2023년 Case Rep Gastroenterol 에 실린 case 입니다.
79-year-old female was referred to our institution for further evaluation and treatment of multiple enlarged hyperplastic polyps in the gastric antrum. The patient had AIH for 7 years and was under treatment with prednisolone (5 mg daily) and esomeprazole (10 mg daily). The initial prednisolone dose, which was 40 mg/day at the diagnosis, was gradually tapered to 5 mg/day 4 years ago. The patient was a nonsmoker and a nondrinker and had no allergies. Previous upper gastrointestinal endoscopy (GIE), performed 3 years prior, revealed three small hyperplastic polyps and mild mucosal atrophy (Fig. a, d).
A blood test revealed positive PCA and negative intrinsic factor antibodies. Pepsinogen 1 and 2 levels were 32.0 ng/mL and 14.2 ng/mL, respectively. The serum antibody test result for Helicobacter pylori was negative.
Endoscopic mucosal resection was performed for all polyps. The sizes of the polyps were 13 mm × 10 mm × 10 mm, 15 mm × 10 mm × 10 mm, and 16 mm × 13 mm × 10 mm (Fig. 3a).
The patient was discharged uneventfully 2 days after treatment. Follow-up using upper GIE was planned 6 months after the treatment.
Figure 1. Endoscopic findings. Three small hyperplastic polyps (a) and no mucosal atrophy (d) 3 years before the referral. (b), (e) Hyperplastic polyps at the greater curvature of the angulus at the referral. (c), (f) Background mucosa showed corpus-dominant gastric atrophy and sticky adherent mucous at the referral.
Figure 2. Histopathological findings of biopsy samples from greater curvature of the corpus. Hematoxylin and eosin staining showed decreased parietal cells and diffuse lymphocytic infiltration of the deep lamina propria (a: ×20, b: ×100). Immunohistochemistry revealed chromogranin A-positive endocrine cell micronest (ECM) and enterochromaffin-like cell (ECL) hyperplasia (c: ×40, d: ×100).
Figure 3. Gross photograph and histopathological findings of a polyp. a Gross photograph. Hematoxylin and eosin staining showed elongated, branched, dilated foveolar epithelium and edematous inflamed stroma (b: ×20, c: ×40, d: ×100).
AIH is known to be associated with other autoimmune disorders such as chronic thyroiditis, Sjögren syndrome, primary biliary cholangitis, and rheumatoid arthritis. The prevalence of AIH in the standardized Japanese population is 0.024%. Patients with comorbid AIH and AIG are rare because both AIG and AIH have low prevalence. Actually, only one previous case of comorbid AIG with AIH has been reported in the English literature.
* Enlargement of the hyperplastic polyps
(1) The development and progression of hyperplastic polyps in the stomach are strongly associated with the repair of mucosal damage caused by chronic gastritis.
(2) Hypergastrinemia and duodenal reflux also play crucial roles. Long-term therapy with proton pump inhibitors (PPIs) induced serum hypergastrinemia. In this regard, gastrin induces proliferative effects on the gastric mucosa, enhancing the effects of growth factors, such as epidermal growth factor and tumor growth factor-α families, thereby promoting the proliferation of crypt epithelial cells (Kim GH. Proton pump inhibitor-related gastric mucosal changes. Gut Liver. 2021 Sep;15(5):646–52.)
<PPI-induced and AIG-related hypergastrinemia may have caused the formation and enlargement of the hyperplastic polyp.>
The dose reduction of prednisolone may have contributed to the progression of AIG. However, other studies have suggested that the prednisolone dose does not affect gastric atrophy,
In conclusion, we reported a case of comorbid AIG and AIH that was treated with prednisolone. Reduction of prednisolone might affect the progression of AIG. In this regard, when the enlargement of hyperplastic polyps and progression of gastric atrophy is detected, serum antibodies should be evaluated to diagnose AIG, and other manifestations of AIG should be screened.
Abstract
Autoimmune gastritis is immune-mediated gastritis that destroys the oxyntic mucosa. Autoimmune hepatitis is an inflammatory liver disease caused by an autoimmune reaction. These diseases share similar pathogeneses as organ-specific autoimmune disorders; however, cases involving both diseases are quite rare and scarcely reported. Herein, we report a patient with concurrent autoimmune gastritis and hepatitis who developed enlargement of hyperplastic polyps and progression of gastric atrophy. The patient was a 79-year-old female referred to our hospital for the treatment of hyperplastic polyps detected on a follow-up upper gastrointestinal endoscopy. The patient’s previous upper gastrointestinal endoscopy from 3 years prior revealed small hyperplastic polyps and no mucosal atrophy. However, the current upper gastrointestinal endoscopy revealed three 10-mm red polyps, severe mucosal atrophy in the corpus, and mild atrophy in the antral area. In addition, biopsy samples from the gastric body revealed decreased parietal cells and diffuse lymphocytic infiltration of the deep mucosa. Further, chromogranin A-positive endocrine cell micronests and enterochromaffin-like cell hyperplasia were detected. After confirming the diagnosis of autoimmune gastritis, endoscopic mucosal resection was performed for all the polyps, which were histopathologically diagnosed as hyperplastic polyps without malignancy. Therefore, clinicians should consider autoimmune gastritis for enlarged hyperplastic polyps and gastric atrophy progression.
2023년 Case Rep Gastroenterol 에 실린 case 입니다.
79-year-old female was referred to our institution for further evaluation and treatment of multiple enlarged hyperplastic polyps in the gastric antrum. The patient had AIH for 7 years and was under treatment with prednisolone (5 mg daily) and esomeprazole (10 mg daily). The initial prednisolone dose, which was 40 mg/day at the diagnosis, was gradually tapered to 5 mg/day 4 years ago. The patient was a nonsmoker and a nondrinker and had no allergies. Previous upper gastrointestinal endoscopy (GIE), performed 3 years prior, revealed three small hyperplastic polyps and mild mucosal atrophy (Fig. a, d).
A blood test revealed positive PCA and negative intrinsic factor antibodies. Pepsinogen 1 and 2 levels were 32.0 ng/mL and 14.2 ng/mL, respectively. The serum antibody test result for Helicobacter pylori was negative.
Endoscopic mucosal resection was performed for all polyps. The sizes of the polyps were 13 mm × 10 mm × 10 mm, 15 mm × 10 mm × 10 mm, and 16 mm × 13 mm × 10 mm (Fig. 3a).
The patient was discharged uneventfully 2 days after treatment. Follow-up using upper GIE was planned 6 months after the treatment.
Figure 1. Endoscopic findings. Three small hyperplastic polyps (a) and no mucosal atrophy (d) 3 years before the referral. (b), (e) Hyperplastic polyps at the greater curvature of the angulus at the referral. (c), (f) Background mucosa showed corpus-dominant gastric atrophy and sticky adherent mucous at the referral.
Figure 2. Histopathological findings of biopsy samples from greater curvature of the corpus. Hematoxylin and eosin staining showed decreased parietal cells and diffuse lymphocytic infiltration of the deep lamina propria (a: ×20, b: ×100). Immunohistochemistry revealed chromogranin A-positive endocrine cell micronest (ECM) and enterochromaffin-like cell (ECL) hyperplasia (c: ×40, d: ×100).
Figure 3. Gross photograph and histopathological findings of a polyp. a Gross photograph. Hematoxylin and eosin staining showed elongated, branched, dilated foveolar epithelium and edematous inflamed stroma (b: ×20, c: ×40, d: ×100).
AIH is known to be associated with other autoimmune disorders such as chronic thyroiditis, Sjögren syndrome, primary biliary cholangitis, and rheumatoid arthritis. The prevalence of AIH in the standardized Japanese population is 0.024%. Patients with comorbid AIH and AIG are rare because both AIG and AIH have low prevalence. Actually, only one previous case of comorbid AIG with AIH has been reported in the English literature.
* Enlargement of the hyperplastic polyps
(1) The development and progression of hyperplastic polyps in the stomach are strongly associated with the repair of mucosal damage caused by chronic gastritis.
(2) Hypergastrinemia and duodenal reflux also play crucial roles. Long-term therapy with proton pump inhibitors (PPIs) induced serum hypergastrinemia. In this regard, gastrin induces proliferative effects on the gastric mucosa, enhancing the effects of growth factors, such as epidermal growth factor and tumor growth factor-α families, thereby promoting the proliferation of crypt epithelial cells (Kim GH. Proton pump inhibitor-related gastric mucosal changes. Gut Liver. 2021 Sep;15(5):646–52.)
<PPI-induced and AIG-related hypergastrinemia may have caused the formation and enlargement of the hyperplastic polyp.>
The dose reduction of prednisolone may have contributed to the progression of AIG. However, other studies have suggested that the prednisolone dose does not affect gastric atrophy,
In conclusion, we reported a case of comorbid AIG and AIH that was treated with prednisolone. Reduction of prednisolone might affect the progression of AIG. In this regard, when the enlargement of hyperplastic polyps and progression of gastric atrophy is detected, serum antibodies should be evaluated to diagnose AIG, and other manifestations of AIG should be screened.
Abstract
Autoimmune gastritis is immune-mediated gastritis that destroys the oxyntic mucosa. Autoimmune hepatitis is an inflammatory liver disease caused by an autoimmune reaction. These diseases share similar pathogeneses as organ-specific autoimmune disorders; however, cases involving both diseases are quite rare and scarcely reported. Herein, we report a patient with concurrent autoimmune gastritis and hepatitis who developed enlargement of hyperplastic polyps and progression of gastric atrophy. The patient was a 79-year-old female referred to our hospital for the treatment of hyperplastic polyps detected on a follow-up upper gastrointestinal endoscopy. The patient’s previous upper gastrointestinal endoscopy from 3 years prior revealed small hyperplastic polyps and no mucosal atrophy. However, the current upper gastrointestinal endoscopy revealed three 10-mm red polyps, severe mucosal atrophy in the corpus, and mild atrophy in the antral area. In addition, biopsy samples from the gastric body revealed decreased parietal cells and diffuse lymphocytic infiltration of the deep mucosa. Further, chromogranin A-positive endocrine cell micronests and enterochromaffin-like cell hyperplasia were detected. After confirming the diagnosis of autoimmune gastritis, endoscopic mucosal resection was performed for all the polyps, which were histopathologically diagnosed as hyperplastic polyps without malignancy. Therefore, clinicians should consider autoimmune gastritis for enlarged hyperplastic polyps and gastric atrophy progression.