TY - JOUR
T1 - Autoimmune gastritis
T2 - Pathologist's viewpoint
AU - Coati, Irene
AU - Fassan, Matteo
AU - Farinati, Fabio
AU - Graham, David Y.
AU - Genta, Robert M.
AU - Rugge, Massimo
N1 - Publisher Copyright:
© 2015 Baishideng Publishing Group Inc. All rights reserved.
PY - 2015/11/14
Y1 - 2015/11/14
N2 - Western countries are seeing a constant decline in the incidence of Helicobacter pylori-associated gastritis, coupled with a rising epidemiological and clinical impact of autoimmune gastritis. This latter gastropathy is due to autoimmune aggression targeting parietal cells through a complex interaction of auto-antibodies against the parietal cell proton pump and intrinsic factor, and sensitized T cells. Given the specific target of this aggression, autoimmune gastritis is typically restricted to the gastric corpus-fundus mucosa. In advanced cases, the oxyntic epithelia are replaced by atrophic (and metaplastic) mucosa, creating the phenotypic background in which both gastric neuroendocrine tumors and (intestinal-type) adenocarcinomas may develop. Despite improvements in our understanding of the phenotypic changes or cascades occurring in this autoimmune setting, no reliable biomarkers are available for identifying patients at higher risk of developing a gastric neoplasm. The standardization of autoimmune gastritis histology reports and classifications in diagnostic practice is a prerequisite for implementing definitive secondary prevention strategies based on multidisciplinary diagnostic approaches integrating endoscopy, serology, histology and molecular profiling.
AB - Western countries are seeing a constant decline in the incidence of Helicobacter pylori-associated gastritis, coupled with a rising epidemiological and clinical impact of autoimmune gastritis. This latter gastropathy is due to autoimmune aggression targeting parietal cells through a complex interaction of auto-antibodies against the parietal cell proton pump and intrinsic factor, and sensitized T cells. Given the specific target of this aggression, autoimmune gastritis is typically restricted to the gastric corpus-fundus mucosa. In advanced cases, the oxyntic epithelia are replaced by atrophic (and metaplastic) mucosa, creating the phenotypic background in which both gastric neuroendocrine tumors and (intestinal-type) adenocarcinomas may develop. Despite improvements in our understanding of the phenotypic changes or cascades occurring in this autoimmune setting, no reliable biomarkers are available for identifying patients at higher risk of developing a gastric neoplasm. The standardization of autoimmune gastritis histology reports and classifications in diagnostic practice is a prerequisite for implementing definitive secondary prevention strategies based on multidisciplinary diagnostic approaches integrating endoscopy, serology, histology and molecular profiling.
KW - Autoimmune gastritis
KW - Carcinoids
KW - Metaplasia
KW - Operative link for gastritis assessment staging
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U2 - 10.3748/wjg.v21.i42.12179
DO - 10.3748/wjg.v21.i42.12179
M3 - Review article
C2 - 26576102
AN - SCOPUS:84947460429
SN - 1007-9327
VL - 21
SP - 12179
EP - 12189
JO - World Journal of Gastroenterology
JF - World Journal of Gastroenterology
IS - 42
ER -