Anticancer research · 2011
Evidence for acute vascular toxicity of cisplatin-based chemotherapy in patients with germ cell tumour.
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Dieckmann Klaus-Peter, Struss Werner Jan, Budde Ulrich
Аннотация
BACKGROUND: Acute early vascular toxicity of chemotherapy for germ cell tumour (GCT) is poorly understood. To explore the pathogenesis of this complication we evaluated laboratory parameters associated with vascular disease.
PATIENTS AND METHODS: In 33 GCT patients the following parameters were investigated with routine laboratory methods before and after chemotherapy: von Willebrand factor antigen (vWF:AG), collagen binding capacity (vWF:CB), lipoprotein (a), homocysteine, plasminogen activator inhibitor I, total cholesterol, high density lipoprotein, low density lipoprotein, troponine I. Statistical evaluation involved descriptive analysis and the Wilcoxon signed rank test.
RESULTS: Levels of vWF:AG and vWF:CB increased significantly upon therapy (p=0.002). All other parameters remained unchanged. Upon late measurement, vWF:AG and vWF:CB were normalised.
CONCLUSION: As von Willebrand factor is released from endothelial cells upon damage, we postulate that early vascular toxicity of chemotherapy is caused by direct damage of the vascular endothelium. Long-term vascular complications of chemotherapy appear to be different, pathogenetically.
PATIENTS AND METHODS: In 33 GCT patients the following parameters were investigated with routine laboratory methods before and after chemotherapy: von Willebrand factor antigen (vWF:AG), collagen binding capacity (vWF:CB), lipoprotein (a), homocysteine, plasminogen activator inhibitor I, total cholesterol, high density lipoprotein, low density lipoprotein, troponine I. Statistical evaluation involved descriptive analysis and the Wilcoxon signed rank test.
RESULTS: Levels of vWF:AG and vWF:CB increased significantly upon therapy (p=0.002). All other parameters remained unchanged. Upon late measurement, vWF:AG and vWF:CB were normalised.
CONCLUSION: As von Willebrand factor is released from endothelial cells upon damage, we postulate that early vascular toxicity of chemotherapy is caused by direct damage of the vascular endothelium. Long-term vascular complications of chemotherapy appear to be different, pathogenetically.