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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Slappendel, R. Articles by de Bruijne, J. Search for Related Content PubMed PubMed Citation Articles by Slappendel, R. Articles by de Bruijne, J. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Normal cations and abnormal membrane lipids in the red blood cells of dogs with familial stomatocytosis-hypertrophic gastritis RJ Slappendel, W Renooij and JJ de Bruijne Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, University of Utrecht, The Netherlands. 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. Volume 84, Issue 3, pp. 904-909, 08/01/1994 Copyright © 1994 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. S. Rallis, M. N. Patsikas, M. E. Mylonakis, M. J. Day, T. A. Petanides, L. G. Papazoglou, and A. F. Koutinas Giant Hypertrophic Gastritis (Menetrier's-like Disease) in an Old English Sheepdog J. Am. Anim. Hosp. Assoc., March 1, 2007; 43(2): 122 - 127. [Abstract] [Full Text] [PDF]

	Copyright © 1994 by American Society of Hematology         Online ISSN: 1528-0020