Abstract

INTRODUCTION: The serrated group of colorectal polyps include hyperplastic polyps (HPs), sessile serrated polyps (SSPs), and traditional serrated adenomas (TSAs). HPs are generally non-precancerous whereas SSPs and TSAs are considered precancerous. TSAs are associated with high risk of subsequent (metachronous) advanced neoplasms, suggesting that TSAs reflect a predisposition for neoplastic progression. If true, the presence of one or more TSAs should be associated with synchronous advanced neoplasms. METHODS: Data was extracted from UCICQD—a prospectively collected database (2012–2019) inclusive of locations, sizes and pathology of all polyps and masses. A “neoplasm” was defined as carcinoma, adenoma, SSP, or TSAs regardless of size. Cases with advanced neoplasm were defined if any neoplasm was malignant, ≥1 cm, contained villous features or high grade dysplasia, or if ≥3 neoplasms of any size were found. TSAs cases were compared to cases of other lesions for rates and odds ratios of synchronous neoplasms and advanced neoplasms. RESULTS: A total of 6023 procedures with at least one HP, adenoma, SSP or TSA were included, of which 70 had one or more TSAs (TSA cases). No significant differences in age, body mass index, or gender were seen between TSA and non-TSA cases. TSA cases had a mean of 2.44 neoplasms compared to 1.72 in non-TSA cases (IIR = 1.42 [CI 1.05–1.92] P = 0.022) and were associated with increased numbers of SSPs (IIR = 1.83 [CI 1.04–3.22] P = 0.038) (Table 1). The fraction of cases with synchronous advanced neoplasia was significantly higher in TSA cases (0.786 ± 0.115) compared to cases with one or more adenomas (0.487 ± 0.016), HPs (0.327 ± 0.019) or SSPs (0.592 ± 0.034), P = 0.0002. Relative to cases with one or more HPs, odds ratios for advanced neoplasia were 1.95 (1.75–2.17), 2.98 (2.54–3.5) and 7.54 (4.23–13.44) for cases with adenoma, SSP and TSA, respectively (Table 2). CONCLUSION: Prior studies have shown that one or more index TSA(s) predict later risk for metachronous advanced neoplasms, more so than an index colorectal carcinoma. We show that the presence of one or more TSAs is also associated with higher risk for synchronous neoplasms and advanced neoplasms, especially SSPs. This suggests that TSA presence may reflect an unknown genetic predisposition and/or intestinal field defect that promotes tumor initiation and malignant progression. Regardless of underlying mechanisms, our data support an aggressive surveillance strategy for patients with one or more TSAs.

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