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|Title:||Clinical and endoscopic predictors of cytological dysplasia or cancer in a prospective multicentre study of large sessile serrated adenomas/polyps|
|Epworth Authors:||Brown, Gregor|
|Other Authors:||Burgess, Nicholas|
|Keywords:||Trial Registration Number NCT01368289|
|Citation:||Gut. 2016 Mar;65(3):437-46.|
|Abstract:||The serrated neoplasia pathway accounts for up to 30% of all sporadic colorectal cancers (CRCs). Sessile serrated adenomas/polyps (SSA/Ps) with cytological dysplasia (SSA/P-D) are a high-risk serrated CRC precursor with little existing data. We aimed to describe the clinical and endoscopic predictors of SSA/P-D and high grade dysplasia (HGD) or cancer. Prospective multicentre data of SSA/Ps ≥20 mm referred for treatment by endoscopic mucosal resection (September 2008–July 2013) were analysed. Imaging and lesion assessment was standardised. Histological findings were correlated with clinical and endoscopic findings. 268 SSA/Ps were found in 207/1546 patients (13.4%). SSA/P-D comprised 32.4% of SSA/Ps ≥20 mm. Cancer occurred in 3.9%. On multivariable analysis, SSA/P-D was associated with increasing age (OR=1.69 per decade; 95% CI (1.19 to 2.40), p0.004) and increasing lesion size (OR=1.90 per 10 mm; 95% CI (1.30 to 2.78), p0.001), an ‘adenomatous’ pit pattern (Kudo III, IV or V) (OR=3.98; 95% CI (1.94 to 8.15), p<0.001) and any 0-Is component within a SSA/P (OR=3.10; 95% CI (1.19 to 8.12) p0.021). Conventional type dysplasia was more likely to exhibit an adenomatous pit pattern than serrated dysplasia. HGD or cancer was present in 7.2% and on multivariable analysis, was associated with increasing age (OR=2.0 per decade; 95% CI 1.13 to 3.56) p0.017) and any Paris 0-Is component (OR=10.2; 95% CI 3.18 to 32.4, p<0.001). Simple assessment tools allow endoscopists to predict SSA/P-D or HGD/cancer in SSA/Ps ≥20 mm. Correct prediction is limited by failure to recognise SSA/P-D which may mimic conventional adenoma. Understanding the concept of SSA/P-D and the pitfalls of SSA/P assessment may improve detection, recognition and resection and potentially reduce interval cancer.|
|Affiliated Organisations:||Department of Gastroenterology and Hepatology, Westmead Hospital, Sydney, New South Wales, Australia|
Westmead Clinical School, University of Sydney, Sydney, New South Wales, Australia
Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Queensland, Australia
Department of Gastroenterology and Hepatology, Greenslopes Private Hospital, Brisbane, Queensland, Australia.
Department of Gastroenterology and Hepatology, The Alfred Hospital, Melbourne, Victoria, Australia
Department of Gastroenterology and Hepatology, Western Hospital, Melbourne, Victoria, Australia
Department of Gastroenterology and Hepatology, Lyell McEwin Hospital, Adelaide, South Australia, Australia
Department of Gastroenterology and Hepatology, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
University of Sydney NHMRC Clinical Trials Centre, Sydney, New South Wales, Australia
Institute of Clinical Pathology and Medical Research, Westmead Hospital, Sydney, New South Wales, Australia
|Type of Clinical Study or Trial:||Prospective Observational Study|
|Appears in Collections:||Cancer Services|
General Surgery and Gastroenterology
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