The Korean Journal of Helicobacter and Upper Gastrointestinal Research 2023;23(2):137-142.
Published online: June 12, 2023 // DOI: https://doi.org/10.7704/kjhugr.2023.0021
<Case Report>
* 54/F, Past history: non-specific
* Serologic finding
- pepsinogen Ⅰ level: 22.4 ng/mL; pepsinogen Ⅱ level, 13.2 ng/mL; and pepsinogen Ⅰ/Ⅱ ratio, 1.7
- serum gastrin level: 205 pg/mL
- anti-Helicobacter pylori antibody level: 0.73 U/mL
* Endoscopic finding
Figure 1. Upper gastrointestinal endoscopy findings. (A) Erythematous nodules, flattened mucosal folds, and atrophic mucosa are observed in the gastric body and fundus. (B) Flattened gastric mucosal folds and prominent submucosal vasculature are observed along the greater curvature of the gastric body. (C) The gastric antrum appears normal.
* Pathologic finding
Figure 2. Histopathological findings of the greater curvature of the gastric body. (A) Endoscopic images showing slightly elevated erythematous nodules (blue arrow) and advanced mucosal atrophy (yellow arrow) along the greater curvature of the gastric mid body. (B) Specimen obtained from an erythematous nodule showing mild inflammation and atrophic oxyntic gastric mucosa (H&E stain, ×100). (C) Specimen obtained from the mucosa in an area of advanced atrophy showing moderate inflammation and atrophic oxyntic gastric mucosa (H&E stain, ×100). (D) Image of the same specimen as that shown in (B); mildly increased numbers of neuroendocrine cells are observed (chromogranin A stain, ×100). (E) Image of the same specimen as that shown in (C); a mild-to-moderate increase in the numbers of neuroendocrine cells and linear neuroendocrine cell hyperplasia is visualized (chromogranin A stain, ×100).
* Subepithelial tumor evaluation
Figure 3. Images of the subepithelial tumor. (A) Endoscopic images showing a subepithelial tumor (slightly >1 cm) at the greater curvature of the gastric lower body. (B) Contrast-enhanced computed tomography scan showing an enhanced exophytic mass (1.2 cm) in the gastric body. (C) Endoscopic ultrasonography scan showing an oval hypoechoic mass (1.1×0.8 cm) with a clearly demarcated border, beneath the muscularis propria layer. (D) Specimen showing interlacing bundles of spindle cells with elongated and palisading nuclei (hematoxylin & eosin stain, ×100). (E) Specimen showing stained cytoplasm and nuclei of tumor cells (S-100 protein stain, ×100).
* AIG accampanied by SET
Table 1. Reported Cases of Autoimmune Gastritis with Concomitant Subepithelial Tumors
* Discussion
- This case is an example of an ongoing AIG stage, not early or advanced atrophy stage. AIG is a progressive inflammatory disease that can appear as various features on endoscopy depending on its stage, and show ambiguous serologic results, thus biopsy should be performed even if widespread atrophy is not apparent, and remnant oxyntic mucosal lesions mixed with atrophic mucosa and flattened folds are observed in the gastric body.
- NETs accompanied by AIG may appear as SETs, occur in various locations, and may hide malignancy when they are <2 cm.
- Hypergastrinemia resulting from the hypochlorhydria environment may contribute to ECL cell proliferation from hyperplasia to NETs.
- There are no definitive guidelines for assessment and treatment of SETs in patients with AIG.
- As SETs can manifest in various forms in patients with AIG, a systematic follow-up of similar cases, such as this one, is required.
<Abstract>
Autoimmune gastritis (AIG), a chronic inflammatory disease occurs as a result of a complex interaction between host-related and environmental factors. AIG may progress to severe atrophic gastritis secondary autoimmune-mediated parietal cell destruction in the stomach. AIG can be diagnosed based on anti-parietal cell antibody tests and endoscopy, which reveals widespread gastric corpus atrophy in patients with low serum pepsinogen I levels, a low pepsinogen I/II ratio, and elevated serum gastrin levels on serological testing. Tissue biopsy findings, which include mucosal atrophy and lymphocytic infiltration of the lamina propria may be useful for diagnostic confirmation. Decreased gastric acid secretion causes hypergastrinemia and enterochromaffin-like (ECL) cell proliferation, which can lead to neuroendocrine tumor development. Additionally, an autoimmune response results in parietal and chief cell injury, and proliferating ECL cells are detected in the deep mucosal layers in patients with AIG. Therefore, this condition may easily be misdiagnosed as a subepithelial tumor, and establishing a differential diagnosis for other types of subepithelial tumor accompanied by AIG is challenging. We present the case of a 54-year-old woman who was diagnosed with AIG with a concomitant subepithelial tumor based on serologic tests and biopsy findings and underwent wedge resection, which confirmed diagnosis of a schwannoma.
The Korean Journal of Helicobacter and Upper Gastrointestinal Research 2023;23(2):137-142.
Published online: June 12, 2023 // DOI: https://doi.org/10.7704/kjhugr.2023.0021
<Case Report>
* 54/F, Past history: non-specific
* Serologic finding
- pepsinogen Ⅰ level: 22.4 ng/mL; pepsinogen Ⅱ level, 13.2 ng/mL; and pepsinogen Ⅰ/Ⅱ ratio, 1.7
- serum gastrin level: 205 pg/mL
- anti-Helicobacter pylori antibody level: 0.73 U/mL
* Endoscopic finding
* Pathologic finding
Figure 2. Histopathological findings of the greater curvature of the gastric body. (A) Endoscopic images showing slightly elevated erythematous nodules (blue arrow) and advanced mucosal atrophy (yellow arrow) along the greater curvature of the gastric mid body. (B) Specimen obtained from an erythematous nodule showing mild inflammation and atrophic oxyntic gastric mucosa (H&E stain, ×100). (C) Specimen obtained from the mucosa in an area of advanced atrophy showing moderate inflammation and atrophic oxyntic gastric mucosa (H&E stain, ×100). (D) Image of the same specimen as that shown in (B); mildly increased numbers of neuroendocrine cells are observed (chromogranin A stain, ×100). (E) Image of the same specimen as that shown in (C); a mild-to-moderate increase in the numbers of neuroendocrine cells and linear neuroendocrine cell hyperplasia is visualized (chromogranin A stain, ×100).
* Subepithelial tumor evaluation
Figure 3. Images of the subepithelial tumor. (A) Endoscopic images showing a subepithelial tumor (slightly >1 cm) at the greater curvature of the gastric lower body. (B) Contrast-enhanced computed tomography scan showing an enhanced exophytic mass (1.2 cm) in the gastric body. (C) Endoscopic ultrasonography scan showing an oval hypoechoic mass (1.1×0.8 cm) with a clearly demarcated border, beneath the muscularis propria layer. (D) Specimen showing interlacing bundles of spindle cells with elongated and palisading nuclei (hematoxylin & eosin stain, ×100). (E) Specimen showing stained cytoplasm and nuclei of tumor cells (S-100 protein stain, ×100).
* AIG accampanied by SET
Table 1. Reported Cases of Autoimmune Gastritis with Concomitant Subepithelial Tumors
* Discussion
- This case is an example of an ongoing AIG stage, not early or advanced atrophy stage. AIG is a progressive inflammatory disease that can appear as various features on endoscopy depending on its stage, and show ambiguous serologic results, thus biopsy should be performed even if widespread atrophy is not apparent, and remnant oxyntic mucosal lesions mixed with atrophic mucosa and flattened folds are observed in the gastric body.
- NETs accompanied by AIG may appear as SETs, occur in various locations, and may hide malignancy when they are <2 cm.
- Hypergastrinemia resulting from the hypochlorhydria environment may contribute to ECL cell proliferation from hyperplasia to NETs.
- There are no definitive guidelines for assessment and treatment of SETs in patients with AIG.
- As SETs can manifest in various forms in patients with AIG, a systematic follow-up of similar cases, such as this one, is required.
<Abstract>
Autoimmune gastritis (AIG), a chronic inflammatory disease occurs as a result of a complex interaction between host-related and environmental factors. AIG may progress to severe atrophic gastritis secondary autoimmune-mediated parietal cell destruction in the stomach. AIG can be diagnosed based on anti-parietal cell antibody tests and endoscopy, which reveals widespread gastric corpus atrophy in patients with low serum pepsinogen I levels, a low pepsinogen I/II ratio, and elevated serum gastrin levels on serological testing. Tissue biopsy findings, which include mucosal atrophy and lymphocytic infiltration of the lamina propria may be useful for diagnostic confirmation. Decreased gastric acid secretion causes hypergastrinemia and enterochromaffin-like (ECL) cell proliferation, which can lead to neuroendocrine tumor development. Additionally, an autoimmune response results in parietal and chief cell injury, and proliferating ECL cells are detected in the deep mucosal layers in patients with AIG. Therefore, this condition may easily be misdiagnosed as a subepithelial tumor, and establishing a differential diagnosis for other types of subepithelial tumor accompanied by AIG is challenging. We present the case of a 54-year-old woman who was diagnosed with AIG with a concomitant subepithelial tumor based on serologic tests and biopsy findings and underwent wedge resection, which confirmed diagnosis of a schwannoma.