Introduction: Meningioma comprises approximately 33%of all primary brain tumours .Overall incidence in general population is 2.3/100000. The incidence increases with each decade of life and peaks in the 5-6th decade. Despite being benign in pathophysiology in 90% of histology, like carcinomas, they always result from clonal outgrowth derived from a single cell as exemplified by cytogenetic and array-comparative genomic hybridization studies. Approximately 12% of all human cancers are caused by oncoviruses, however the causal relationship between meningioma and viruses, although suggested has not been proven.

Methods: A retrospective chart review of all consecutive patients with pathologically confirmed intracranial meningioma in our institution over a period of 15 years. Data was extracted from electronic filing system and images from the pax. All patients had MRI prior to surgery. Each chart was reviewed for the demographic, histology, tumour location, HIV status, CD4 count and anti-retroviral therapy.

Results: Our search identified 388 patients with pathologically confirmed intracranial meningioma. Median age was 47 years. Male: Female ratio of 1:3.5. Sixty four (17%) of the patients were HIV positive, and 62.5% (40) of them had their CD4 count known. 18(28%) of this patient who are HIV positive were on ARVs. Median age of HIV positive patient (38 years) was significantly younger than the rest of the group. WHO Grade 2 accounted for 19.2% which is higher than expected. Patients who are HIV positive harbored even higher percentage of WHO grade 2 (38%) and WHO Grade 3 (11%).

Conclusions: Intracranial meningioma among patients who are HIV positive occur at a younger age and tend to harbor histologically higher grade. Failure of immune-Surveillance alone may not fully account for the behavior of meningioma in HIV infected patients. There is body of evidence which suggest that HIV-Tat protein may directly play a role in meningioma development and progression.

Patient Care: By recognising that HIV may directly play a role in the development and/or progression towards higher grade of meningioma, particularly in younger patients, will argue strongly towards early commencement of antiretroviral therapies irrespective of the level of CD4 Counts. If the spectra of Non-AIDS defining malignancies if verified, including meningioma,strategies in HIV treatment will not only aim to prevent development of AIDS defining tumours but also prevention of those disease that are not AIDS defining. This research will also stimulate interest in development of novel therapies that will target the viral specific particles proven to cause tumours including meningioma.

Learning Objectives: By conclusion of this session, the participants should be able to: 1) To recognise that meningioma in HIV infected patients occur at younger age and usually harbour higher incidence of WHO grade 2 and WHO grade 3 than seen in general population. 2)To discuss in small groups why such a high incidence of WHO grade 2 and 3 meningiomas seen in HIV positive patients, is not seen in association with other immunosuppressive diseases or in patients on immunosuppressive therapies, if failure of immune-surveillance is responsible for malignant transformation. 3)To identify potential novel therapies that may inhibit the virulent particles of HIV such as Tat-Protein in the armamentorium of preventative and treatment strategies of meningioma in HIV infected patients.

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