Jasper L A Vleugels1, Husna Sahin1, Yark Hazewinkel1, Lianne Koens2, Jose G van den Berg3, Monique E van Leerdam4, Evelien Dekker1. 1. Department of Gastroenterology and Hepatology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. 2. Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. 3. Department of Pathology, Antoni van Leeuwenhoek Hospital, Netherlands Cancer Institute, Amsterdam, the Netherlands. 4. Department of Gastroenterology and Hepatology, Antoni van Leeuwenhoek Hospital, Netherlands Cancer Institute, Amsterdam, the Netherlands.
Abstract
BACKGROUND AND AIMS: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND AND AIMS: 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 syndromepatients with a matched control population. METHODS: We collected data of Lynch syndromepatients 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. RESULTS: We identified 321 patients with Lynch syndrome who underwent at least 1 colonoscopy. Of these, 223 Lynch syndromepatients (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 syndromepatients and in 6.7% (95% confidence interval, 4.1-10.8) of control subjects (P = .86). None of the detected SSLs in Lynch syndromepatients contained dysplasia. CONCLUSIONS: The detection rate of SSLs in Lynch syndromepatients 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.
Authors: Britt B S L Houwen; Jasper L A Vleugels; Maria Pellisé; Liseth Rivero-Sánchez; Francesc Balaguer; Raf Bisschops; Sabine Tejpar; Alessandro Repici; D Ramsoekh; M A J M Jacobs; Ramon-Michel Schreuder; Michal F Kamiński; Maria Rupińska; Pradeep Bhandari; M G H van Oijen; L Koens; Barbara A J Bastiaansen; K M A J Tytgat; Paul Fockens; Evelien Dekker; Yark Hazewinkel Journal: Endosc Int Open Date: 2022-01-14
Authors: Tanja E Argillander; Jan J Koornstra; Mariette van Kouwen; Alexandra Mj Langers; Fokko M Nagengast; Juda Vecht; Wouter H de Vos Tot Nederveen Cappel; Evelien Dekker; Peter van Duijvendijk; Hans Fa Vasen Journal: United European Gastroenterol J Date: 2018-06-11 Impact factor: 4.623