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Tumor necrosis factor infusions have a procoagulant effect on the
hemostatic mechanism of humans
KA Bauer, H ten Cate, S Barzegar, DR Spriggs, ML Sherman and RD Rosenberg
Charles A. Dana Research Institute, Beth Israel Hospital, Boston, MA 02215.
Several investigators have reported that tumor necrosis factor (TNF) can
alter the hemostatic properties of vascular endothelial cells in vitro. We
have examined the in vivo effects on the hemostatic mechanism of
recombinant human TNF administered as a continuous intravenous infusion to
23 cancer patients with active disease. A battery of sensitive and specific
immunochemical techniques were used to monitor changes in blood
coagulability. Serial determinations of F1 + 2, the protein C activation
peptide (PCP), and fibrinopeptide A (FPA) were obtained prior to the
initiation of the TNF infusions and at three and 24 hours after the start
of therapy in 12 individuals who received greater than 3 x 10(5) U/m2/24h.
The mean levels of F1 + 2, PCP, and FPA were significantly elevated at both
time points as compared to the baseline values. The metabolic behavior of
125I-F1 + 2 in an animal model was not affected by infusions of the
cytokine. We therefore conclude that the observed elevations in the
concentration of this marker in humans receiving TNF result from hemostatic
system hyperactivity. In 11 subjects infused with 1 x 10(5) to 2.4 x 10(5)
U/m2/24 h of the cytokine, the mean levels of F1 + 2, PCP, and FPA were not
significantly greater at 24 hours as compared with the baseline values,
indicating that there is a threshold dose at which the cytokine can exert a
biochemical effect on the coagulation system. Our studies demonstrate that
TNF is able to provide a substantial net procoagulant stimulus to the
hemostatic mechanism, and suggest that this cytokine may be a mediator of
certain hypercoagulable states in humans.
Volume 74,
Issue 1,
pp. 165-172,
07/01/1989
Copyright © 1989 by The American Society of Hematology
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