Post written by Jasper L.A. Vleugels, MD, from the Department of Gastroenterology and Hepatology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.

We compared endoscopic detection rates and distribution of sessile serrated lesions in Lynch syndrome patients to a matched control population in this case-control study.

Cancers in Lynch syndrome are generally assumed to go through the conventional adenoma-to-carcinoma development sequence, but there has been speculation as to whether the serrated neoplasia pathway plays a role. To investigate this hypothesis, we retrospectively examined results from colonoscopies and removed polyps were reviewed by specialist pathologists who were blinded to the initial diagnosis.

Endoscopic detection rates and distribution of sessile serrated lesions were compared in individuals with Lynch syndrome (n = 223) and matched controls (n = 223). In all, 7.6% of colonoscopies performed in Lynch patients and 6.7% in controls turned up sessile serrated lesions (P = 0.86), comparable rates. Moreover, none of the sessile serrated lesions were detected with any dysplasia in this high-risk population. Hence, we concluded that the function of the serrated neoplasia pathway in terms of colorectal cancer development appears to be comparable between people with Lynch syndrome and the general population. Future studies should molecularly evaluate colorectal cancers in Lynch syndrome to determine to what extent these can be attributed to the serrated neoplasia pathway.

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