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Abstract
Hepatic veno-occlusive disease (VOD) is a major cause of morbidity and mortality following
high dose cytotoxic therapy for stem cell transplantation (SCT). Pre-existing liver
damage, SCT-related therapy, and genetic polymorphisms all appear to increase the
risk of developing VOD. Studies of biological markers during SCT suggest that cytokines,
haemostasis, and hepatic drug metabolism via the glutathione pathway are all involved
in the pathogenesis of VOD. Until recently, treatment options were limited and experimental
therapies directed at the pathogenesis of the disease were mostly unsuccessful. However,
Defibrotide, a relatively new agent that has modulatory effects on vascular endothelium,
cytokine release, and haemostasis, has been used with some success in the management
and prophylaxis of VOD. In the future, a better understanding of genetic polymorphisms
and biological markers which may be important in the pathogenesis of VOD, may enable
us to predict which patients are most likely to be affected.