Published online Nov 14, 2015. doi: 10.3748/wjg.v21.i42.12179
Peer-review started: February 26, 2015
First decision: June 2, 2015
Revised: June 15, 2015
Accepted: September 2, 2015
Article in press: September 2, 2015
Published online: November 14, 2015
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.
Core tip: Autoimmune gastritis (AIG) is an emerging gastropathy with a significant epidemiological and clinical impact on Western populations. Despite a better understanding of the phenotypic changes or cascades occurring in this autoimmune setting, the etiopathogenic mechanisms behind the disease are still poorly understood, histology reporting is not standardized, and both the AIG-associated cancer risk and its secondary prevention strategies remain confusing.