PostScript believe that both the timeframe and study design imply a major negative effect on the external validity of this study. First of all, the long-term risk for CRC is assessed after an initial screening sigmoidoscopy performed between 1999 and 2001. As acknowledged by the authors, around this time, awareness of the neoplastic potential of SPs was not yet widespread and the general quality of colonoscopy was inferior compared with current practice. Therefore, many large SPs will probably not have been detected and, if detected, might not have been reported. Second, only those individuals with an adenoma or a large SP in the rectosigmoid were invited for full colonoscopy. Therefore, all large SPs in the right-sided colon in patients without relevant distal lesions were not detected. As a result, only 0.8% of participants were identified with at least one large SP. In a recent study, a prevalence rate of 2.7% was described in a similar, average risk-patient population.2 In this cohort, 1.1% of patients were diagnosed with at least one large SP in the right-sided colon without a synchronic adenoma or large SP in the distal colon (unpublished data). Analyses in the study of Holme et al are therefore performed on a minority of patients with large SPs making the outcome of this study unreliable. Since CRCs arising via the serrated neoplasia pathway are most often described in the right-sided colon, external validity seems even more compromised.3 Although providing unique data, the analysis concerning the natural course of large SPs seems underpowered. Analyses were performed on 23 detected but unresected large SPs. In a majority of cases, retrospectively collected data of the first follow-up colonoscopy were used to assess the behaviour of these lesions. In
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total, eight out of 23 lesions would have disappeared but these might as well have been missed during follow-up colonoscopy performed by non-expert endoscopists not aware of the significance of serrated lesions. Since no tattoo was placed next to the unresected polyp, it is unclear if endoscopists have evaluated the same lesion at follow-up colonoscopy. One patient with an unresected large SP developed CRC in another segment, while CRC developed in three patients in whom large SPs were detected at initial colonoscopy. Given the fact that all adenomas were removed in these patients, the CRC might also have resulted from missed SPs as well. Studies like the one performed by Holme et al are very important to gain a better understanding about the actual risk of SPs and the authors have tried to enhance the small amount of knowledge on this subject. However, only a prospectively designed study with expert endoscopists and structured colonoscopy reports will help resolve the uncertainty about this topic. Ethical considerations will have to be taken into account before such a study could be established. J E G IJspeert, B A J Bastiaansen, P Fockens, E Dekker Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands Correspondence to Dr Evelien Dekker, Department of Gastroenterology and Hepatology, Academic Medical Centre, Meibergdreef 9 1105 AZ, Amsterdam, The Netherlands; [email protected]
To cite IJspeert JEG, Bastiaansen BAJ, Fockens P, et al. Gut 2015;64:1007–1008. Received 13 December 2014 Revised 22 December 2014 Accepted 24 December 2014 Published Online First 14 January 2015
▸ http://dx.doi.org/10.1136/gutjnl-2014-307793 Gut 2015;64:1007–1008. doi:10.1136/gutjnl-2014-309020
REFERENCES 1
2
3
Holme O, Bretthauer M, Eide TJ, et al. Long-term risk of colorectal cancer in individuals with serrated polyps. Gut 2015;64:929–36. Hazewinkel Y, de Wijkerslooth TR, Stoop EM, et al. Prevalence of serrated polyps and association with synchronous advanced neoplasia in screening colonoscopy. Endoscopy 2014;46:219–24. Lash RH, Genta RM, Schuler CM. Sessile serrated adenomas: prevalence of dysplasia and carcinoma in 2139 patients. J Clin Pathol 2010;63:681–6.
Correction Kalla R, Ventham NT, Kennedy NA, et al. MicroRNAs: new players in inflammatory bowel disease. Gut 2015;64:504–13. The Open Access licence has been corrected to CC BY.
Contributors All authors contributed equally to this manuscript. Funding This research received no specific funding. Competing interests None. Provenance and peer review Not commissioned; internally peer reviewed.
Gut 2015;64:1008. doi:10.1136/gut.2014.307891corr1
Gut June 2015 Vol 64 No 6
Copyright of Gut is the property of BMJ Publishing Group and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
1008
total, eight out of 23 lesions would have disappeared but these might as well have been missed during follow-up colonoscopy performed by non-expert endoscopists not aware of the significance of serrated lesions. Since no tattoo was placed next to the unresected polyp, it is unclear if endoscopists have evaluated the same lesion at follow-up colonoscopy. One patient with an unresected large SP developed CRC in another segment, while CRC developed in three patients in whom large SPs were detected at initial colonoscopy. Given the fact that all adenomas were removed in these patients, the CRC might also have resulted from missed SPs as well. Studies like the one performed by Holme et al are very important to gain a better understanding about the actual risk of SPs and the authors have tried to enhance the small amount of knowledge on this subject. However, only a prospectively designed study with expert endoscopists and structured colonoscopy reports will help resolve the uncertainty about this topic. Ethical considerations will have to be taken into account before such a study could be established. J E G IJspeert, B A J Bastiaansen, P Fockens, E Dekker Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands Correspondence to Dr Evelien Dekker, Department of Gastroenterology and Hepatology, Academic Medical Centre, Meibergdreef 9 1105 AZ, Amsterdam, The Netherlands; [email protected]
To cite IJspeert JEG, Bastiaansen BAJ, Fockens P, et al. Gut 2015;64:1007–1008. Received 13 December 2014 Revised 22 December 2014 Accepted 24 December 2014 Published Online First 14 January 2015
▸ http://dx.doi.org/10.1136/gutjnl-2014-307793 Gut 2015;64:1007–1008. doi:10.1136/gutjnl-2014-309020
REFERENCES 1
2
3
Holme O, Bretthauer M, Eide TJ, et al. Long-term risk of colorectal cancer in individuals with serrated polyps. Gut 2015;64:929–36. Hazewinkel Y, de Wijkerslooth TR, Stoop EM, et al. Prevalence of serrated polyps and association with synchronous advanced neoplasia in screening colonoscopy. Endoscopy 2014;46:219–24. Lash RH, Genta RM, Schuler CM. Sessile serrated adenomas: prevalence of dysplasia and carcinoma in 2139 patients. J Clin Pathol 2010;63:681–6.
Correction Kalla R, Ventham NT, Kennedy NA, et al. MicroRNAs: new players in inflammatory bowel disease. Gut 2015;64:504–13. The Open Access licence has been corrected to CC BY.
Contributors All authors contributed equally to this manuscript. Funding This research received no specific funding. Competing interests None. Provenance and peer review Not commissioned; internally peer reviewed.
Gut 2015;64:1008. doi:10.1136/gut.2014.307891corr1
Gut June 2015 Vol 64 No 6
Copyright of Gut is the property of BMJ Publishing Group and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
