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Pathology · Systemic pathology: Menetrier disease
Sample itemA 50-year-old man has epigastric pain, weight loss and peripheral oedema with low serum albumin. Endoscopy shows giant cerebriform gastric folds in the body and fundus. Biopsy shows marked foveolar hyperplasia with few parietal cells. Which mechanism underlies this?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. Overexpression of TGF-alpha, activating the epidermal growth factor receptor
Menetrier disease is hypertrophic gastropathy in which excess TGF-alpha stimulates the mucous cells. Parietal cells are lost, acid falls, and protein leaks across the hyperplastic mucosa, producing hypoalbuminaemia.
Option by option
A. Gastrin overproduction by a pancreatic neuroendocrine tumour
Gastrinoma causes parietal cell hyperplasia with acid hypersecretion rather than parietal loss.
B. Autoantibodies against parietal cells and intrinsic factor
Autoimmune gastritis causes atrophy of the body with achlorhydria and pernicious anaemia, not giant folds.
C. Overexpression of TGF-alpha, activating the epidermal growth factor receptor (correct)
Correct. Excess TGF-alpha signalling via EGFR causes foveolar hyperplasia and protein-losing gastropathy.
D. Loss of E-cadherin with infiltration by signet ring cells
Diffuse gastric cancer with E-cadherin loss causes a rigid, thickened stomach, not hyperplasia with protein loss.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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