Risk for gastric neoplasias in patients with chronic atrophic gastritis： A critical reappraisal

Chronic atrophic gastritis （CAG） is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue （non-metaplastic atrophy） or by glandular structures inappropriate for location （metaplastic atrophy）. Epidemiological data suggest that CAG...

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Bibliographic Details
Published in:World journal of gastroenterology : WJG 2012-03, Vol.18 (12), p.1279-1285
Main Authors: Vannella, Lucy, Lahner, Edith, Annibale, Bruno
Format: Article
Language:English
Subjects:
CAG
Carcinoid Tumor - etiology
Carcinoid Tumor - pathology
Gastric Mucosa - pathology
Gastritis, Atrophic - complications
Gastritis, Atrophic - epidemiology
Gastritis, Atrophic - pathology
Helicobacter Infections - complications
Helicobacter Infections - pathology
Helicobacter pylori - pathogenicity
Humans
Metaplasia - complications
Metaplasia - pathology
Neuroendocrine Tumors - etiology
Neuroendocrine Tumors - pathology
Risk Factors
Stomach Neoplasms - etiology
Stomach Neoplasms - pathology
幽门螺杆菌
患者
慢性炎症
胃炎
萎缩性
评估
风险因素
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Summary:Chronic atrophic gastritis （CAG） is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue （non-metaplastic atrophy） or by glandular structures inappropriate for location （metaplastic atrophy）. Epidemiological data suggest that CAG is associated with two different types of tumors： Intestinal-type gastric cancer （GC） and type I gastric carcinoid （T I GC）. The pathophysiological mechanisms which lead to the development of these gastric tumors are different, It is accepted that a multistep process initiating from Helico- bacterpylori-related chronic inflammation of the gastric mucosa progresses to CAG, intestinal metaplasia, dysplasia and, finally, leads to the development of GC. The T I GC is a gastrin-dependent tumor and the chronic elevation of gastrin, which is associated with CAG, stimulates the growth of enterochromaffin-like cells with their hyperplasia leading to the development of T I GC. Thus, several events occur in the gastric mucosa before the development of intestinatype GC and/ or T I GC and these take several years. Knowledge ofCAG incidence from superficial gastritis, its prevalence in different clinical settings and possible risk factors as- sociated with the progression of this condition to gastric neoplasias are important issues. This editorial intends to provide a brief review of the main studies regarding incidence and prevalence of CAG and risk factors for the development of gastric neoplasias.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v18.i12.1279