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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 Stuart, M. J. Articles by Allen, J. B. Search for Related Content PubMed PubMed Citation Articles by Stuart, M. J. Articles by Allen, J. B. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Abnormal platelet function and arachidonate metabolism in chronic idiopathic thrombocytopenic purpura MJ Stuart, JG Kelton and JB Allen We observed several patients with chronic idiopathic thrombocytopenic purpura (ITP) whose bleeding times were more prolonged than would have been expected from their platelet counts. To investigate this further, we performed in vivo and in vitro platelet function studies, assessed arachidonate metabolism, and measured platelet-associated IgG (PAIGG) in seven patients with chronic ITP. The bleeding times of three of the patients were prolonged for greater than 7 min, and all of these patients had impaired platelet aggregation and abnormal platelet arachidonic acid metabolism as reflected by increased production of the lipoxygenase product HETE and a concomitant decrease in cyclooxygenase products, TXB2 and HHT (p less than 0.001). The abnormalities noted were not due to concomitant drug ingestion, since they were present on repeated evaluation. There was no relationship between the platelet count and the bleeding time; however, there was a significant inverse correlation between the bleeding time and TXB2 production in all patients evaluated (r = 0.81; p less than 0.05). There was no relationship between the level of platelet-associated IgG and any parameter of platelet aggregation or arachidonate metabolism. The abnormalities noted should be looked for in the individual patient with chronic ITP, since the bleeding tendency is exacerbated by the superimposed impairment of platelet function even at platelet counts of greater than 50,000/cu mm, levels generally regarded as "safe." Volume 58, Issue 2, pp. 326-329, 08/01/1981 Copyright © 1981 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: S. Kosugi, Y. Tomiyama, S. Honda, H. Kato, T. Kiyoi, H. Kashiwagi, Y. Kurata, and Y. Matsuzawa Platelet-associated anti-GPIIb-IIIa autoantibodies in chronic immune thrombocytopenic purpura recognizing epitopes close to the ligand-binding site of glycoprotein (GP) IIb Blood, September 15, 2001; 98(6): 1819 - 1827. [Abstract] [Full Text] [PDF] F. Alves-Rosa, C. Stanganelli, J. Cabrera, N. van Rooijen, M. S. Palermo, and M. A. Isturiz Treatment with liposome-encapsulated clodronate as a new strategic approach in the management of immune thrombocytopenic purpura in a mouse model Blood, October 15, 2000; 96(8): 2834 - 2840. [Abstract] [Full Text] [PDF] C. A. Koch, T. P. Archer, and E. H. Kraut Myocardial Ischemia in a Patient With Chronic Refractory Idiopathic Thrombocytopenic Purpura Arch Intern Med, December 8, 1997; 157(22): 2668 - 2668. [Abstract] [PDF]

	Copyright © 1981 by American Society of Hematology         Online ISSN: 1528-0020