Background Ménétrier’s disease is a rare protein-losing gastropathy characterized by markedly enlarged gastric folds, excessive mucus secretion, and hypoalbuminemia. Histologically, it features pronounced foveolar hyperplasia, cystic dilation of gastric glands, and loss of parietal and chief cells. Although first described in humans, a small number of comparable cases have been reported in dogs, where the condition is referred to as Ménétrier-like disease. In veterinary medicine, this disorder remains poorly defined and appears to be uncommon. Case presentation A 6-year-old intact male French Bulldog was referred for a severe progressive weight loss and acute onset anorexia. Clinical and laboratory findings were suggestive of a protein-losing enteropathy. Abdominal ultrasonography revealed marked thickening of the gastric and small intestinal walls. Gastroscopy showed severe, non-reducible hypertrophy of the gastric folds involving both the fundus and body of stomach. Endoscopic biopsies revealed marked foveolar hyperplasia and cystic glandular dilation without evidence of glandular atrophy. Ménétrierlike hypertrophic gastropathy was considered the most likely diagnosis. Given that the owner declined gastrectomy and treatment with somatostatin analogues for financial constraints, medical management with glucocorticoids and H₂-receptor antagonists was administered. After 10 days, the clinical condition progressively worsened, with the onset of new and evolving neurological deficits. The dog subsequently developed severe neurological signs, and euthanasia was ultimately elected. Histopathological examination of a full-thickness gastric sample confirmed mucosal hypert rophy characterized by branching foveolar hyperplasia and cystic dilation of the glands, again without evidence of parietal cell loss. Conclusions This case suggests that canine Ménétrier-like disease may occur even in the absence of glandular atrophy, thereby broadening the currently recognized histologic spectrum of the condition.

Ménétrier-like disease in a dog without glandular atrophy: expanding the morphologic spectrum

Pugliese, Michela
Ultimo
Membro del Collaboration Group
2026-01-01

Abstract

Background Ménétrier’s disease is a rare protein-losing gastropathy characterized by markedly enlarged gastric folds, excessive mucus secretion, and hypoalbuminemia. Histologically, it features pronounced foveolar hyperplasia, cystic dilation of gastric glands, and loss of parietal and chief cells. Although first described in humans, a small number of comparable cases have been reported in dogs, where the condition is referred to as Ménétrier-like disease. In veterinary medicine, this disorder remains poorly defined and appears to be uncommon. Case presentation A 6-year-old intact male French Bulldog was referred for a severe progressive weight loss and acute onset anorexia. Clinical and laboratory findings were suggestive of a protein-losing enteropathy. Abdominal ultrasonography revealed marked thickening of the gastric and small intestinal walls. Gastroscopy showed severe, non-reducible hypertrophy of the gastric folds involving both the fundus and body of stomach. Endoscopic biopsies revealed marked foveolar hyperplasia and cystic glandular dilation without evidence of glandular atrophy. Ménétrierlike hypertrophic gastropathy was considered the most likely diagnosis. Given that the owner declined gastrectomy and treatment with somatostatin analogues for financial constraints, medical management with glucocorticoids and H₂-receptor antagonists was administered. After 10 days, the clinical condition progressively worsened, with the onset of new and evolving neurological deficits. The dog subsequently developed severe neurological signs, and euthanasia was ultimately elected. Histopathological examination of a full-thickness gastric sample confirmed mucosal hypert rophy characterized by branching foveolar hyperplasia and cystic dilation of the glands, again without evidence of parietal cell loss. Conclusions This case suggests that canine Ménétrier-like disease may occur even in the absence of glandular atrophy, thereby broadening the currently recognized histologic spectrum of the condition.
2026
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3353509
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