title: 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.
abstract: 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.
authors: Department of Pathology, University of Pavia and Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Policlinico San Matteo, 27100 Pavia, Italy.
authors: Alessandro
authors: A
authors: Vanoli
authors: Stefano
authors: S
authors: La Rosa
authors: Ombretta
authors: O
authors: Luinetti
authors: Catherine
authors: C
authors: Klersy
authors: Rachele
authors: R
authors: Manca
authors: Costanza
authors: C
authors: Alvisi
authors: Sandro
authors: S
authors: Rossi
authors: Erminio
authors: E
authors: Trespi
authors: Adriano
authors: A
authors: Zangrandi
authors: Fausto
authors: F
authors: Sessa
authors: Carlo
authors: C
authors: Capella
authors: Enrico
authors: E
authors: Solcia
mesh_terms: D015897:Comorbidity; D018450:Disease Progression; D016099:Endoscopy, Gastrointestinal; D004759:Enterochromaffin Cells / Q000473:pathology*; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000150:complications / Q000401:mortality / Q000473:pathology*; D006801:Humans; D006965:Hyperplasia; D007558:Italy / Q000453:epidemiology; D053208:Kaplan-Meier Estimate; D018358:Neuroendocrine Tumors / Q000209:etiology / Q000401:mortality / Q000473:pathology*; D011230:Precancerous Conditions / Q000473:pathology*; D011379:Prognosis; D011706:Pyloric Antrum / Q000473:pathology; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000150:complications / Q000401:mortality / Q000473:pathology*; D015996:Survival Rate
keywords: Dysplasia; ECL cell; Hyperplasia; Neuroendocrine tumor; Preneoplastic lesions; Stomach