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Treatment of hepatic venocclusive disease with recombinant human tissue
plasminogen activator and heparin in 42 marrow transplant patients
SI Bearman, JL Lee, AE Baron and GB McDonald
Division of Clinical Research, Fred Hutchinson Cancer Research Center,
Seattle, USA.
The purpose of this report is to review the Fred Hutchinson Cancer Research
Center experience of treating patients with venocclusive disease of the
liver (VOD) after marrow transplantation using recombinant human tissue
plasminogen activator (rh-tPA) and heparin. The charts of 42 patients who
had received rh-tPA and heparin for the treatment of VOD between February
1991 and December 1995 were reviewed. Response to rh-tPA and heparin was
defined as a reduction in total serum bilirubin by 50% within 10 days of
starting treatment. Total serum bilirubin, percent weight gain, and serum
creatinine before, after, and at the start of rh-tPA and heparin were
examined to determine whether these laboratory values distinguished
patients who responded to treatment from those who did not. We also
evaluated whether evidence of multiorgan failure (requirement for
supplemental oxygen, requirement for hemodialysis, requirement for
mechanical ventilation) or whether the calculated probability of a fatal
outcome from VOD could discriminate responders from nonresponders. In
addition, the incidence and outcome of bleeding as a major complication of
thrombolytic therapy was examined. Twelve patients responded to rh-tPA and
heparin and 30 patients did not. There were no statistically significant
differences between responders and nonresponders in the day treatment was
started, dose of rh-tPA, total serum billirubin, and percent weight gain
before, after, or at the start of treatment, or the calculated probability
of dying from VOD on the day treatment with rh- tPA and heparin was begun.
More nonresponding patients required dialysis or mechanical ventilation (11
of 30) before or at the start of rh-tPA and heparin than responding
patients (0 of 12), P = .0183. Serum creatinine was greater at the start of
treatment in nonresponding patients (1.9 +/- 1.3 mg/dL) than in responding
patients (1.1 +/- 0.4 mg/dL), P = .0794. Ten patients had severe bleeding
episodes, which resulted in death in three patients and may have
contributed to death in an additional three patients. Treatment for VOD
using rh-tPA and heparin was successful in 29% of patients but was
associated with a significant risk of life-threatening hemorrhage.
Requirement for supplemental oxygen, dialysis, or mechanical ventilation
before the start of treatment were prognostic indicators of no response to
thrombolytic therapy. We do not recommend treatment using tPA and heparin
in patients with severe VOD who have already developed multiorgan
dysfunction.
Volume 89,
Issue 5,
pp. 1501-1506,
03/01/1997
Copyright © 1997 by The American Society of Hematology
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