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Increasing rates of SSA/P detection in a large open-access Australian colonoscopy cohort

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      Abstract

      Background and study aims  There are limited longitudinal data regarding detection rates for sessile serrated adenoma/polyps (SSADR) and right-sided hyperplastic polyps (RHPDR) that constitute the proximal serrated lesion detection rate (PSLDR). Recently, a minimum PSLDR of 4.5 % has been suggested. This study was designed to assess SSADR, PSLDR and adenoma detection rate (ADR) for a newly qualified gastroenterologist and compare them to published data and to assess the change in SSADR, PSLDR and ADR over time for potential improvement with experience. Patients and methods  All colonoscopies performed by a single colonoscopist (AM), at one Australian ambulatory direct-access endoscopy center over 4 years from 2011 to 2015 were retrospectively analyzed. Histology was reported by a single expert pathologist (SL). ADR, SSADR, RHPDR and PSLDR were recorded. Results  A total of 841 colonoscopies were performed on 637 patients. Of them, 454 (54 %) were males. Mean age was 59 years. Of the colonoscopies, 87 % were performed for patients with ASA scores of 1 – 2, 422 (50.2 %) were for screening or surveillance, 374 (44.5 %) for investigation of symptoms and 45 (5.4 %) had therapeutic indications. Conventional adenomas were detected in 346 colonoscopies (ADR = 41.1 %), SSA/P in 124 (SSADR = 14.7 %) and RHP in the absence of SSA/P in 35 (RHPDR = 4.2 %). PSLDR was 18.9 %. ADR was stable over time (range 33 %-50 %). SSADR and PSLDR increased over time [SSADR: 8.6 % (2011), 8.4 % (2012), 14.9 % (2013), 18.5 % (2014), 25.0 % (2015); PSLDR: 10.5 % (2011), 11.3 % (2012), 16.8 % (2013), 27.2 % (2014), 29.4 % (2015)]. There was a statistically significant improvement in SSADR (IRR 1.37) and PSLDR (IRR 1.36) over the study period ( P  < 0.001), whereas the ADR remained stable (IRR 1.04, P  = 0.334). Conclusions  SSADR and PSLDR in this unselected direct-access cohort are high and exceed previously reported detection rates in the final 2 years. Detection rates improved with experience, likely representing a learning effect. The minimum expected PSLDR may need to be revised upwards and further studies are required, particularly in areas where screening colonoscopies are offered only for patients with increased colorectal cancer risk (family history or fecal immunochemical test-positive).

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      Most cited references 13

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      Genetic alterations during colorectal-tumor development.

      Because most colorectal carcinomas appear to arise from adenomas, studies of different stages of colorectal neoplasia may shed light on the genetic alterations involved in tumor progression. We looked for four genetic alterations (ras-gene mutations and allelic deletions of chromosomes 5, 17, and 18) in 172 colorectal-tumor specimens representing various stages of neoplastic development. The specimens consisted of 40 predominantly early-stage adenomas from 7 patients with familial adenomatous polyposis, 40 adenomas (19 without associated foci of carcinoma and 21 with such foci) from 33 patients without familial polyposis, and 92 carcinomas resected from 89 patients. We found that ras-gene mutations occurred in 58 percent of adenomas larger than 1 cm and in 47 percent of carcinomas. However, ras mutations were found in only 9 percent of adenomas under 1 cm in size. Sequences on chromosome 5 that are linked to the gene for familial adenomatous polyposis were not lost in adenomas from the patients with polyposis but were lost in 29 to 35 percent of adenomas and carcinomas, respectively, from other patients. A specific region of chromosome 18 was deleted frequently in carcinomas (73 percent) and in advanced adenomas (47 percent) but only occasionally in earlier-stage adenomas (11 to 13 percent). Chromosome 17p sequences were usually lost only in carcinomas (75 percent). The four molecular alterations accumulated in a fashion that paralleled the clinical progression of tumors. These results are consistent with a model of colorectal tumorigenesis in which the steps required for the development of cancer often involve the mutational activation of an oncogene coupled with the loss of several genes that normally suppress tumorigenesis.
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        Quality indicators for colonoscopy and the risk of interval cancer.

        Although rates of detection of adenomatous lesions (tumors or polyps) and cecal intubation are recommended for use as quality indicators for screening colonoscopy, these measurements have not been validated, and their importance remains uncertain. We used a multivariate Cox proportional-hazards regression model to evaluate the influence of quality indicators for colonoscopy on the risk of interval cancer. Data were collected from 186 endoscopists who were involved in a colonoscopy-based colorectal-cancer screening program involving 45,026 subjects. Interval cancer was defined as colorectal adenocarcinoma that was diagnosed between the time of screening colonoscopy and the scheduled time of surveillance colonoscopy. We derived data on quality indicators for colonoscopy from the screening program's database and data on interval cancers from cancer registries. The primary aim of the study was to assess the association between quality indicators for colonoscopy and the risk of interval cancer. A total of 42 interval colorectal cancers were identified during a period of 188,788 person-years. The endoscopist's rate of detection of adenomas was significantly associated with the risk of interval colorectal cancer (P=0.008), whereas the rate of cecal intubation was not significantly associated with this risk (P=0.50). The hazard ratios for adenoma detection rates of less than 11.0%, 11.0 to 14.9%, and 15.0 to 19.9%, as compared with a rate of 20.0% or higher, were 10.94 (95% confidence interval [CI], 1.37 to 87.01), 10.75 (95% CI, 1.36 to 85.06), and 12.50 (95% CI, 1.51 to 103.43), respectively (P=0.02 for all comparisons). The adenoma detection rate is an independent predictor of the risk of interval colorectal cancer after screening colonoscopy. 2010 Massachusetts Medical Society
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          Serrated lesions of the colorectum: review and recommendations from an expert panel.

          Serrated lesions of the colorectum are the precursors of perhaps one-third of colorectal cancers (CRCs). Cancers arising in serrated lesions are usually in the proximal colon, and account for a disproportionate fraction of cancer identified after colonoscopy. We sought to provide guidance for the clinical management of serrated colorectal lesions based on current evidence and expert opinion regarding definitions, classification, and significance of serrated lesions. A consensus conference was held over 2 days reviewing the topic of serrated lesions from the perspectives of histology, molecular biology, epidemiology, clinical aspects, and serrated polyposis. Serrated lesions should be classified pathologically according to the World Health Organization criteria as hyperplastic polyp, sessile serrated adenoma/polyp (SSA/P) with or without cytological dysplasia, or traditional serrated adenoma (TSA). SSA/P and TSA are premalignant lesions, but SSA/P is the principal serrated precursor of CRCs. Serrated lesions have a distinct endoscopic appearance, and several lines of evidence suggest that on average they are more difficult to detect than conventional adenomatous polyps. Effective colonoscopy requires an endoscopist trained in the endoscopic appearance of serrated lesions. We recommend that all serrated lesions proximal to the sigmoid colon and all serrated lesions in the rectosigmoid > 5 mm in size, be completely removed. Recommendations are made for post-polypectomy surveillance of serrated lesions and for surveillance of serrated polyposis patients and their relatives.
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            Author and article information

            Affiliations
            [1 ]Department of Endoscopic Services, Western Health, Melbourne, Australia
            [2 ]Department of Medicine – Western Health, Melbourne Medical School, The University of Melbourne, Victoria, Australia
            [3 ]Department of Anatomical Pathology, St John of God Pathology, Victoria, Australia
            [4 ]Chesterville Endoscopy, Chesterville Day Hospital, Cheltenham, Victoria, Australia
            Author notes
            Corresponding author Alan Moss Director of Endoscopic Services, Western Health Gordon St, Footscray 3011Melbourne, VictoriaAustralia+61 3 83457378 alan.moss@ 123456wh.org.au
            Journal
            Endosc Int Open
            Endosc Int Open
            10.1055/s-00025476
            Endoscopy International Open
            © Georg Thieme Verlag KG (Stuttgart · New York )
            2364-3722
            2196-9736
            March 2019
            28 February 2019
            : 7
            : 3
            : E310-E316
            6395094
            10.1055/a-0808-3523

            This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited.

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