Goedert James J, Purdue Mark P, McNeel Timothy S, McGlynn Katherine A, Engels Eric A
Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20892, USA.
Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1266-9. doi: 10.1158/1055-9965.EPI-07-0042.
Men with HIV/acquired immunodeficiency syndrome (AIDS) are reported to be at increased risk for germ cell tumors (GCT), particularly testicular seminoma. We investigated correlates of this association to improve understanding of GCTs.
Testicular and extratesticular seminoma and nonseminoma cases were found by linking population-based cancer and HIV/AIDS registry data for 268,950 men who developed AIDS in 1980 to 2003. Standardized incidence ratios (SIR) with 95% confidence intervals (95% CI) were used to compare these cases with the number of cases expected in the demographically matched population.
Overall, seminoma risk (161 cases: SIR, 1.9; 95% CI, 1.6-2.2) was increased significantly with HIV/AIDS, whereas nonseminoma risk was not (56 cases: SIR, 1.3; 95% CI, 0.96-1.7). Extratesticular GCT risk also was increased (11 cases: SIR, 2.1; 95% CI, 1.1-3.7). Seminoma risk was elevated regardless of age, race, or HIV/AIDS transmission group. It was highest for disseminated disease (SIR, 4.7; 95% CI, 2.9-7.2) and within 9 months of AIDS onset (SIR, 7.6; 95% CI, 5.8-9.6), but it was unrelated to CD4 count and duration of HIV/AIDS. The excess risk of seminoma declined in more recent calendar periods, and it was no longer elevated (SIR, 1.4; 95% CI, 0.9-1.9) in the highly active antiretroviral treatment era.
Men with HIV/AIDS had an increased risk of seminoma, but this risk may have attenuated with improving anti-HIV/AIDS treatments. Although detection bias could partly explain the excess of this cancer, various lines of evidence support a causal relationship. Possible mechanisms underlying this association include impaired tumor immunosurveillance or AIDS-related testicular atrophy.
据报道，感染人类免疫缺陷病毒/获得性免疫缺陷综合征（HIV/AIDS）的男性患生殖细胞肿瘤（GCT）的风险增加，尤其是睾丸精原细胞瘤。我们研究了这种关联的相关因素，以增进对GCT的了解。
通过将1980年至2003年期间患艾滋病的268,950名男性的基于人群的癌症登记数据与HIV/AIDS登记数据相链接，发现了睾丸和睾丸外精原细胞瘤及非精原细胞瘤病例。使用标准化发病比（SIR）及95%置信区间（95%CI）将这些病例与人口统计学匹配人群中预期的病例数进行比较。
总体而言，HIV/AIDS患者患精原细胞瘤的风险（161例：SIR，1.9；95%CI，1.6 - 2.2）显著增加，而非精原细胞瘤的风险未增加（56例：SIR，1.3；95%CI，0.96 - 1.7）。睾丸外GCT的风险也增加（11例：SIR，2.1；95%CI，1.1 - 3.7）。无论年龄、种族或HIV/AIDS传播途径如何，精原细胞瘤的风险均升高。在疾病播散时（SIR，4.7；95%CI，2.9 - 7.2）以及AIDS发病后9个月内（SIR，7.6；95%CI，5.8 - 9.6）风险最高，但与CD4细胞计数及HIV/AIDS病程无关。精原细胞瘤的额外风险在最近几个时期有所下降，在高效抗逆转录病毒治疗时代不再升高（SIR，1.4；95%CI，0.9 - 1.9）。
HIV/AIDS男性患精原细胞瘤的风险增加，但随着抗HIV/AIDS治疗的改善，这种风险可能已经减弱。尽管检测偏倚可能部分解释了这种癌症的超额发生，但各种证据支持因果关系。这种关联的潜在机制可能包括肿瘤免疫监视受损或与AIDS相关的睾丸萎缩。
