Choy Winward, Lagman Carlito, Lee Seung J, Bui Timothy T, Safaee Michael, Yang Isaac
Department of Neurosurgery, University of California, Los Angeles, Los Angeles, CA, USA.
Department of Neurosurgery, University of California, Los Angeles, Los Angeles, CA, USA.; Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles, CA, USA.
Brain Tumor Res Treat. 2016 Oct;4(2):77-86. doi: 10.14791/btrt.2016.4.2.77. Epub 2016 Oct 31.
Improvement in antiviral therapies have been accompanied by an increased frequency of non-Acquired Immune Deficiency Syndrome (AIDS) defining malignancies, such as glioblastoma multiforme. Here, we investigated all reported cases of human immunodeficiency virus (HIV)-positive patients with glioblastoma and evaluated their clinical outcomes. A comprehensive review of the molecular pathogenetic mechanisms underlying glioblastoma development in the setting of HIV/AIDS is provided.
We performed a PubMed search using keywords "HIV glioma" AND "glioblastoma," and "AIDS glioma" AND "glioblastoma." Case reports and series describing HIV-positive patients with glioblastoma (histologically-proven World Health Organization grade IV astrocytoma) and reporting on HAART treatment status, clinical follow-up, and overall survival (OS), were included for the purposes of quantitative synthesis. Patients without clinical follow-up data or OS were excluded. Remaining articles were assessed for data extraction eligibility.
A total of 17 patients met our inclusion criteria. Of these patients, 14 (82.4%) were male and 3 (17.6%) were female, with a mean age of 39.5±9.2 years (range 19-60 years). Average CD4 count at diagnosis of glioblastoma was 358.9±193.4 cells/mm. Tumor progression rather than AIDS-associated complications dictated patient survival. There was a trend towards increased median survival with HAART treatment (12.0 vs 7.5 months, =0.10).
Our data suggests that HAART is associated with improved survival in patients with HIV-associated glioblastoma, although the precise mechanisms underlying this improvement remain unclear.
抗病毒治疗的改进伴随着非获得性免疫缺陷综合征(AIDS)定义的恶性肿瘤发病率增加,如多形性胶质母细胞瘤。在此,我们调查了所有报告的人类免疫缺陷病毒(HIV)阳性胶质母细胞瘤患者病例,并评估了他们的临床结局。提供了对HIV/AIDS背景下胶质母细胞瘤发生的分子致病机制的全面综述。
我们使用关键词“HIV胶质瘤”和“胶质母细胞瘤”以及“AIDS胶质瘤”和“胶质母细胞瘤”在PubMed上进行搜索。纳入病例报告和系列研究,这些研究描述了HIV阳性胶质母细胞瘤患者(经组织学证实为世界卫生组织IV级星形细胞瘤),并报告了高效抗逆转录病毒治疗(HAART)的治疗状态、临床随访和总生存期(OS),用于定量综合分析。排除没有临床随访数据或OS的患者。对其余文章进行数据提取资格评估。
共有17例患者符合我们的纳入标准。其中,14例(82.4%)为男性,3例(17.6%)为女性,平均年龄为39.5±9.2岁(范围19 - 60岁)。胶质母细胞瘤诊断时的平均CD4细胞计数为358.9±193.4个细胞/mm。决定患者生存的是肿瘤进展而非AIDS相关并发症。HAART治疗有使中位生存期增加的趋势(12.0对7.5个月,P = 0.10)。
我们的数据表明,HAART与HIV相关胶质母细胞瘤患者生存期改善相关,尽管这种改善的确切机制尚不清楚。