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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Styles, L. A. Articles by Kuypers, F. A. Search for Related Content PubMed PubMed Citation Articles by Styles, L. A. Articles by Kuypers, F. A. Related Collections Red Cells Brief Reports Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 November 2000, Vol. 96, No. 9, pp. 3276-3278 BRIEF REPORT Secretory phospholipase A2 predicts impending acute chest syndrome in sickle cell disease Lori A. Styles, Anton J. Aarsman, Elliott P. Vichinsky, and Frans A. Kuypers From the Department of Hematology/Oncology, Children's Hospital Oakland, and Children's Hospital Oakland Research Institute, Oakland, CA; and the Center for Biomembranes and Lipid Enzymology, Department of Lipid Biochemistry, University of Utrecht, the Netherlands. Acute chest syndrome (ACS) is the leading cause of death in sickle cell disease. Severe ACS often develops in the course of a vaso-occlusive crisis (VOC), but currently there are no predictors for its development. Secretory phospholipase A2 (sPLA2), a potent inflammatory mediator, is elevated in ACS, and previous work suggests that sPLA2 predicts impending ACS. We prospectively evaluated sPLA2 concentration during 21 admissions for VOC; 6 of these patients went on to develop ACS. Elevation of sPLA2 was detected all 6 patients 24 to 48 hours before ACS was clinically diagnosed. Adding the requirement for fever raised the specificity of sPLA2 to 87% while retaining 100% sensitivity. These data indicate that sPLA2 can be useful in alerting the clinician to patients with impending ACS. In addition, sPLA2 may be useful for instituting early therapies to prevent or reduce the clinical morbidity of ACS. © 2000 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: N. A. Neidlinger, S. K. Larkin, A. Bhagat, G. P. Victorino, and F. A. Kuypers Hydrolysis of Phosphatidylserine-exposing Red Blood Cells by Secretory Phospholipase A2 Generates Lysophosphatidic Acid and Results in Vascular Dysfunction J. Biol. Chem., January 13, 2006; 281(2): 775 - 781. [Abstract] [Full Text] [PDF] E. M. Bargoma, J. K. Mitsuyoshi, S. K. Larkin, L. A. Styles, F. A. Kuypers, and S. T. Test Serum C-reactive protein parallels secretory phospholipase A2 in sickle cell disease patients with vasoocclusive crisis or acute chest syndrome Blood, April 15, 2005; 105(8): 3384 - 3385. [Full Text] [PDF] G. R. Buchanan, M. R. DeBaun, C. T. Quinn, and M. H. Steinberg Sickle Cell Disease Hematology, January 1, 2004; 2004(1): 35 - 47. [Abstract] [Full Text] [PDF] V Mak and S C Davies The pulmonary physician in critical care * Illustrative case 6: Acute chest syndrome of sickle cell anaemia Thorax, August 1, 2003; 58(8): 726 - 728. [Full Text] [PDF] M. C. Walters, A. W. Nienhuis, and E. Vichinsky Novel Therapeutic Approaches in Sickle Cell Disease Hematology, January 1, 2002; 2002(1): 10 - 34. [Abstract] [Full Text]

	Copyright © 2000 by American Society of Hematology         Online ISSN: 1528-0020