Sage Journals: Discover world-class research

Abstract

The most common adult primary brain tumor is glioblastoma multiforme (GBM). Current treatment is surgical resection, adjuvant radiation and chemotherapy, which can extend the median survival 20—36 weeks (Mansky et al. Central nervous system tumors. In Abraham J, Allegra CJ, Gulley J, eds. Bethesda Handbook of clinical oncology, 2nd edn. Philadelphia, Pennsylvania: Lippincott Williams and Wilkins, 2000: 440—2; Knox S. Intracranial tumors. In Pillot G, Chantler M, Magiera H, Peles S, et al., eds. The Washington Manual Hematology and Oncology Subspecialty Consult. Philadelphia, Pennsylvania: Lippincott Williams and Wilkins, 2004: 204—6.). But treatment efficacy is limited, mandating the exploration of more effective treatments. We report on a patient with GBM treated as per a clinical protocol with high-dose methotrexate (12 g/m²), who expired within hours after the initiation of treatment secondary to transtentorial herniation. Although it is not completely clear what caused the patient's herniation, we think that high-dose methotrexate therapy may have played a crucial role. We suggest that high-dose methotrexate should be used cautiously in patients with GBM. J Oncol Pharm Practice (2008) 14: 57—60.

Keywords

methotrexate glioblastoma multiforme neurotoxicity

Get full access to this article

View all access options for this article.

References

Vezmar S. , Becker A. , Bode U. , Jaehde U. Biochemical and clinical aspects of methotrexate neurotoxicity. Chemotherapy 2003; 49: 92—104.

McManus C. , Valley A. Cancer treatment and chemotherapy. In: Dipiro J , Talbert R , Yee G , et al., eds. Fifth edition Pharmacotherapy a Pathophysiologic Approach 2002; New York: McGraw-Hill, 2002:2196.

Bleyer WA Neurologic sequelae of methotrexate and ionizing radiation: A new classification . Cancer Treat Rep 1981; 65 (Suppl 1): 89—98.

Allen JC , Rosen G. Transient cerebral dysfunction following chemotherapy for osteogenic sarcoma . Ann Neurol 1978; 3441—4.

Walker RW , Allen JC , Rosen G. , Caparros B. Transient cerebral dysfunction secondary to high-dose methotrexate. J Clin Oncol 1986; 4: 1845—50.

Yim YS , Mahoney Jr DH , Oshman DG Hemiparesis and ischemic changes of the white matter after intrathecal therapy for children with acute lymphocytic leukemia . Cancer 1991; 67: 2058—61.

Kaplan RS , Wiernik PH Neurotoxicity of antineoplastic drugs. Semin Oncol 1982; 9: 103—30.

Bleyer WA , Drake JC , Chabner BA Neurotoxicity and elevated cerebrospinal-fluid methotrexate concentration in meningeal leukemia. N Engl J Med 1973; 289: 770—3.

Bleyer WA Neurologic sequelae of methotrexate and ionizing radiation. Cancer Treat Rep 1981; 65 (Suppl 1): 89—98.

10.

Chambers , et al. Acute hyperhomocysteinemia and endothelial dysfunction. Lancet 1998; 351: 36—7.

11.

Crontein , et al. The anti-inflammatory mechanism of methotrexate. Increased adenosine release at inflamed sites diminishes leukocyte accumulation in an in vivo model of inflammation. J Clin Invest 1993; 92: 2675—82.

A fatal outcome in a patient with glioblastoma multiforme after receiving high-dose methotrexate

Abstract

Keywords

Get full access to this article

References