• Title/Summary/Keyword: M$\acute{e}$n$\acute{e}$trier's disease

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Co-Infection with Cytomegalovirus and Helicobacter pylori in a Child with $M\acute{e}n\acute{e}$trier's Disease

  • Yoo, Yangho;Lee, Yoon;Lee, Yoo Min;Choe, Yon Ho
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.16 no.2
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    • pp.123-126
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    • 2013
  • $M\acute{e}n\acute{e}$trier's disease is a rare protein-losing gastropathy characterized by hypertrophic gastric fold, foveolar hyperplasia, and hypoproteinemia with resulting peripheral edema. It is clinically evident as nonspecific gastrointestinal symptoms, including abdominal discomfort, nausea and vomiting, abdominal pain, weight loss, diarrhea, and edema. Pediatric $M\acute{e}n\acute{e}$trier's disease usually has an insidious onset and progressive, chronic clinical course and it spontaneously resolves in weeks or months. The pathogenesis of $M\acute{e}n\acute{e}$trier's disease is not clearly understood. $M\acute{e}n\acute{e}$trier's disease is thought to be associated with some gastric infections. But the cause of $M\acute{e}n\acute{e}$trier's disease is unknown, an association with cytomegalovirus (CMV) and Helicobacter pylori has been suggested. In Korea, We present the first a case of pediatric $M\acute{e}n\acute{e}$trier's disease with positive evidence of CMV and H. pylori.

A case of cytomegalovirus-negative M$\acute{e}$n$\acute{e}$trier's disease with eosinophilia in a child

  • Son, Keun-Hyung;Kwak, Jeong-Ja;Park, Jae-Ock
    • Clinical and Experimental Pediatrics
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    • v.55 no.8
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    • pp.293-296
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    • 2012
  • M$\acute{e}$n$\acute{e}$trier's disease is a rare form of acquired gastropathy characterized by giant rugal folds in the stomach and protein-losing gastropathy. Children with M$\acute{e}$n$\acute{e}$trier's disease tend to follow a benign self-limited course with symptoms typically completely resolving within 2 to 10 weeks in contrast to the chronic course in adults. A 9-year-old girl presented with a history of gradually worsening abdominal distension, increasing body weight, and abdominal pain for 2 weeks. Physical examination on admission indicated periorbital swelling, pitting edema in both the legs, and abdominal distension with mild diffuse tenderness and shifting dullness. Laboratory tests on admission showed hypoalbuminemia, hypoproteinemia, and peripheral eosinophilia. The test result for anti-cytomegalovirus immunoglobulin M was negative. Increased fecal alpha 1 anti-trypsin excretion was observed. Radiological findings showed massive ascites and pleural effusion in both the lungs. On gastroscopy, large gastric folds, erythema, erosion, and exudation were noted in the body and fundus of the stomach. Microscopic findings showed infiltration of eosinophils and neutrophils in the gastric mucosa. Her symptoms improved with conservative treatment from day 7 of hospitalization and resolved completely.