Histologic changes in type A chronic atrophic gastritis indicating increased risk of neuroendocrine tumor development: the predictive role of dysplastic and severely hyperplastic enterochromaffin-like cell lesions.

Détails

ID Serval
serval:BIB_16AE590F7D3F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Histologic changes in type A chronic atrophic gastritis indicating increased risk of neuroendocrine tumor development: the predictive role of dysplastic and severely hyperplastic enterochromaffin-like cell lesions.
Périodique
Human Pathology
Auteur(s)
Vanoli A., La Rosa S., Luinetti O., Klersy C., Manca R., Alvisi C., Rossi S., Trespi E., Zangrandi A., Sessa F., Capella C., Solcia E.
ISSN
1532-8392 (Electronic)
ISSN-L
0046-8177
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
44
Numéro
9
Pages
1827-1837
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
The role of putative preneoplastic enterochromaffin-like cell lesions, either hyperplastic or dysplastic, in the genesis of type 1 enterochromaffin-like cell neuroendocrine tumors associated with type A chronic atrophic gastritis, their actual neoplastic risk, and their precise histogenetic mechanism deserve further clarification by specific histopathologic studies coupled with patient follow-up. A total of 100 patients with severe type A chronic atrophic gastritis, enterochromaffin-like cell hyperplasia, and antral G-cell hyperplasia were endoscopically and histologically followed up for a median of 90.1 months (total of 9118 person-months). Preneoplastic enterochromaffin-like cell lesions and newly developed neuroendocrine tumors were investigated histologically and histochemically, in parallel with enterochromaffin-like cell lesions found in nontumor mucosa of another 32 well-characterized and previously reported type 1 neuroendocrine tumors. Both neuroendocrine and nonneuroendocrine mucosa changes were analyzed and statistically evaluated. During follow-up, 7 of 100 patients developed neuroendocrine tumors: 5 were in a group of 20 cases with previous enterochromaffin-like cell dysplasia and 2 were among 80 cases showing only enterochromaffin-like cell hyperplasia throughout the study (hazard ratio, 20.7; P < .001). The severity of enterochromaffin-like cell hyperplasia at first biopsy, with special reference to linear hyperplasia with 6 chains or more per linear millimeter, also increased the risk of neuroendocrine tumor development during follow-up (hazard ratio, 13.0; P < .001). Enterochromaffin-like cell microinvasive dysplastic lesions arising at the epithelial renewal zone level, in connection with immature proliferating mucous-neck cells, were found to be linked to early intramucosal neuroendocrine tumor histogenesis. Both enterochromaffin-like cell dysplasia and severe hyperplasia indicate increased risk of neuroendocrine tumor development in type A chronic atrophic gastritis with hypergastrinemia/G-cell hyperplasia.
Mots-clé
Comorbidity, Disease Progression, Endoscopy, Gastrointestinal, Enterochromaffin Cells/pathology, Follow-Up Studies, Gastric Mucosa/pathology, Gastritis, Atrophic/complications, Gastritis, Atrophic/mortality, Humans, Hyperplasia, Italy/epidemiology, Kaplan-Meier Estimate, Neuroendocrine Tumors/etiology, Neuroendocrine Tumors/mortality, Precancerous Conditions/pathology, Prognosis, Pyloric Antrum/pathology, Risk Factors, Stomach Neoplasms/complications, Stomach Neoplasms/mortality, Survival Rate
Pubmed
Web of science
Création de la notice
06/09/2016 12:57
Dernière modification de la notice
20/08/2019 12:46
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