scholarly journals A Rare case of Menetrier’s disease presenting with Protein Losing Gastropathy Mimicking Carcinoma Stomach

2021 ◽  
Vol 5 (4) ◽  
pp. 01-03
Author(s):  
Richmond Ronald Gomes

Ménétrier's disease (MD) (also known as giant hypertrophic gastritis or hypoproteinemic hypertrophic gastropathy) is a rare premalignant entity characterized by markedly hypertrophied mucosal folds of the fundus and the gastric corpus typically associated with , hypochlorhydria, protein losing enteropathy causing hypoalbuminemia and anemia. However, the natural history of MD in adults remains unclear and is rarely reported in the literature. Its constellation of classic symptoms includes nausea, vomiting, abdominal pain and peripheral edema, and it is associated with increased risk of gastric cancer. Nevertheless, its pathophysiology is not yet fully understood and clinical and endoscopic diagnosis can be difficult to establish. Malignant transformation in MD should not be overlooked, and regular monitoring of the gastric mucosa via endoscopy is necessary.

2009 ◽  
Vol 195 (1-6) ◽  
pp. 247-252 ◽  
Author(s):  
Heino Raotma ◽  
Lennart Angervall ◽  
Ingvar Dahl ◽  
Gerhard Dotevall

2013 ◽  
Vol 144 (5) ◽  
pp. S-680 ◽  
Author(s):  
Joshua D. Penfield ◽  
Ann E. Almazar ◽  
Yuri A. Saito ◽  
Giles R. Locke ◽  
Katherine E. Tilkes ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-5
Author(s):  
Michael Chung ◽  
Jaime Pittenger ◽  
Deborah Flomenhoft ◽  
Jeffrey Bennett ◽  
Eun-Young Lee ◽  
...  

Ménétrier's disease is one of the rarest protein-losing gastropathies in childhood. It is characterized clinically by non-specific gastrointestinal symptoms and edema, biochemically by hypoalbuminemia, and pathologically by enlarged gastric folds. In adults, this disease can be devastating with significant morbidity and mortality. In childhood, it is a self-limiting, transient and benign illness. Its treatment is largely supportive with total parenteral nutrition (TPN) while oral intake is encouraged. Acute onset of vomiting in healthy school age children can be initially explained by acute viral gastroenteritis. However, persistent vomiting associated with hematemesis and severe abdominal pain should warrant further work-up. This case report illustrates a self-limiting and rare cause of protein-losing enteropathy called Ménétrier's disease that presented with several variant clinical features not typically described in association with this entity.


Blood ◽  
1994 ◽  
Vol 84 (3) ◽  
pp. 904-909 ◽  
Author(s):  
RJ Slappendel ◽  
W Renooij ◽  
JJ de Bruijne

Examination of the red blood cells (RBCs) of eight dogs with familial stomatocytosis-hypertrophic gastritis (FS-HG), a multiorgan disease associated with hemolytic anemia, hereditary stomatocytosis (HSt), and hypertrophic gastritis resembling Menetrier's disease in man, showed abnormal osmotic fragility, normal mean corpuscular volume, slightly increased cell water, and normal cation content and cation fluxes. Cholesterol was decreased in RBC and increased in plasma. In both RBCs and plasma, total phospholipid (PL) was normal, phosphatidylcholine (PC) decreased, and sphingomyelin increased. The palmitic acid content of PC was increased, and the stearic acid content of PC was decreased. Sodium dodecyl sulfate electrophoresis of RBC membrane proteins was normal. These findings have not been described previously in HSt. They suggest that in FS-HG, abnormal composition of the PL in RBCs secondary to abnormal PL in plasma causes defective membrane function and stomatocytic shape-change. This conclusion was supported by a shortened half-life of 51Cr-labeled RBCs from normal dogs after transfusion in dogs with FS-HG. It was concluded (1) that not all hereditary forms of stomatocytosis are necessarily associated with an intrinsic structural defect of the RBC membrane, but that the change in shape of RBC may also be induced by abnormal composition of the plasma; (2) that stomatocytosis may be caused by loss of membrane surface area rather than by the increased cation uptake such as has been shown in some human kindreds with HSt, (3) that FS-HG is a disorder of lipid metabolism, and by consequence, (4) that abnormal lipid metabolism might be involved in the pathogenesis of Menetrier's disease.


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