Summary
Hepatic venocclusive disease causes considerable morbidity and mortality following
bone marrow transplantation. There are two hypotheses regarding 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
intravascular deposition of fibrin. We have investigated these mechanisms by measuring
the changes in proteins C and S and factors VII and X in the post transplant period
and by using the plasma concentration of factor Vila as an in vivo marker of potential
endothelial cell tissue factor 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 dysfunction induced by the
chemo-radiotherapy. Factor Vila 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 there are both anticoagulant and procoagulant changes. The absence
of any changes in factor Vila levels suggests that tissue factor was not exposed to
the general circulation following BMT but does not exclude focal expression at the
sites of thrombosis.
