Menetrier disease (giant hypertrophic gastritis) is a rare premalignant gastropathy characterized by massive hypertrophy of the mucosal folds in the gastric fundus and body. Patients present with protein-losing enteropathy, hypoalbuminemia, and mucoid gastric hypersecretion. The etiology involves overexpression of TGF-alpha and activation of the EGF receptor; transient CMV-associated forms have been described in children. On imaging, CT typically demonstrates pronounced thickening of mucosal folds with a serpentine cerebriform pattern and fundus-body predominance. Definitive diagnosis requires endoscopic biopsy showing foveolar hyperplasia and glandular atrophy as histological hallmarks. The disease is a risk factor for gastric carcinoma, and treatment may include cetuximab therapy or gastrectomy.
Age Range
30-70
Peak Age
50
Gender
Male predominant
Prevalence
Rare
The pathophysiology of Menetrier disease centers on hyperactivation of the EGF receptor (EGFR) signaling pathway. Local overproduction of TGF-alpha chronically stimulates EGFR, triggering foveolar (surface mucous cell) hyperplasia and atrophy of oxyntic (parietal and chief cell) glands. Foveolar hyperplasia results in massive enlargement of mucosal folds, producing the characteristic thick cerebriform mucosal folds seen on CT. Increased mucus production and glandular atrophy lead to decreased acid secretion and increased protein loss — manifesting clinically as hypochlorhydria and hypoalbuminemia. Mucosal hyperplasia causes corticomedullary edema and interstitial fluid accumulation that further thickens the gastric wall, showing pronounced enhancement on CT. Chronic EGFR stimulation creates a preneoplastic state predisposing to dysplasia and gastric carcinoma; cetuximab (anti-EGFR monoclonal antibody) blocking EGFR is used as a therapeutic option.
The cerebriform appearance of massively thickened mucosal folds in the gastric fundus and body resembling brain gyri on CT — a characteristic imaging finding for Menetrier disease. This pattern combined with antral sparing strongly suggests the diagnosis.
Massive thickening of mucosal folds (>10 mm, typically 20-40 mm) in the gastric fundus and body on portal venous phase. Folds demonstrate a cerebriform (brain gyrus-like) or polypoid appearance. The antrum is typically spared. The thickened mucosa shows pronounced enhancement while the submucosal layer appears hypodense. Total wall thickness may reach 2-4 cm.
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Pronounced mucosal fold thickening (approximately ___ mm) with cerebriform configuration in the gastric fundus and body with antral sparing is observed, consistent with Menetrier disease.
Pronounced early enhancement of the hyperplastic mucosa in the arterial phase. Intense arterial enhancement is seen in the thickened mucosal folds while the submucosal layer is not yet enhanced, creating a distinct mucosal-submucosal demarcation. This early enhancement reflects increased vascular perfusion of the mucosa.
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Pronounced early enhancement of the thickened mucosal folds in the gastric fundus and body is noted in the arterial phase with clear demarcation from the submucosal layer.
Diffuse gastric wall thickening and increased intraluminal fluid content on non-contrast CT. Mucosal fold thickening is appreciable on non-contrast CT although mucosal-submucosal distinction is not as clear as post-contrast. Increased intraluminal fluid reflects mucus hypersecretion. Peripheral edema or ascites may be present due to protein-losing enteropathy.
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Diffuse gastric wall thickening with increased intraluminal fluid content is observed in the fundus and body on non-contrast CT.
Increased signal intensity in the thickened mucosal folds on T2-weighted images. The edematous submucosal layer appears markedly T2 hyperintense while the mucosal layer is moderately hyperintense. Total wall thickness is increased paralleling CT findings. T2 sequences confirm the mucosal-submucosal double-contour appearance on MRI.
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Pronounced mucosal fold thickening with increased signal intensity in the edematous submucosal layer is observed in the gastric fundus and body on T2-weighted MRI.
On contrast-enhanced T1-weighted images (post-gadolinium), a stratified wall appearance with pronounced mucosal enhancement, decreased submucosal enhancement, and moderate muscularis propria enhancement. This pattern parallels CT findings and is valuable in differentiating benign thickening from malignant infiltration.
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Stratified enhancement pattern of the gastric wall on contrast-enhanced MRI with pronounced mucosal enhancement and double-contour appearance due to submucosal edema, consistent with Menetrier disease.
Prominent thickening of rugal folds in the gastric fundus and body on ultrasound. The thickened folds show a layered appearance with hypoechoic mucosa and hyperechoic submucosa. Increased echo-free or hypoechoic fluid within the lumen is seen. Total wall thickness is increased (>10 mm) with preserved normal gastric wall stratification — a feature distinguishing from malignant infiltration.
Report Sentence
Prominent rugal fold thickening in the gastric fundus and body with preserved wall stratification and increased intraluminal fluid on ultrasound.
Persistent low density in the submucosal layer (edema retention) with still visible mucosal enhancement on delayed phase CT. Although mucosal enhancement decreases in the delayed phase, submucosal edema remains persistent and the double-contour appearance continues. This finding supports the chronic inflammatory process and protein loss.
Report Sentence
Persistent submucosal edema with continued double-contour appearance on delayed phase CT, consistent with chronic gastropathy.
Criteria
Chronic progressive course in adults (40-60 years) with foveolar hyperplasia, protein-losing enteropathy, and premalignant potential. Associated with TGF-alpha/EGFR overactivation.
Distinct Features
Fundus and body predominance, antral sparing, pronounced mucosal hypertrophy (>20 mm), hypoalbuminemia, hypochlorhydria. Giant cerebriform folds on CT. May require cetuximab or gastrectomy.
Criteria
Transient form triggered by CMV infection in children (typically <10 years). Acute onset of protein loss and gastric fold thickening. Spontaneous regression expected.
Distinct Features
Milder mucosal thickening, positive CMV serology/PCR, spontaneous resolution within 4-6 weeks. Less pronounced thickening on CT compared to adult form. Accelerated recovery with antiviral treatment.
Criteria
Hypertrophic gastropathy occurring in association with H. pylori infection. Shows partial or complete regression after H. pylori eradication.
Distinct Features
H. pylori-positive biopsy, regression of mucosal thickening after eradication therapy, better prognosis than classic adult form. Moderate mucosal thickening on CT.
Distinguishing Feature
In gastric lymphoma, wall thickening is diffuse and homogeneous with disrupted normal stratification; in Menetrier disease, mucosal folds are prominently thickened while normal wall stratification is preserved. Lymphoma may be accompanied by perigastric lymphadenopathy and splenic involvement.
Distinguishing Feature
In gastric adenocarcinoma, wall thickening is asymmetric, focal, and wall stratification is disrupted; Menetrier shows symmetric fundus-body predominant mucosal fold thickening with preserved stratification. Carcinoma may be accompanied by perigastric invasion, lymphadenopathy, and distant metastasis.
Distinguishing Feature
In linitis plastica, the gastric wall is diffusely thickened with a rigid narrowed appearance (leather bottle stomach); in Menetrier, folds are thick but luminal narrowing is not prominent. Linitis plastica may affect the entire stomach including the antrum; in Menetrier, the antrum is typically spared.
Distinguishing Feature
Acute/chronic gastritis shows diffuse but milder wall thickening (usually <10 mm); Menetrier has much more pronounced fold thickening (>20 mm). Gastritis may affect the entire stomach including the antrum; Menetrier is fundus-body limited. Hypoalbuminemia is not seen in gastritis.
Urgency
routineManagement
medicalBiopsy
NeededFollow-up
6-monthMenetrier disease is premalignant with a risk of gastric carcinoma (2-15%). Definitive diagnosis requires endoscopic biopsy. Cetuximab (anti-EGFR) therapy may provide symptomatic improvement. Gastrectomy may be needed in refractory cases. Nutritional support and albumin replacement are important due to protein-losing enteropathy. Regular endoscopic surveillance is recommended.
Ménétrier disease is considered premalignant (2-15% risk of gastric cancer). Hypoalbuminemia and peripheral edema occur due to protein-losing gastropathy. Cetuximab therapy may be effective. Gastrectomy may be needed in refractory cases.