Song Huan, Ekheden Isabella Guncha, Zheng Zongli, Ericsson Jan, Nyrén Olof, Ye Weimin
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden.
Department of Pathology, Karolinska Hospital, Sweden.
BMJ. 2015 Jul 27;351:h3867. doi: 10.1136/bmj.h3867.
To accurately measure the incidence of gastric cancer among patients with gastric precancerous lesions, and to quantify the excess incidence in comparison with people with normal mucosa on endoscopy and a general population.
Population based cohort study.
Population of Sweden using data from its national disease registers.
405,172 patients who had gastric biopsy samples taken for non-malignant indications between 1979 and 2011.
Incidence of gastric cancer, reported separately for patients with different mucosal changes in biopsy samples. Standardised incidence ratios provided estimation of the relative risk, using the general Swedish population as reference; and hazard ratios were derived from Cox regression modelling for internal comparisons with patients with normal gastric mucosa.
After excluding the first two years of follow-up, 1599 cases of gastric cancer were identified. The annual crude incidence of gastric cancer was 20 × 10(-5) for those in the normal mucosa group (standardised incidence ratio 1.0), 42 × 10(-5) for those with minor changes (1.5), 59 × 10(-5) for the gastritis group (1.8), 100 × 10(-5) for the atrophic gastritis group (2.8), 129 × 10(-5) for the intestinal metaplasia group (3.4), and 263 × 10(-5) for the dysplasia group (6.5). Cox regression modelling confirmed that excess risks increased monotonically with progressive severity of gastric lesions, with the highest hazard ratio of 10.9 (dysplasia versus normal mucosa, 95% confidence interval 7.7 to 15.4). The increased incidence was stable throughout the follow-up period, and the gaps between cumulative incidence curves grew continuously.
Among patients who undergo gastroscopy with biopsy for clinical indications, approximately 1 in 256 with normal mucosa, 1 in 85 with gastritis, 1 in 50 with atrophic gastritis, 1 in 39 with intestinal metaplasia, and 1 in 19 with dysplasia will develop gastric cancer within 20 years. These numbers, along with cost-benefit analyses, should guide future surveillance policies for these particular patient groups.
准确测量胃癌前病变患者中胃癌的发病率，并与内镜检查显示黏膜正常的人群及普通人群相比，量化额外发病率。
基于人群的队列研究。
利用瑞典国家疾病登记数据的瑞典人群。
1979年至2011年间因非恶性指征接受胃活检的405,172名患者。
胃癌发病率，按活检样本中不同黏膜变化的患者分别报告。标准化发病率比以瑞典普通人群为参照估计相对风险；风险比通过Cox回归模型得出，用于与胃黏膜正常的患者进行内部比较。
排除随访的前两年后，共确诊1599例胃癌。正常黏膜组患者胃癌的年粗发病率为20×10⁻⁵（标准化发病率比为1.0），轻度变化组为42×10⁻⁵（1.5），胃炎组为59×10⁻⁵（1.8），萎缩性胃炎组为100×10⁻⁵（2.8），肠化生组为129×10⁻⁵（3.4），发育异常组为263×10⁻⁵（6.5）。Cox回归模型证实，随着胃部病变严重程度的增加，额外风险呈单调上升，发育异常组与正常黏膜组相比风险比最高，为10.9（95%置信区间7.7至15.4）。整个随访期间发病率增加稳定，累积发病率曲线之间的差距持续扩大。
在因临床指征接受胃镜活检的患者中，正常黏膜者约256人中1人、胃炎患者约85人中1人、萎缩性胃炎患者约50人中1人、肠化生患者约39人中1人以及发育异常患者约19人中1人在20年内会发生胃癌。这些数据以及成本效益分析应指导针对这些特定患者群体的未来监测策略。
