Objective: We present the case of a 57-year-old man with a history of Roux-en-Y gastric bypass (RYGB) and colonic polyps who presented with an upper gastrointestinal obstruction based on massive stomach polyposis in the pouch.
Methods: Two months prior to this acute admission, he had undergone resection of the gastric remnant due to massive refractory intraluminal bleeding from a polypoid mass. Ten years earlier, right colectomy was performed due to hypertrophic polyposis unsuitable for endoscopic polypectomy. Upper gastrointestinal endoscopy showed a polypoid mass in the pouch causing obstruction. Benign biopsies were obtained. A resection of the stomach pouch with esophagojejunostomy was performed. Macroscopic evaluation of the pouch lumen showed massive polyposis with a sharp demarcation near the Z-line and at the gastrojejunostomy. On clinical examination, the presence of atrophic nail changes, alopecia, and palmar hyperpigmentation was noticed.
Results: Postoperative course was uneventful and feeding was restarted successfully. Histological analysis revealed hyperplastic polypoid tissue, which resembled the polyps in the stomach remnant and colon. Together with the ectodermal changes, the diagnose of Cronkhite-Canada syndrome was established.
Conclusion: Diffuse polyposis in Cronkhite-Canada syndrome is a rare cause for pouch obstruction after RYGB. Clinical examination should focus on dermatologic findings.
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http://dx.doi.org/10.1080/00015458.2017.1411556 | DOI Listing |
Clin Nucl Med
December 2024
From the Department of Neurology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine.
Gardner syndrome is characterized by multiple intestinal polyps and extraintestinal lesions. We describe FDG PET/CT findings of the extraintestinal lesions in a patient with Gardner syndrome. FDG PET/CT showed 2 hypermetabolic desmoid tumors in the abdominal wall, sclerotic areas with multifocal activity in the maxilla and mandible, multiple osteomas in the bilateral parietal, left frontal, sphenoid and ethmoid bones, an impacted tooth in the right maxilla, and bone islands in the T2 and T5 vertebral bodies.
View Article and Find Full Text PDFBJS Open
December 2024
Unit of Hereditary Digestive Tract Tumours, Fondazione IRCCS Istituto Nazionale dei Tumouri, Milan, Italy.
Background: Familial adenomatous polyposis is a cancer-predisposing syndrome caused by germline pathogenic variants of the adenomatous polyposis coli gene, leading to numerous colorectal polyps and a high risk of colorectal cancer. Desmoid tumours have become significant in the management of familial adenomatous polyposis after a colectomy, yet the exact incidence remains undetermined due to a lack of dedicated surveillance.
Methods: This retrospective study accessed data from the prospectively maintained Hereditary Digestive Tumours Registry from 2000 to 2023.
Transgenic Res
January 2025
Laboratory of Cell and Developmental Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Videnska 1083, 142 20, Prague 4, Czech Republic.
Proto-oncogene KRAS, GTPase (KRAS) is one of the most intensively studied oncogenes in cancer research. Although several mouse models allow for regulated expression of mutant KRAS, selective isolation and analysis of transforming or tumor cells that produce the KRAS oncogene remains a challenge. In our study, we present a knock-in model of oncogenic variant KRAS that enables the "activation" of KRAS expression together with production of red fluorescent protein tdTomato.
View Article and Find Full Text PDFNature
January 2025
Department of Medical Oncology and Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Oncogenic mutations that drive colorectal cancer can be present in healthy intestines for long periods without overt consequence. Mutation of Adenomatous polyposis coli (Apc), the most common initiating event in conventional adenomas, activates Wnt signalling, hence conferring fitness on mutant intestinal stem cells (ISCs). Apc mutations may occur in ISCs that arose by routine self-renewal or by dedifferentiation of their progeny.
View Article and Find Full Text PDFFam Cancer
January 2025
Department of Gastroenterology and Hepatology, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, Cancer Center Amsterdam, Amsterdam, The Netherlands.
Several extra-colonic manifestations, including duodenal polyposis and desmoid tumors, are well-described manifestations in familial adenomatous polyposis (FAP). More recently, an increase in gastric cancer diagnoses has been observed in FAP. This case series presents nine patients with FAP who were diagnosed with gastric cancer at our FAP expertise center, of whom eight were diagnosed between 2017 and 2023, while before 2017 the only diagnosis of gastric cancer was in 2001.
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