Gastric Adenocarcinoma Arising From the Ménétrier Disease

CASE REPORT A 62-year-old man presenting with nausea, vomiting, epigastric pain, loose stool, and hypoalbuminemia was diagnosed with the biopsy-proven Ménétrier disease (MD) in 2014 (Figure 1) and received octreotide for ∼11 years (2014–2025), achieving excellent response with marked symptomatic improvement. Surveillance upper endoscopy was performed every 2–3 years. In 2018, biopsies showed low-grade dysplasia (LGD); repeat biopsies in late 2018 and 2019 were negative. In 2022, biopsies were indefinite for dysplasia. In 2024, surveillance biopsies again demonstrated LGD with persistent and diffuse hypertrophic gastric folds (Figure 2) and protein-losing gastropathy. Given recurrent/multifocal dysplasia involving a diffusely affected stomach on surveillance and persistent hypoalbuminemia despite medical therapy, the patient underwent total gastrectomy in August 2025. Grossly, the stomach showed markedly thickened rugal folds (Figure 3A). Histology revealed foveolar hyperplasia consistent with MD, with low and high-grade dysplasia (Figure 3B) and early gastric adenocarcinoma with focal submucosal invasion (Figure 3C, arrows); 16 lymph nodes were negative, consistent with pT1bN0M0 disease. Postoperatively, serum albumin normalized (3.0 to 4.2 g/dL) and symptoms improved. This case highlights malignant progression in MD1-5 despite medical therapy and supports close surveillance and consideration of definitive surgery when dysplasia recurs or becomes multifocal, particularly with ongoing protein loss.Figure 1.: Initial computed tomography scan image showing thickening of the gastric wall.Figure 2.: Upper endoscopic image demonstrating irregular, thickened gastric folds in the body.Figure 3.: Pathologic examination of the gastrectomy specimen: (A) serially sectioned stomach revealing markedly thickened gastric folds; (B) Low-power photomicrography showing severe foveolar hyperplasia and low-grade dysplasia (hematoxylin and eosin, ×2); (C) high-power photomicrography demonstrating tumor cell invasion into the submucosa (arrows) (hematoxylin and eosin, ×20).DISCLOSURES Author contributions: G. Lee integrated the patient's data, wrote the manuscript, interpreted pathologic findings, and generated the figures; JB Rose provided the case with radiologic images, reviewed and edited the manuscript; F. Weber obtained patient consent, contributed endoscopic image, reviewed the patient's history, and edited the manuscript. G. Lee is the article guarantor. Conflicts of interest: The authors have no potential conflicts of interest. Financial disclosure: None to report. Informed consent was obtained for this case report.

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Journal
ACG Case Reports Journal
Published
2026-04-01
DOI
https://doi.org/10.14309/crj.0000000000002074
Primary Topic
Neuroendocrine Tumor Research Advances
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article
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article

Gastric Adenocarcinoma Arising From the Ménétrier Disease

Goo Lee, Frederick Weber, J. Bart Rose
ACG Case Reports Journal
Neuroendocrine Tumor Research Advances
article

Gastric Adenocarcinoma Arising From the Ménétrier Disease

Goo Lee, Frederick Weber, J. Bart Rose
article en

Abstract

CASE REPORT A 62-year-old man presenting with nausea, vomiting, epigastric pain, loose stool, and hypoalbuminemia was diagnosed with the biopsy-proven Ménétrier disease (MD) in 2014 (Figure 1) and received octreotide for ∼11 years (2014–2025), achieving excellent response with marked symptomatic improvement. Surveillance upper endoscopy was performed every 2–3 years. In 2018, biopsies showed low-grade dysplasia (LGD); repeat biopsies in late 2018 and 2019 were negative. In 2022, biopsies were indefinite for dysplasia. In 2024, surveillance biopsies again demonstrated LGD with persistent and diffuse hypertrophic gastric folds (Figure 2) and protein-losing gastropathy. Given recurrent/multifocal dysplasia involving a diffusely affected stomach on surveillance and persistent hypoalbuminemia despite medical therapy, the patient underwent total gastrectomy in August 2025. Grossly, the stomach showed markedly thickened rugal folds (Figure 3A). Histology revealed foveolar hyperplasia consistent with MD, with low and high-grade dysplasia (Figure 3B) and early gastric adenocarcinoma with focal submucosal invasion (Figure 3C, arrows); 16 lymph nodes were negative, consistent with pT1bN0M0 disease. Postoperatively, serum albumin normalized (3.0 to 4.2 g/dL) and symptoms improved. This case highlights malignant progression in MD1-5 despite medical therapy and supports close surveillance and consideration of definitive surgery when dysplasia recurs or becomes multifocal, particularly with ongoing protein loss.Figure 1.: Initial computed tomography scan image showing thickening of the gastric wall.Figure 2.: Upper endoscopic image demonstrating irregular, thickened gastric folds in the body.Figure 3.: Pathologic examination of the gastrectomy specimen: (A) serially sectioned stomach revealing markedly thickened gastric folds; (B) Low-power photomicrography showing severe foveolar hyperplasia and low-grade dysplasia (hematoxylin and eosin, ×2); (C) high-power photomicrography demonstrating tumor cell invasion into the submucosa (arrows) (hematoxylin and eosin, ×20).DISCLOSURES Author contributions: G. Lee integrated the patient's data, wrote the manuscript, interpreted pathologic findings, and generated the figures; JB Rose provided the case with radiologic images, reviewed and edited the manuscript; F. Weber obtained patient consent, contributed endoscopic image, reviewed the patient's history, and edited the manuscript. G. Lee is the article guarantor. Conflicts of interest: The authors have no potential conflicts of interest. Financial disclosure: None to report. Informed consent was obtained for this case report.

ACG Case Reports JournalVol. 13(4)
University of Alabama at Birmingham (US)
Good health and well-being
Openalex Percentile: Top 18%
Neuroendocrine Tumor Research Advances
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