Carcinogenesis in Lynch syndrome involves fast progression of adenomas to colorectal cancer (CRC) due to 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 to 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. Controls 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 one colonoscopy. Of these, 223 Lynch patients (mean age 49.3, female 59%, index colonoscopy 56%) were matched to 223 controls. SSLs were detected in 7.6% (CI, 4.8-11.9) of colonoscopies performed in Lynch patients and in 6.7% (CI, 4.1-10.8) of controls (p = 0.86). None of the detected SSLs in Lynch patients contained dysplasia.
The detection rate of SSLs in Lynch patients undergoing colonoscopy is comparable to a matched population. These findings suggest that the role of the serrated neoplasia pathway in CRC development in Lynch syndrome seems to be comparable to that in the general population.
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weblog.maimonides.edu/farmacia/archives/0216_Admin_FarmEcon.pdf - //
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