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2015 ; 21
(42
): 12179-89
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Autoimmune gastritis: Pathologist s viewpoint
#MMPMID26576102
Coati I
; Fassan M
; Farinati F
; Graham DY
; Genta RM
; Rugge M
World J Gastroenterol
2015[Nov]; 21
(42
): 12179-89
PMID26576102
show ga
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.