ANZ journal of surgery · 2020
Patterns of polyp histology: predictors of peril in the mucosa.
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Dean Meara, Plesec Thomas, Kalady Matthew F, Church James
Аннотация
BACKGROUND: Precursor colonic polyps of varied subtypes correlate with the known neoplastic pathways. When patients present with synchronous pre-malignant polyps of multiple histologies, multiple genetic mechanisms are likely to be active, potentially resulting in a more unstable, tumourigenic mucosa.
METHODS: We hypothesized that patients with a combination of sessile serrated adenomas/polyps (SSA/Ps), hyperplastic (HP) polyps and adenomas would be at highest risk of developing dysplasia/cancer compared to SSA/Ps alone, due to the synergistic effect of multiple active carcinogenic pathways. A prospective colonoscopy database was examined for patients with a history of SSA/P. Patients were placed into four groups based on patterns of polyp histology as follows: (i) only SSA/Ps; (ii) SSA/P + HP; (iii) SSA/Ps + adenomas; and (iv) SSA/Ps + HP + adenomas. These groups were compared in terms of the numbers, size, location and histology of polyps and personal or family history of colorectal cancer.
RESULTS: A total of 374 patients were included. The average age was 70 years (range 21-88), and 43% were male. There was a trend towards the most aggressive neoplastic pattern in group 4, associated with a tendency to larger SSA/Ps, more villous architecture in the adenomas and more high-grade dysplasia in both types of polyps. It was also associated with multiplicity of both SSA/Ps and adenomas. No SSA/Ps existing in the absence of adenomas had cytological dysplasia.
CONCLUSION: The combination of SSA/Ps, HP and adenomas in the colorectal epithelium seems to be a marker for aggressive carcinogenesis and suggests that accurate and effective surveillance is important to manage this risk.
METHODS: We hypothesized that patients with a combination of sessile serrated adenomas/polyps (SSA/Ps), hyperplastic (HP) polyps and adenomas would be at highest risk of developing dysplasia/cancer compared to SSA/Ps alone, due to the synergistic effect of multiple active carcinogenic pathways. A prospective colonoscopy database was examined for patients with a history of SSA/P. Patients were placed into four groups based on patterns of polyp histology as follows: (i) only SSA/Ps; (ii) SSA/P + HP; (iii) SSA/Ps + adenomas; and (iv) SSA/Ps + HP + adenomas. These groups were compared in terms of the numbers, size, location and histology of polyps and personal or family history of colorectal cancer.
RESULTS: A total of 374 patients were included. The average age was 70 years (range 21-88), and 43% were male. There was a trend towards the most aggressive neoplastic pattern in group 4, associated with a tendency to larger SSA/Ps, more villous architecture in the adenomas and more high-grade dysplasia in both types of polyps. It was also associated with multiplicity of both SSA/Ps and adenomas. No SSA/Ps existing in the absence of adenomas had cytological dysplasia.
CONCLUSION: The combination of SSA/Ps, HP and adenomas in the colorectal epithelium seems to be a marker for aggressive carcinogenesis and suggests that accurate and effective surveillance is important to manage this risk.