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Demonstration of Rickettsia conorii-induced endothelial injury in vivo by
measuring circulating endothelial cells, thrombomodulin, and von Willebrand
factor in patients with Mediterranean spotted fever [see comments]
F George, P Brouqui, MC Boffa, M Mutin, M Drancourt, C Brisson, D Raoult and J Sampol
Laboratoire d'Immuno-Hematologie, Faculte de Pharmacie, Marseille, France.
The endothelial cell (EC) is the primary target for Rickettsia conorii (RC)
in Mediterranean spotted fever (MSF). Clinical manifestations such as
thrombosis and vasculitis are mediated by pathologic changes localized in
blood vessels. To study the in vivo endothelial injury induced by RC,
markers of endothelial damage, including circulating EC (CEC), plasmatic
thrombomodulin (TM), and von Willebrand factor (vWF), were investigated in
12 patients with MSF. CEC were counted in whole blood by a new
immunomagnetic separation assay using a specific anti-EC antibody, S-Endo
1. Plasmatic TM and vWF antigens were measured by enzyme-linked
immunosorbent assay. High levels of CEC and cell fragments were found in
patients with a severe or malignant form of MSF. Sequential studies of CEC
showed a decrease from 162 +/- 454 cells/mL before treatment to 6 +/- 7
cells/mL during treatment and recovery. Mean plasma TM and vWF levels that
were also elevated before therapy (TM, 106 +/- 27 ng/mL; vWF, 420% +/-
164%) decreased progressively (TM, 55 +/- 43 ng/mL; vWF, 148% +/- 26%)
during treatment. The measurement of cellular and molecular markers of
vascular damage such as CEC, plasmatic TM, and vWF contributes to the
definition of the Rickettsia-induced endothelial injury in vivo.
Volume 82,
Issue 7,
pp. 2109-2116,
10/01/1993
Copyright © 1993 by The American Society of Hematology
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