Cancers (Basel). 2024 Mar 28;16(7):1310. doi: 10.3390/cancers16071310.
AIG에 대해 최근까지 발표된 내용들을 정리한 review 가 있어서 올려 봅니다.
1. Introduction
* Autoimmune atrophic gastritis (AAG): chronic "condition" in which the immune system attacks and damages the oxyntic mucosa of the stomach through the production of anti-parietal cell antibodies and/or anti-intrinsic factor antibodies. (condition과 lesion은 전혀 다른 의미이며, AIG는 chronic condition 입니다.)
* Pathogenesis: primary involvement of cellular immunity promoted by the CD4+Th1 response; gastric parietal cells에 대한 autoantibodies는 autoreactive Th1 cells을 유도하여 H+/K+ ATPase의 손상을 일으킴.
* The inflammatory response leads to the destruction or loss of parietal cells normally involved in the production of gastric acid and intrinsic factors.
Figure 1. Pathogenesis, diagnosis, clinical presentation of autoimmune atrophic gastritis, and risk of malignancy.
ECL: enterochromaffin-like.
Table 1. Recent findings in the topic of atrophic autoimmune gastritis.
Figure 2. Histological features of autoimmune atrophic gastritis. (a). Oxyntic mucosa with diffuse pseudopyloric and intestinal metaplasia (hematoxylin-eosin staining) (10× magnification). (b). Intraglandular linear and nodular hyperplasia of the enterochromaffin-like cells (chromogranin A staining) (20× magnification). (c). Hyperplasia of gastrin G cells in antrum (hematoxylin-eosin staining) (20× magnification).
Figure 3. Neuroendocrine tumor (NET) G1, diameter: 3 mm, ki-67: 1.4%. (a). Hematoxylin-eosin staining (20× magnification). (b). Immunohistochemical staining for synaptophysin (20× magnification). (c). Immunohistochemical staining for SSTR2 (20× magnification). (d). Immunohistochemical staining for ki67 (40× magnification).
8. Conclusions
The epidemiology of AAG is still unclear, as this condition is often misdiagnosed, especially in subclinical forms, and is potentially underestimated due to the absence of standard diagnostic criteria. The etiopathogenesis of AAG is not well defined, requiring further studies investigating the possible pathogenesis of this condition. Recently, a new concept of “potential” AAG has been introduced, defined by the presence of anti-parietal cell antibodies in the absence of gastric histopathological atrophy and H. pylori infection. More studies are needed to investigate the natural history of AAG and to highlight possible risk factors associated with a more rapid and severe evolution of the disease. While the association between NETs and AAG is well known, the risk of gastric cancer is still under debate. Several cohort studies with a long follow-up on AAG patients reported the absence of gastric cancer cases and explained how the presence of gastric cancer could plausibly result from previous/current H. pylori infection rather than AAG. Autoimmune atrophic gastritis does not benefit from specific treatment, and the management of patients with AAG aims to correct iron and vitamin deficiencies; therefore, an early diagnosis of AAG is required to guarantee appropriate iron and vitamin B12 supplementation, possibly before the onset of anemia and neurological symptoms. An appropriate endoscopic follow-up is required for the early detection of gastric neoplasia in patients with AAG. New treatments able to reduce gastric inflammation and prevent the development and progression of atrophy are needed.
Simple Summary: Autoimmune atrophic gastritis can lead to serious conditions, including malabsorption and vitamin deficiencies, that may cause anemia, neurological disorders, and gastric malignancies. This paper provides recent evidence on the pathogenesis, diagnosis, clinical presentation, risk of malignancies, endoscopic surveillance, and treatment of autoimmune atrophic gastritis. This review provides a valuable update for healthcare professionals and researchers, and the findings may help improve the diagnosis and management of patients with autoimmune atrophic gastritis, leading to improved outcomes and shaping future research directions.
Abstract: Autoimmune atrophic gastritis (AAG) is a chronic condition characterized by the presence of atrophy in the oxyntic mucosa due to anti-parietal cell antibodies. This review provides a comprehensive and up-to-date overview of autoimmune atrophic gastritis, reporting recent evidence on epidemiology, pathogenesis, diagnosis, clinical presentation, risk of malignancies, and management. The prevalence of AAG has been estimated at between 0.3% and 2.7% in the general population. The diagnosis of AAG is based on a combination of the serologic profile and the histological examination of gastric biopsies. Patients with AAG are often asymptomatic but can also have dyspeptic or reflux symptoms. The atrophy of the oxyntic mucosa leads to iron and vitamin B12 malabsorption, which may result in anemia and neurological affections. Autoimmune atrophic gastritis is associated with an increased risk of type I neuroendocrine tumors (NETs) and gastric cancer, with an incidence rate of 2.8% and 0.5% per person/year, respectively. Management is directed to reinstate vitamins and iron and to prevent malignancies with endoscopic surveillance. In conclusion, atrophic autoimmune gastritis is an infrequent condition, often asymptomatic and misdiagnosed, that requires an early diagnosis for appropriate vitamin supplementation and endoscopic follow-up for the early diagnosis of NETs and gastric cancer. Keywords: autoimmune atrophic gastritis; anti-parietal cell antibodies; gastric carcinoids
Cancers (Basel). 2024 Mar 28;16(7):1310. doi: 10.3390/cancers16071310.
AIG에 대해 최근까지 발표된 내용들을 정리한 review 가 있어서 올려 봅니다.
1. Introduction
* Autoimmune atrophic gastritis (AAG): chronic "condition" in which the immune system attacks and damages the oxyntic mucosa of the stomach through the production of anti-parietal cell antibodies and/or anti-intrinsic factor antibodies. (condition과 lesion은 전혀 다른 의미이며, AIG는 chronic condition 입니다.)
* Pathogenesis: primary involvement of cellular immunity promoted by the CD4+Th1 response; gastric parietal cells에 대한 autoantibodies는 autoreactive Th1 cells을 유도하여 H+/K+ ATPase의 손상을 일으킴.
* The inflammatory response leads to the destruction or loss of parietal cells normally involved in the production of gastric acid and intrinsic factors.
Figure 1. Pathogenesis, diagnosis, clinical presentation of autoimmune atrophic gastritis, and risk of malignancy.
ECL: enterochromaffin-like.
Table 1. Recent findings in the topic of atrophic autoimmune gastritis.
Figure 2. Histological features of autoimmune atrophic gastritis. (a). Oxyntic mucosa with diffuse pseudopyloric and intestinal metaplasia (hematoxylin-eosin staining) (10× magnification). (b). Intraglandular linear and nodular hyperplasia of the enterochromaffin-like cells (chromogranin A staining) (20× magnification). (c). Hyperplasia of gastrin G cells in antrum (hematoxylin-eosin staining) (20× magnification).
Figure 3. Neuroendocrine tumor (NET) G1, diameter: 3 mm, ki-67: 1.4%. (a). Hematoxylin-eosin staining (20× magnification). (b). Immunohistochemical staining for synaptophysin (20× magnification). (c). Immunohistochemical staining for SSTR2 (20× magnification). (d). Immunohistochemical staining for ki67 (40× magnification).
8. Conclusions
The epidemiology of AAG is still unclear, as this condition is often misdiagnosed, especially in subclinical forms, and is potentially underestimated due to the absence of standard diagnostic criteria. The etiopathogenesis of AAG is not well defined, requiring further studies investigating the possible pathogenesis of this condition. Recently, a new concept of “potential” AAG has been introduced, defined by the presence of anti-parietal cell antibodies in the absence of gastric histopathological atrophy and H. pylori infection. More studies are needed to investigate the natural history of AAG and to highlight possible risk factors associated with a more rapid and severe evolution of the disease. While the association between NETs and AAG is well known, the risk of gastric cancer is still under debate. Several cohort studies with a long follow-up on AAG patients reported the absence of gastric cancer cases and explained how the presence of gastric cancer could plausibly result from previous/current H. pylori infection rather than AAG. Autoimmune atrophic gastritis does not benefit from specific treatment, and the management of patients with AAG aims to correct iron and vitamin deficiencies; therefore, an early diagnosis of AAG is required to guarantee appropriate iron and vitamin B12 supplementation, possibly before the onset of anemia and neurological symptoms. An appropriate endoscopic follow-up is required for the early detection of gastric neoplasia in patients with AAG. New treatments able to reduce gastric inflammation and prevent the development and progression of atrophy are needed.
Simple Summary: Autoimmune atrophic gastritis can lead to serious conditions, including malabsorption and vitamin deficiencies, that may cause anemia, neurological disorders, and gastric malignancies. This paper provides recent evidence on the pathogenesis, diagnosis, clinical presentation, risk of malignancies, endoscopic surveillance, and treatment of autoimmune atrophic gastritis. This review provides a valuable update for healthcare professionals and researchers, and the findings may help improve the diagnosis and management of patients with autoimmune atrophic gastritis, leading to improved outcomes and shaping future research directions.
Abstract: Autoimmune atrophic gastritis (AAG) is a chronic condition characterized by the presence of atrophy in the oxyntic mucosa due to anti-parietal cell antibodies. This review provides a comprehensive and up-to-date overview of autoimmune atrophic gastritis, reporting recent evidence on epidemiology, pathogenesis, diagnosis, clinical presentation, risk of malignancies, and management. The prevalence of AAG has been estimated at between 0.3% and 2.7% in the general population. The diagnosis of AAG is based on a combination of the serologic profile and the histological examination of gastric biopsies. Patients with AAG are often asymptomatic but can also have dyspeptic or reflux symptoms. The atrophy of the oxyntic mucosa leads to iron and vitamin B12 malabsorption, which may result in anemia and neurological affections. Autoimmune atrophic gastritis is associated with an increased risk of type I neuroendocrine tumors (NETs) and gastric cancer, with an incidence rate of 2.8% and 0.5% per person/year, respectively. Management is directed to reinstate vitamins and iron and to prevent malignancies with endoscopic surveillance. In conclusion, atrophic autoimmune gastritis is an infrequent condition, often asymptomatic and misdiagnosed, that requires an early diagnosis for appropriate vitamin supplementation and endoscopic follow-up for the early diagnosis of NETs and gastric cancer. Keywords: autoimmune atrophic gastritis; anti-parietal cell antibodies; gastric carcinoids