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Clinical and endoscopic predictors of cytological dysplasia or cancer in a prospective multicentre study of large sessile serrated adenomas/polyps
  1. Nicholas G Burgess1,2,
  2. Maria Pellise1,
  3. Kavinderjit S Nanda1,
  4. Luke F Hourigan3,4,
  5. Simon A Zanati5,6,
  6. Gregor J Brown5,7,
  7. Rajvinder Singh8,
  8. Stephen J Williams1,
  9. Spiro C Raftopoulos9,
  10. Donald Ormonde9,
  11. Alan Moss6,
  12. Karen Byth10,
  13. Heok P'Ng11,
  14. Duncan McLeod11,
  15. Michael J Bourke1,2
    1. 1Department of Gastroenterology and Hepatology, Westmead Hospital, Sydney, New South Wales, Australia
    2. 2Westmead Clinical School, University of Sydney, Sydney, New South Wales, Australia
    3. 3Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    4. 4Department of Gastroenterology and Hepatology, Greenslopes Private Hospital, Brisbane, Queensland, Australia
    5. 5Department of Gastroenterology and Hepatology, The Alfred Hospital, Melbourne, Victoria, Australia
    6. 6Department of Gastroenterology and Hepatology, Western Hospital, Melbourne, Victoria, Australia
    7. 7Department of Gastroenterology and Hepatology, Epworth Hospital, Melbourne, Victoria, Australia
    8. 8Department of Gastroenterology and Hepatology, Lyell McEwin Hospital, Adelaide, South Australia, Australia
    9. 9Department of Gastroenterology and Hepatology, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
    10. 10University of Sydney NHMRC Clinical Trials Centre, Sydney, New South Wales, Australia
    11. 11Institute of Clinical Pathology and Medical Research, Westmead Hospital, Sydney, New South Wales, Australia
    1. Correspondence to Professor Michael J Bourke, Director of Endoscopy, Department of Gastroenterology and Hepatology, Westmead Hospital, c/- Suite 106a, 151-155 Hawkesbury Road, Westmead, Sydney, NSW 2143, Australia; michael{at}


    Objective 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.

    Design 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.

    Results 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).

    Conclusions 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.

    Trial registration number NCT01368289.


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