J R Hall1, S C Short. 1. Department of Oncology, Kent and Canterbury Hospital, Ethelbert Road, Canterbury CT1 3NG, UK. julia.hall1@nhs.net
Abstract
AIMS: HIV infection is associated with an increased incidence of glioblastoma multiforme (GBM). Here we report four new cases of HIV-associated GBM, discuss these in the context of previously reported cases, and consider aspects of current glioma management in HIV-positive patients. METHODS AND RESULTS: Twenty-one cases of GBM in HIV-positive patients, including four treated recently at our own institution, are discussed. The median age at presentation of the whole series was 38 years (range 19-60 years). The median CD4 count at GBM presentation was 400 cells/mm(3) (range 80-610 cells/mm(3)). Patients had been HIV positive for a median of 3 years (range 0-11 years) before tumour presentation. Treatment and survival were analysed in 16 of the 21 patients (five published cases were excluded: three due to lack of further information and two spinal cord tumours). Treatment included surgical debulking, radical radiotherapy and chemotherapy, all of which were well tolerated. The median survival was 8 months for the 16 patients with assessable data. CONCLUSIONS: GBM occurs at an increased frequency and younger age in the HIV population than in the general population. HIV itself is not found in glioma specimens, but the effect of HIV infection on reduced immune surveillance is thought to promote the development of these tumours. The approach to management of HIV-positive patients with GBM should be the same as the general population, using surgery, radiotherapy and chemotherapy. Vincristine should be used with caution due to potential interactions with highly active antiretroviral therapy, causing an increased rate of autonomic neuropathy. Continuous low-dose temozolomide treatment should also be used cautiously because of potential additive lymphopenia. Survival of glioma patients with HIV is dictated by their tumour, not their HIV status.
AIMS: HIV infection is associated with an increased incidence of glioblastoma multiforme (GBM). Here we report four new cases of HIV-associated GBM, discuss these in the context of previously reported cases, and consider aspects of current glioma management in HIV-positivepatients. METHODS AND RESULTS: Twenty-one cases of GBM in HIV-positivepatients, including four treated recently at our own institution, are discussed. The median age at presentation of the whole series was 38 years (range 19-60 years). The median CD4 count at GBM presentation was 400 cells/mm(3) (range 80-610 cells/mm(3)). Patients had been HIV positive for a median of 3 years (range 0-11 years) before tumour presentation. Treatment and survival were analysed in 16 of the 21 patients (five published cases were excluded: three due to lack of further information and two spinal cord tumours). Treatment included surgical debulking, radical radiotherapy and chemotherapy, all of which were well tolerated. The median survival was 8 months for the 16 patients with assessable data. CONCLUSIONS: GBM occurs at an increased frequency and younger age in the HIV population than in the general population. HIV itself is not found in glioma specimens, but the effect of HIV infection on reduced immune surveillance is thought to promote the development of these tumours. The approach to management of HIV-positivepatients with GBM should be the same as the general population, using surgery, radiotherapy and chemotherapy. Vincristine should be used with caution due to potential interactions with highly active antiretroviral therapy, causing an increased rate of autonomic neuropathy. Continuous low-dose temozolomide treatment should also be used cautiously because of potential additive lymphopenia. Survival of gliomapatients with HIV is dictated by their tumour, not their HIV status.
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