Clinical Neuroscience

[Chemotherapy of recurrent supratentorial malignant gliomas (Phase II study)]

ÁFRA Dénes, SIPOS László, VITANOVICS Dusan

FEBRUARY 20, 2002

Clinical Neuroscience - 2002;55(01-02)

[At the Hungarian National Institute of Neurosurgery 73 recurrent supratentorial malignant tumours were treated by chemotherapy during the last ten years. Chemotherapy was applied after postoperative radiotherapy but in some cases following reoperation only. All cases were clinically and by CT or MRI verified recurrences. Forty-three patients received BCNU-DBD (dibromodulcitol) treatment (23 anaplastic astrocytoma - AA, and 20 glioblastoma multiforme - GM): day 1. BCNU 150 mg/sq.m. in iv. infusion, day 2. dibromdulcitol 1000 mg/sq orally was given. This course was repeated every six weeks, altogether 2-8 times. Sixteen patients with AA responded with complete or partial regression but only 6 did with GM. Median survival was 14 and 7 months, the difference proved to be significant, p=0.0091. PCV combination (procarbazine, CCNU, vincristine) was applied to 16 patients with AA and 14 cases with recurrent oligodendroglioma (O). Treatment started with vincristine 1.5 mg/sq. m. iv. (2.0 mg maximum), the next day CCNU 100 mg/sq.m. was given, followed by procarbazine 60 mg/sq.m. on days 8-22. and finished by the same dose of vincristine on day 30. The course was repeated after one month, mostly six times. Six patients with AA did not respond; in cases of oligodendroglioma all but one responded with complete or partial improvement. It is remarkable that no significant difference was found between the survivals of BCNU-DBD or PCV treated AA patients. Chemotherapy of supratentorial malignant glioma recurrences with nitroso-ureas and their combination proved to be efficacious. It also seems, that in recurrent cases lower grade gliomas show better response rate than glioblastomas.]

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[In the development of a cholesterol granuloma both cellular and vascular permeability factors have to be taken into consideration. It may arise as a special degradation product in a chronic cerebral infarct because of the partial insufficient activity of the macrophages. Consequently, the degradation of brain sphingolipids and other compounds does not follow the usual route of degradation and transportation by granular cells to the stage of neutral fat but the necrotic mass transforms into cholesterol esters. Cholesterol crystals produce an irritative effect to neighbouring tissues which may result in the formation of young fibroblasts with proliferative tendency in the vessel wall. Some of the fibroblasts take part in the proliferation of connective tissue, while the rest degenerate, producing more cholesterol or xanthomatous material. Inflammatory changes may also be associated with these lesions. The amount of cholesterol sometimes increases in the inner side of the thickening connective tissue layer. The final result may be an intracranial space occupying mass or it may end as a small cholesterol granuloma, as demonstrated in our incidental cases. By the time a granuloma has developed, the original vessel usually disappears completely, but sometimes remnants of vessels might prove the vascular origin. Other pathomechanisms should also be taken into consideration, such as a cholesterol embolus or anomalous vessel with a large cholesterol plaque in the wall. This also explains why trauma (hemorrhage, granulation), cholesterol embolus, inflammation, metabolic imbalance may predispose to the formation of a granuloma, as well as the hypercholesterolaemia. The nine cases demonstrate the significance of the intracranial granuloma from pathological, clinical and neurosurgical points of view. Such cases have not yet been reported in the national or international literature.]

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