Autoimmune Gastritis: Distinct Histological and Immunohistochemical Findings Before Complete Loss of Oxyntic Glands

Abstract

Autoimmune gastritis (AG) can be easily recognized when the histological features are fully developed, but recognizing AG before the complete loss of the oxyntic mucosa is more challenging. One feature of fully developed AG is enterochromaffin cell-like (ECL) hyperplasia, but its presence or absence in earlier stages of AG has not been fully evaluated. A retrospective study of biopsy specimens from 40 patients was performed; all of the patients were originally diagnosed with possible AG based on the presence of lymphocytic infiltration and damage to oxyntic glands and/or the presence of metaplastic epithelium that disproportionately involved the body mucosa. Nineteen cases had follow-up serological studies for anti-parietal cells and/or antiintrinsic factor antibodies: 13 were positive and 6 negative. The remaining 21 cases were indeterminate because of incomplete testing. The histological findings were similar in the patients who were serologically positive and those who were indeterminate for AG. In all of these cases, the oxyntic mucosa showed lymphoplasmacytic infiltrates within the lamina propria with focal gland infiltration and damage. Sixty-five percent (22/34) of the cases showed intestinal and/or pyloric metaplasia, and 85% (29/34) showed parietal cell pseudohypertrophy. Chromogranin stains were performed in 11 of 13 cases with positive serological markers for AG, and all showed at least linear ECL cell hyperplasia. In contrast, none of the six cases with negative serological studies had linear ECL cell hyperplasia, P < .001. In conclusion, the following constellation of findings supports a diagnosis of AG before the complete loss of oxyntic mucosa: deep or diffuse lymphoplasmacytic infiltrates within the lamina propria with foci of gland infiltration and damage, epithelial metaplasia, parietal cell pseudohypertrophy, and ECL cell hyperplasia at the linear or greater level.

Immunological and morphogenic basis of gastric mucosa atrophy and metaplasia

“…These results correspond well with the findings of anti-H,KATPase reactivity of antigastric autoantibodies in H. pylori gastritis just mentioned [17] and support the idea that in genetically susceptible individuals H. pylori infection triggers or accelerates the development of gastric autoimmunity [6]. Thus, H. pylori gastritis could progress to autoimmune gastritis via an intermediate stage described as active autoimmune gastritis without complete loss of glands [76,82]. This concept is strengthened by observations that this particular pre-atrophic phenotype of autoimmune gastritis improves after H. pylori therapy [58].…”

Gastrin suppresses the interdependent expression of p16 and anion exchanger 1 favoring growth inhibition of gastric cancer cells

“…Clinical studies showed that the hypergastrinemia was common in the patients with type A gastritis and gastric body cancer. 28,29 To clarify the relationship between gastrin and p16 in vivo, we first detected the expression of p16 in primary gastric body carcinoma by immunohistochemistry (86 cases, 25 early and 61 advanced gastric cancer patients). The results showed that the p16 protein was abundantly expressed in gastric cancer cell and mainly located in cytoplasm, compared with that in surrounding normal tissue (Figs.…”

Gastritis and gastropathy

“…Az intestinalis metaplasia ebben a szakaszban ritka és gócos. A parietalis sejtek számának nem egyértelmű csökkenésével járó korai AMAG jó jelzője a lamina propria mirigypusztulással járó, mély és diffúz lymphoplasmocytás beszű-rődése, az epithelialis metaplasia, a lineáris enterochromaffi n-like (ECL) -sejtes hyperplasia és a parietalis sejtek pseudohypertrophiája [17].…”