C Andersen1, F T Jensen. 1. Department of Neurosurgery, Aarhus University Hospital, Denmark.
Abstract
PURPOSE: To study differences in tumour capillary permeability as expressed by the unidirectional transport rate constant Ki, extracellular distribution volume Vd and relaxation time T1 in human intracranial tumours using a recently described MRI method, and apply the model to study differences in these parameters after glucocorticoid (GC) treatment. PATIENTS AND METHODS: Seventeen brain tumour patients were studied. There were seven glioblastoma (GLI), four metastasis (MET), and six meningioma (MM) patients. Nine patients were studied before and after an average of 6 days of GC treatment. A 1.5 Tesla MR imaging scanner was used, and a two compartment diffusion model for Gd-DTPA was applied. RESULTS: There was a significant difference between pre-treatment Ki in GLI's and MM's, MM's having the highest permeability. There were no significant differences between pre-treatment Vd or T1 among the different tumour types. After GC treatment Ki decreased 15% on average (52% in GLI's and MET's, but only 4% in MM's). Vd decreased 14% on average in all tumours, but 47% in GLI's and MET's (p < 0.04), but increased 2% during treatment of MM's. T1 decreased 9% in all tumours (p < 0.04), but 11% in GLI's and MET's (p < 0.003), and only 6% in MM's. CONCLUSIONS: It is possible to estimate Ki, Vd and T1 simultaneously in brain tumour patients in a clinical MRI system. Ki was significantly higher in MM's compared to GLI's and MET's suggesting that MM's differ in some physiological parameter at the blood-tumour interface. MM's did not respond to GC treatment, neither in Ki, Vd nor in T1, whereas GLI's and MET's primarily decreased their extracellular distribution volume, suggesting that this may be an important effect in GC's mode of action in these tumour types.
PURPOSE: To study differences in tumour capillary permeability as expressed by the unidirectional transport rate constant Ki, extracellular distribution volume Vd and relaxation time T1 in humanintracranial tumours using a recently described MRI method, and apply the model to study differences in these parameters after glucocorticoid (GC) treatment. PATIENTS AND METHODS: Seventeen brain tumourpatients were studied. There were seven glioblastoma (GLI), four metastasis (MET), and six meningioma (MM) patients. Nine patients were studied before and after an average of 6 days of GC treatment. A 1.5 Tesla MR imaging scanner was used, and a two compartment diffusion model for Gd-DTPA was applied. RESULTS: There was a significant difference between pre-treatment Ki in GLI's and MM's, MM's having the highest permeability. There were no significant differences between pre-treatment Vd or T1 among the different tumour types. After GC treatment Ki decreased 15% on average (52% in GLI's and MET's, but only 4% in MM's). Vd decreased 14% on average in all tumours, but 47% in GLI's and MET's (p < 0.04), but increased 2% during treatment of MM's. T1 decreased 9% in all tumours (p < 0.04), but 11% in GLI's and MET's (p < 0.003), and only 6% in MM's. CONCLUSIONS: It is possible to estimate Ki, Vd and T1 simultaneously in brain tumourpatients in a clinical MRI system. Ki was significantly higher in MM's compared to GLI's and MET's suggesting that MM's differ in some physiological parameter at the blood-tumour interface. MM's did not respond to GC treatment, neither in Ki, Vd nor in T1, whereas GLI's and MET's primarily decreased their extracellular distribution volume, suggesting that this may be an important effect in GC's mode of action in these tumour types.
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