous lesions after H. pylori infection than the relatives of H. pylori-infected patients with only DUs. H. pylori eradication can reverse gastric COX-2 expression in patients without IM but not in patients with IM.
本研究旨在确定胃癌患者的亲属（GCF）在幽门螺杆菌感染后是否表现出更高的胃环氧化酶-2（COX-2）表达或癌前病变的更高发生率，以及根除幽门螺杆菌是否能降低COX-2表达。
本研究招募了300名受试者：一半是50名幽门螺杆菌感染的胃癌患者的亲属，另一半是50名幽门螺杆菌感染的十二指肠溃疡（DU）患者的亲属（对照组）。每位亲属均接受内镜检查以检测幽门螺杆菌感染及相关胃组织学情况。发现120名GCF感染了幽门螺杆菌。在根除幽门螺杆菌后，对这120名GCF中的90名在接下来的2年中每年进行内镜检查随访。对从这些患者收集的所有标本中的胃COX-2强度进行免疫化学染色，并从0到4进行分级。
GCF中幽门螺杆菌感染、胃萎缩和肠化生（IM）比幽门螺杆菌感染的DU患者的亲属更普遍（P<0.05）。幽门螺杆菌感染的GCF也比幽门螺杆菌感染的DU患者的亲属表现出更高的COX-2强度（89.1%对62.7%，P<0.001；相对风险：4.9；95%置信区间：约2.34 - 10.29）。在幽门螺杆菌感染的GCF中，COX-2强度与萎缩和IM相关（P<0.001）。根除幽门螺杆菌后，仅在没有IM的亲属中胃COX-2表达消失（P<0.001）。
与仅患有DU的幽门螺杆菌感染患者的亲属相比，GCF在幽门螺杆菌感染后更有可能表现出更高的胃COX-2表达和更高的癌前病变发生率。根除幽门螺杆菌可使没有IM的患者的胃COX-2表达逆转，但不能使有IM的患者逆转。
