scholarly journals Progression From Antral G-Cell Hyperplasia to Gastric Neuroendocrine Tumor in a Patient With Autoimmune Gastritis

2021 ◽  
Vol 8 (8) ◽  
pp. e00649
Author(s):  
Patrick Brown ◽  
Bhavana Tetali ◽  
Suraj Suresh ◽  
Adarsh Varma
2021 ◽  
Vol 156 (Supplement_1) ◽  
pp. S59-S60
Author(s):  
S Q Zia ◽  
S Chhetri Aryal ◽  
H Jaratli ◽  
Z Wang

Abstract Introduction/Objective Autoimmune gastritis (AG) is characterized by oxyntic glands destruction, metaplasia, enterochromaffin-like endocrine cell abnormality and G-cell hyperplasia with hypergastrinemia. The gastrin level can be extraordinarily high in certain cases to justify suspicion of Zollinger-Ellison syndrome. We herein report one such case and discuss clinical implication of a grading system for G-cell hyperplasia to correlate histology with gastrin levels. Methods/Case Report The patient was a symptomatic 65 year-old female with hypergastrinemia (2,068 pg/mL), negative abdomen/pelvis CT scan, positive anti-intrinsic factor and anti-parietal cell antibodies. Under esophagogastroduodenoscopy, biopsies were obtained from gastric cardia, fundus, corpus, incisura angularis, and antrum. Morphology and immunostains confirmed autoimmune gastritis. Diffuse linear pattern G-cell hyperplasia was evident in antrum and incisura angularis, counting up to 200 G-cells per linear millimeter. One study defined G-cell hyperplasia as >140 gastrin-positive cells per linear millimeter while another proposed a 2-tier stratification, i.e., simple hyperplasia (4-5 cells for each gland) and linear hyperplasia (continuous chain-like distribution of G-cells). Such scoring, however, was largely qualitative and fell short in delineating the extent of G-cell hyperplasia and correlation with gastrinemia. Results (if a Case Study enter NA) NA Conclusion Lack of G-cell grading system hindered our unequivocal determination of the G-cell hyperplasia as underlying or contributing cause of hypergastrenemia. The unique features of our case highlighted the necessity for installing a practical grading system that incorporates G-cell density, pattern (linear vs. nodular), extent of involved areas, other features of AG to correspond to gastrin level. With accumulation of clinical information, one such grading system is feasible and will improve our knowledge and patient care.


2020 ◽  
Vol 59 (6) ◽  
pp. 799-803
Author(s):  
Hirotaka Watanabe ◽  
Sho Yoneda ◽  
Yuichi Motoyama ◽  
Kosuke Mukai ◽  
Yosuke Okuno ◽  
...  

1988 ◽  
Vol 33 (7) ◽  
pp. 795-800 ◽  
Author(s):  
G. E. Feurle ◽  
K. Tischbirek ◽  
I. Baća

1999 ◽  
Vol 277 (1) ◽  
pp. G209-G218 ◽  
Author(s):  
Louise M. Judd ◽  
Paul A. Gleeson ◽  
Ban-Hock Toh ◽  
Ian R. van Driel

We have investigated the underlying basis of the lesion in murine autoimmune gastritis, a model of the human disease pernicious anemia. The disease is mediated by T lymphocytes and characterized by selective depletion of parietal and zymogenic cells from the gastric unit (gland) together with gastric epithelial cell hyperplasia. The gastric units of gastritic stomachs contained 2.3-fold more cells than normal and accumulated rapidly dividing, short-lived gastric epithelial stem cells and mucous neck cells. Most of these immature cells failed to differentiate into end-stage cells but rather appeared to die by apoptosis. We also found no correlation between anti-parietal cell autoantibody titers and the degree of gastric pathology, providing further evidence that autoantibodies do not play a direct role in the pathogenesis of gastritis. Taken together, the normal developmental pathways of the gastric mucosa are disrupted in autoimmune gastritis, resulting in an amplification of immature cell types. The differentiation of these immature cells appears to be blocked, contributing to depletion of end-stage cells. This scenario provides an explanation for depletion of not only parietal cells but also zymogenic cells even though they are not directly targeted by the immune system.


Sign in / Sign up

Export Citation Format

Share Document