{"title":"Revealing autoimmune gastritis: Polypoid nodule scar development after endoscopic submucosal dissection for early gastric cancer","authors":"Naoya Masuda, Kenji Yamazaki, Yasuhiko Maruyama, Ryoji Kushima, Nae Hasebe, Noritaka Ozawa, Shogo Shimizu, Masahito Shimizu","doi":"10.1002/deo2.70094","DOIUrl":null,"url":null,"abstract":"<p>Endoscopic submucosal dissection (ESD), the standard treatment for early gastric cancer, typically results in homogeneous flat scars. However, in some cases, polypoid nodule scars (PNS) may develop, complicating the cancer recurrence assessment. This case report describes a 60-year-old man with a history of <i>Helicobacter pylori</i> infection who underwent two ESD procedures: first for early antral gastric cancer and then for gastric body adenoma. Subsequently, an erythematous protruding lesion developed at the antral ESD scar site. Lesion biopsy revealed regenerative and hyperplastic tissue growth, consistent with PNS. Despite <i>H. pylori</i> eradication therapy and discontinuation of potassium-competitive acid blockers and H<sub>2</sub>-receptor antagonists, the lesion continued to enlarge. PNS growth may be caused by excessive mucosal regeneration and enhanced antral peristalsis, suggesting that hypergastrinemia, which may enhance these effects, may be an underlying cause. Further, elevated serum gastrin levels, decreased pepsinogen levels, the presence of antiparietal cell antibodies, and consistent pathological findings confirmed autoimmune gastritis (AIG).</p><p>This case highlights the diagnostic challenges of AIG, especially in cases of active or previous <i>H. pylori</i> infection because typical endoscopic features may be obscured. Persistent PNS after ESD warrants the consideration of excessive mucosal regeneration and enhanced peristalsis, with AIG as a potential cause because of its association with hypergastrinemia. To our knowledge, this is the first case report describing a potential link between AIG and PNS.</p>","PeriodicalId":93973,"journal":{"name":"DEN open","volume":"5 1","pages":""},"PeriodicalIF":1.4000,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/deo2.70094","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"DEN open","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/deo2.70094","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Endoscopic submucosal dissection (ESD), the standard treatment for early gastric cancer, typically results in homogeneous flat scars. However, in some cases, polypoid nodule scars (PNS) may develop, complicating the cancer recurrence assessment. This case report describes a 60-year-old man with a history of Helicobacter pylori infection who underwent two ESD procedures: first for early antral gastric cancer and then for gastric body adenoma. Subsequently, an erythematous protruding lesion developed at the antral ESD scar site. Lesion biopsy revealed regenerative and hyperplastic tissue growth, consistent with PNS. Despite H. pylori eradication therapy and discontinuation of potassium-competitive acid blockers and H2-receptor antagonists, the lesion continued to enlarge. PNS growth may be caused by excessive mucosal regeneration and enhanced antral peristalsis, suggesting that hypergastrinemia, which may enhance these effects, may be an underlying cause. Further, elevated serum gastrin levels, decreased pepsinogen levels, the presence of antiparietal cell antibodies, and consistent pathological findings confirmed autoimmune gastritis (AIG).
This case highlights the diagnostic challenges of AIG, especially in cases of active or previous H. pylori infection because typical endoscopic features may be obscured. Persistent PNS after ESD warrants the consideration of excessive mucosal regeneration and enhanced peristalsis, with AIG as a potential cause because of its association with hypergastrinemia. To our knowledge, this is the first case report describing a potential link between AIG and PNS.