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For many years, it was understood that the vast majority of the colorectal carcinomas in the general population evolved from conventional adenomas via the adenoma–carcinoma sequence. In 1990, Longacre and Fenoglio-Preiser first described polyps characterised by serrated architecture and unequivocal dysplasia1; these neoplastic polyps were subsequently called traditional serrated adenomas (TSAs).2 More recently, serrated colorectal polyps—hyperplastic polyps, sessile serrated adenoma/polyps (SSA/P)3 and TSAs3 ,4—have emerged as an alternative pathway of colorectal carcinogenesis. It has been estimated that in the general population about 30% of the CRC progress via the serrated pathway.3
So far, the histogenesis and natural history of TSAs have remained undisclosed.
A 73-year-old woman consulted for gastrointestinal bleeding. The patient had alopecia, nail atrophy, iron deficiency and anaemia. Colonoscopic and gastroscopic examinations disclosed multiple colorectal polyps and confluent gastroduodenal polyps, respectively. Histology showed to be cystic hamartomas. MRI showed no jejunal or ileum polyps. She had no chronic diarrhoea, protein-losing enteropathy, family history of polyposis or of colorectal cancer. Molecular genetic testing disclosed no SMAD4 or BMPR1A genes mutations.
Because of the dense colorectal polyposis and repeated bleedings, a subtotal colectomy was carried out under a diagnosis of Cronkhite-Canada syndrome (CCS). The …