在 283 例早期胃癌内镜切除术后患者中，幽门螺杆菌根除失败和年龄是肿瘤复发的独立危险因素。
Failure of Helicobacter pylori eradication and age are independent risk factors for recurrent neoplasia after endoscopic resection of early gastric cancer in 283 patients.
机构信息
Division of Gastroenterology, Department of Internal Medicine, Kyungpook National University Medical Center, Daegu, South Korea.
出版信息
Aliment Pharmacol Ther. 2014 Mar;39(6):609-18. doi: 10.1111/apt.12633. Epub 2014 Jan 26.
BACKGROUND
Whether the incidence of metachronous gastric dysplasia and cancer could be decreased by eradication of Helicobacter pylori after endoscopic submucosal dissection (ESD) for early gastric cancer (EGC).
AIM
To compare the incidence of metachronous gastric lesion in the eradicated group and the persistent group. Second end point is to evaluate the risk factors for metachronous gastric lesions after ESD for EGC.
METHODS
In a single centre, between May 2007 and May 2010, the patients who had evidence of H. pylori infection at the time of ESD for EGC were included, and the follow-up data were analysed retrospectively.
RESULTS
We enrolled 283 patients who have shown H. pylori infection at the time of ESD for EGC. Successful eradication was achieved for 214 patients (75.6%) (Eradicated group), and 69 patients (24.4%) showed persistent H. pylori infection (Persistent group). Metachronous gastric lesions developed in 13 (18.8%) in the persistent group and 18 (8.4%) in the eradicated group (P = 0.016). In the ≥60-year-old group, the cumulative incidence of metachronous gastric cancer showed a significant increase (P = 0.012). Cumulative hazard ratio of subsequent gastric metachronous lesions differed between the eradication group and the persistent infection group (OR = 2.322, 95% CI = 1.136-4.744, P = 0.021), and ≥60 age at the time of endoscopic resection (OR = 2.803, 95% CI = 1.207-6.509, P = 0.016).
CONCLUSIONS
Both persistent H. pylori infection and old age (≥60) are independent risk factors for the increased incidence of metachronous gastric cancer.
背景
内镜黏膜下剥离术（ESD）治疗早期胃癌（EGC）后，根除幽门螺杆菌（H. pylori）能否降低胃黏膜异型增生和胃癌的发生率。
目的
比较 H. pylori 根除组和持续感染组的胃黏膜异型增生发生率。次要终点是评估 ESD 治疗 EGC 后胃黏膜异型增生的危险因素。
方法
单中心回顾性分析 2007 年 5 月至 2010 年 5 月期间 ESD 治疗 EGC 时 H. pylori 感染患者的随访资料。
结果
共纳入 283 例 ESD 治疗 EGC 时 H. pylori 感染患者。214 例（75.6%）患者 H. pylori 根除成功（根除组），69 例（24.4%）患者 H. pylori 持续感染（持续感染组）。持续感染组中有 13 例（18.8%）发生胃黏膜异型增生，根除组中有 18 例（8.4%）（P=0.016）。≥60 岁患者中，胃黏膜异型增生的累积发生率显著增加（P=0.012）。根除组和持续感染组的胃黏膜异型增生累积风险比不同（OR=2.322，95%CI=1.136-4.744，P=0.021），ESD 时年龄≥60 岁（OR=2.803，95%CI=1.207-6.509，P=0.016）也是胃黏膜异型增生的独立危险因素。
结论
持续 H. pylori 感染和年龄≥60 岁是胃黏膜异型增生和胃癌发生率增加的独立危险因素。
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