Human plasma extrinsic pathway inhibitor activity: II. Plasma levels in
disseminated intravascular coagulation and hepatocellular disease
TA Warr, LV Rao and SI Rapaport
Department of Medicine, University of California, San Diego 92103.
Plasma or serum extrinsic pathway inhibitor (EPI) activity was measured in
24 patients with disseminated intravascular coagulation (DIC) and in 23
patients with severe hepatocellular disease. EPI was measured as activity
in a test sample that inhibited factor VIIa/tissue factor (TF)- catalyzed
activation of 3H-factor IX (activation peptide release) in the presence of
factor X. Of the 24 patients with DIC, 13 had sepsis and five had
metastatic carcinoma, disorders in which tissue factor is believed to
initiate DIC. EPI activity ranged from 68% to 300% (mean 134% +/- 50%).
Serial measurements in nine patients failed to show depletion of EPI
activity coincident with worsening DIC. DIC induced by tissue factor or
other activating materials may progress despite normal EPI levels. In the
patients with liver disease, of whom 15 had decompensated chronic
hepatocellular disease (two fatal cases) and eight had acute fulminant
liver failure (seven fatal cases), plasma or serum EPI activity varied from
less than 20% to 194%. Values were distributed in a bimodal fashion. EPI
activity could not be correlated with either the etiology of the liver
disease or the degree of prolongation of the prothrombin time. Patients
with chronic hepatocellular disease who survived had normal or elevated EPI
activity. Patients with fatal hepatic dysfunction had low, normal, or high
values for EPI activity. This must mean that secretion of EPI from cells
other than hepatocytes can maintain normal plasma EPI levels.
Volume 74,
Issue 3,
pp. 994-998,
08/15/1989
Copyright © 1989 by The American Society of Hematology
