Department of Gastroenterology and Hepatology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Gastrointest Endosc. 2018 May;87(5):1289-1296. doi: 10.1016/j.gie.2017.11.034. Epub 2017 Dec 9.
Carcinogenesis in Lynch syndrome involves fast progression of adenomas to colorectal cancer (CRC) because of microsatellite instability. The role of sessile serrated lesions (SSLs) and the serrated neoplasia pathway in these patients is unknown. The aim of this matched case-control study was to compare endoscopic detection rates and distribution of SSLs in Lynch syndrome patients with a matched control population.
We collected data of Lynch syndrome patients with a proven germline mutation who underwent colonoscopy between January 2011 and April 2016 in 2 tertiary referral hospitals. Control subjects undergoing elective colonoscopy from 2011 and onward for symptoms or surveillance were selected from a prospectively collected database. Patients were matched 1:1 for age, gender, and index versus surveillance colonoscopy. An expert pathology review of serrated polyps was performed. The primary outcomes included the detection rates and distribution of SSLs.
We identified 321 patients with Lynch syndrome who underwent at least 1 colonoscopy. Of these, 223 Lynch syndrome patients (mean age, 49.3; 59% women; index colonoscopy, 56%) were matched to 223 control subjects. SSLs were detected in 7.6% (95% confidence interval, 4.8-11.9) of colonoscopies performed in Lynch syndrome patients and in 6.7% (95% confidence interval, 4.1-10.8) of control subjects (P = .86). None of the detected SSLs in Lynch syndrome patients contained dysplasia.
The detection rate of SSLs in Lynch syndrome patients undergoing colonoscopy is comparable with a matched population. These findings suggest that the role of the serrated neoplasia pathway in CRC development in Lynch syndrome seems to be comparable with that in the general population.
林奇综合征患者的腺瘤向结直肠癌(CRC)快速进展与微卫星不稳定有关。这些患者中无蒂锯齿状病变(SSLs)和锯齿状肿瘤发生途径的作用尚不清楚。本匹配病例对照研究的目的是比较林奇综合征患者和匹配对照人群中内镜检测 SSL 率和 SSL 分布。
我们收集了 2011 年 1 月至 2016 年 4 月期间在 3 家三级转诊医院接受结肠镜检查的具有明确种系突变的林奇综合征患者的数据。从 2011 年开始为症状或监测目的接受择期结肠镜检查的对照受试者从一个前瞻性收集的数据库中选择。对年龄、性别、指数与监测结肠镜检查进行了 1:1 匹配。对锯齿状息肉进行了专家病理审查。主要结果包括 SSL 检出率和分布。
我们确定了 321 例至少接受过 1 次结肠镜检查的林奇综合征患者。其中 223 例林奇综合征患者(平均年龄 49.3 岁;59%为女性;指数结肠镜检查 56%)与 223 例对照患者匹配。在林奇综合征患者中,7.6%(95%置信区间,4.8-11.9)的结肠镜检查中检测到 SSL,在对照患者中,6.7%(95%置信区间,4.1-10.8)的结肠镜检查中检测到 SSL(P=0.86)。在林奇综合征患者中检测到的 SSL 均无异型增生。
在接受结肠镜检查的林奇综合征患者中 SSL 的检出率与匹配人群相当。这些发现表明,锯齿状肿瘤发生途径在林奇综合征患者 CRC 发展中的作用似乎与普通人群相当。