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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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Vicente, V. Articles by Griffin, J. H. Search for Related Content PubMed PubMed Citation Articles by Vicente, V. Articles by Griffin, J. H. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Evidence of activation of the protein C pathway during acute vascular damage induced by Mediterranean spotted fever V Vicente, F Espana, D Tabernero, A Estelles, J Aznar, S Hendl and JH Griffin Department of Medicine, School of Medicine, Murcia, Spain. Mediterranean spotted fever (MSF) is a rickettsiosis that induces widespread microvascular injury. To obtain quantitative information on the in vivo activation and inactivation of the protein C system during the acute phase of endothelial damage, several components of the protein C pathway were studied in 28 MSF patients. Upon admission (day 1), patients showed clear evidence of endothelial damage as reflected by the significant decrease in the ratio VIII:C/vWF:Ag (0.36 +/- 0.14, mean +/- SD) compared with normals (0.98 +/- 0.14), and clinical and laboratory signs of hemostatic alterations such as decreased platelet count, positive fibrinogen/fibrin degradation products, and increased thrombin:antithrombin-III complex levels. Antigenic protein C (72% +/- 18%) and protein C inhibitor (PCI) (41% +/- 20%) were significantly decreased (P less than .001). Complexes of activated protein C (APC) with PCI or with alpha 1-antitrypsin (alpha 1AT) and of plasma kallikrein with PCI (KK:PCI) were measured using sandwich enzyme-linked immunosorbent assays. APC:alpha 1AT complex levels were increased in patients at day 1 (27 +/- 13 ng/mL) compared with controls (7 +/- 2 ng/mL), and APC:PCI and KK:PCI complexes, which were not detectable in any of the controls, were present in 57% and 75% of the 28 MSF patients, with mean levels of 11 +/- 5 and 46 +/- 16 ng/mL, respectively. After remission of the disease (day 30), a trend toward normal values in the majority of the parameters studied was found. This study shows that, in the course of endothelial injury, MSF patients experience a generalized activation of the protein C pathway, resulting in consumption of protein C and PCI, and in the appearance of APC:inhibitor complexes. Moreover, these data provide the evidence that KK:PCI circulating complexes occur in vivo. Volume 78, Issue 2, pp. 416-422, 07/15/1991 Copyright © 1991 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

	Copyright © 1991 by American Society of Hematology         Online ISSN: 1528-0020