Pathology · 2013
Autoimmune gastritis: novel clues to histological diagnosis.
Сравнительное исследованиеСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Bettington Mark, Brown Ian
Аннотация
AIMS: To compare the histological features of a consecutive biopsy series of autoimmune gastritis (AIG) with other forms of chronic gastritis to identify morphological clues to the diagnosis.
METHODS: Morphological features in gastric biopsies were examined in 42 prospectively identified patients with AIG without concomitant neoplasia (n = 184 biopsies), 50 normal controls (NGB; n = 118 biopsies), 52 Helicobacter associated gastritis (HPG; n = 123 biopsies), 16 multifocal atrophic gastritis (MAG; n = 62 biopsies) and 50 chronic pangastritis without defined cause (CG; n = 117 biopsies).
RESULTS: In AIG, inflammation was characterised by lymphocyte infiltration into the epithelium (98%), basal lymphoid aggregates (82.7%), basal predominance (59.6%), eosinophil infiltration [mean 34.5/high power field (HPF), >30 eosinophils/HPF in 46.1%] and neutrophil infiltration (44.2%). Architectural abnormality was characterised by muscularis mucosae thickening (92.9%) and gland irregularity (86.5%). Pancreatic metaplasia was identified in 21.2% of cases. Compared to NGB, HPG, MAG and CG, AIG displayed more eosinophil infiltration (p < 0.001) and more frequent lymphocyte infiltration of the epithelium, basal predominant inflammation and pancreatic acinar metaplasia (all p > 0.05).
CONCLUSIONS: Basal predominance of inflammation, lymphocyte infiltration into gland epithelium, prominent eosinophils, architectural irregularity and muscularis mucosae thickening are common in AIG and are helpful when biopsy site and/or clinical history is uncertain.
METHODS: Morphological features in gastric biopsies were examined in 42 prospectively identified patients with AIG without concomitant neoplasia (n = 184 biopsies), 50 normal controls (NGB; n = 118 biopsies), 52 Helicobacter associated gastritis (HPG; n = 123 biopsies), 16 multifocal atrophic gastritis (MAG; n = 62 biopsies) and 50 chronic pangastritis without defined cause (CG; n = 117 biopsies).
RESULTS: In AIG, inflammation was characterised by lymphocyte infiltration into the epithelium (98%), basal lymphoid aggregates (82.7%), basal predominance (59.6%), eosinophil infiltration [mean 34.5/high power field (HPF), >30 eosinophils/HPF in 46.1%] and neutrophil infiltration (44.2%). Architectural abnormality was characterised by muscularis mucosae thickening (92.9%) and gland irregularity (86.5%). Pancreatic metaplasia was identified in 21.2% of cases. Compared to NGB, HPG, MAG and CG, AIG displayed more eosinophil infiltration (p < 0.001) and more frequent lymphocyte infiltration of the epithelium, basal predominant inflammation and pancreatic acinar metaplasia (all p > 0.05).
CONCLUSIONS: Basal predominance of inflammation, lymphocyte infiltration into gland epithelium, prominent eosinophils, architectural irregularity and muscularis mucosae thickening are common in AIG and are helpful when biopsy site and/or clinical history is uncertain.