ArticleJournal of clinical pathology2007
Gastric duodenal metaplasia in duodenal adenomas.
Article in Journal of clinical pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Duodenal Gastric Metaplasia and Duodenal Neuroendocrine Neoplasms: More Than a Simple Coincidence?Journal of clinical medicine · 2022Article
- Endoscopic assessment and management of sporadic duodenal adenomas: The results of single centre multidisciplinary management.World journal of gastrointestinal endoscopy · 2017Article
- Nonampullary duodenal adenoma: Current understanding of its diagnosis, pathogenesis, and clinical management.World journal of gastroenterology · 2016Review
- Oral benzo[a]pyrene-induced cancer: two distinct types in different target organs depend on the mouse Cyp1 genotype.International journal of cancer · 2010Article
- Stem cells might participate in the cell turnover of duodenal adenomas.International journal of clinical and experimental pathology · 2009Article
- Inverted cystic tubulovillous adenoma involving Brunner's glands of duodenum.World journal of gastroenterology · 2007Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn cases of known aetiology, gastric duodenal metaplasia (GMD) is a reversible lesion. In cases of unknown aetiology, the fate of GMD remains elusive. GMD was recently found in a duodenal adenoma.
aimTo audit the frequency of GMD occurring in a cohort of duodenal adenomas.
methodsFiled H&E-stained sections from 306 consecutive duodenal adenomas were investigated for the presence of GMD.
results68% of the adenomas (n = 208) were from patients with familial adenomatous polyposis (FAP), and the remaining 32% (n = 98) were sporadic. GMD was found in 31.7% (66/208) of the duodenal FAP adenomas and in 59.2% (58/98) of the duodenal sporadic adenomas (p<0.05). The causes for this difference are elusive.
conclusionsAs for other metaplasias of the gastrointestinal tract (intestinal metaplasia of the oesophagus and of the stomach, and metaplastic-hyperplastic polyposis of the colon, known to antedate neoplastic transformation), a subset of GMDs of unknown cause might be present in the duodenal mucosa before adenomatous changes ensue. That subset of GMD might have neoplastic proclivity similar to the metaplastic epithelium in other organs of the gastrointestinal tract. The known carcinogenic effect of high concentrations of bile acids and pancreatic juices bathing the duodenal mucosa carrying an irreversible subset of GDM might set aflame the adenomatous neoplastic transformation in these patients.
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