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Thromb Haemost 2001; 85(02): 250-255
DOI: 10.1055/s-0037-1615705
Review Article
Schattauer GmbH

Whole Blood Tissue Factor Procoagulant Activity Remains Detectable during Severe Aplasia following Bone Marrow and Peripheral Blood Stem Cell Transplantation

Muhit Ozcan
1   Department of Hematology, University of Ankara Medical School, Ibni Sina Hospital, Ankara, Turkey
,
Colleen T. Morton
2   Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
,
Anna Solovey
2   Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
,
Luke Dandelet
2   Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
,
Ronald R. Bach
3   Research Service, Veterans’ Administration Hospital, Minneapolis, MN, USA
,
Robert P. Hebbel
2   Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
,
Arne Slungaard
2   Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
,
Nigel S. Key
2   Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
› Author Affiliations
Supported by grants R29-HL55219 (to N.S.K.) and MO1-RR00400 from the National Center for Research Resources, the National Institutes of Health
Further Information

Publication History

Received 29 May 2000

Accepted after resubmission 30 August 2000

Publication Date:
08 December 2017 (online)

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Summary

Using a novel whole blood assay, we recently demonstrated that tissue factor procoagulant activity (TF PCA) is present in normal individuals. Preliminary experiments suggested that this activity is localized in the mononuclear cell fraction. Postulating that whole blood TF PCA would therefore be undetectable when monocytes and neutrophils are absent from peripheral blood, we assayed TF PCA during the peri-transplant period in 15 consecutive patients undergoing allogeneic (n = 12) or autologous (n = 3) bone marrow transplantation (BMT) or peripheral blood stem cell transplantation (PBSCT). Baseline (pre-transplant) mean TF PCA was higher in patients compared to normal controls (P <0.005). Unexpectedly, although TF PCA during the period of profound aplasia was significantly reduced compared to baseline (p <0.05), fully 55% of the initial activity remained detectable. During the engraftment phase, TF PCA returned to pre-transplant levels, with a linear correlation between monocyte counts and TF PCA (r = 0.63). In contrast to normal whole blood, incubation of aplastic samples with E. Coli lipopolysaccharide ex vivo failed to induce TF PCA. Throughout the period of study – but especially during the aplastic phase – the absolute number of circulating endothelial cells (CECs) that were TF antigen-positive was increased compared to normals (P <0.001). However, removal of these cells from whole blood samples failed to significantly diminish total TF PCA indicating that CECs alone could not account for the detectable TF PCA during aplasia. We conclude that neither circulating mature myelo-monocytic cells nor endothelial cells can account for all the functionally intact TF in peripheral blood. Further studies are needed to identify the other source(s) of TF PCA.

Keywords

Tissue factor - whole blood - bone marrow transplantation - bone marrow aplasia