P. Collins et al., FACTOR VIIA AND OTHER HEMOSTATIC VARIABLES FOLLOWING BONE-MARROW TRANSPLANTATION, Thrombosis and haemostasis, 72(1), 1994, pp. 28-32
Hepatic venocclusive disease causes considerable morbidity and mortali
ty following bone marrow transplantation. There are two hypotheses reg
arding the aetiology of this syndrome; firstly that changes in plasma
coagulation factors and natural anticoagulants lead to a prothrombotic
state and secondly that endothelial cell activation stimulates intrav
ascular deposition of fibrin. We have investigated these mechanisms by
measuring the changes in proteins C and S and factors VII and X in th
e post transplant period and by using the plasma concentration of fact
or VIIa as an in vivo marker of potential endothelial cell tissue fact
or expression. Protein C fell in both allograft and autograft patients
but more so in the allografts. Similar results were found for factors
VII and X. These changes were predominantly due to hepatic dysfunctio
n induced by the chemo-radiotherapy. Factor VIIa levels were unchanged
in both the allograft and autograft patients. We conclude that there
is no convincing evidence for a procoagulant state following BMT as th
ere are both anticoagulant and procoagulant changes. The absence of an
y changes in factor Wa levels suggests that tissue factor was not expo
sed to the general circulation following BMT but does not exclude foca
l expression at the sites of thrombosis.