Chaturvedi Anil K, Pfeiffer Ruth M, Chang Leonard, Goedert James J, Biggar Robert J, Engels Eric A
Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, EPS 7072, Rockville, MD 20852, USA.
AIDS. 2007 Jan 11;21(2):207-13. doi: 10.1097/QAD.0b013e3280118fca.
Lung cancer is a common malignancy among people with AIDS (PWA). Lung cancer risk was compared between PWA and the general population and its relationship with immunosuppression was assessed. The likelihood that excess risk is explained by a high prevalence of smoking was also investigated.
Records on adolescent and adult PWA (N = 397 927) were linked with cancer registries in 11 US regions. Cancer risk was assessed for the period 60 months before to 60 months after AIDS onset, with specific emphasis on the period 4-27 months after onset. Observed incidence was compared with general population rates and rates from a lung cancer prediction model for smokers.
Compared with the general population, lung cancer risk among PWA was elevated overall [n = 1489 cases; standardized incidence ratio (SIR), 3.8; 95% confidence interval (CI), 3.6-4.1] and in the 4-27 months after AIDS (n = 393 cases; SIR, 2.9; 95% CI, 2.6-3.2). In the 4-27 months after AIDS, risk was significantly elevated for all demographic subgroups, and was especially high among young PWA (SIRs for ages 15-29 years, 10.4; 30-39 years, 6.3; 40-49 years, 3.7). Lung cancers generally presented at an advanced stage. Risk was not associated with CD4 cell counts at AIDS (Ptrend = 0.36). Under plausible smoking assumptions, observed incidence was significantly higher than predicted among 40-49 and 50-59-year-old men with AIDS (observed/predicted = 5.03 and 1.43, respectively) and 40-49-year-old women with AIDS (observed/predicted = 1.88), but not among older PWA.
Lung cancer risk was substantially elevated among PWA. Smoking could not entirely account for the observed elevation, especially among younger adults, suggesting a role for additional co-factors.
肺癌是艾滋病患者（PWA）中常见的恶性肿瘤。比较了艾滋病患者与普通人群的肺癌风险，并评估了其与免疫抑制的关系。还研究了吸烟率高是否能解释额外的风险。
美国11个地区的青少年和成年艾滋病患者（N = 397927）的记录与癌症登记处相关联。评估艾滋病发病前60个月至发病后60个月的癌症风险，特别关注发病后4 - 27个月的时期。将观察到的发病率与普通人群的发病率以及吸烟者肺癌预测模型的发病率进行比较。
与普通人群相比，艾滋病患者的肺癌总体风险升高（n = 1489例；标准化发病率（SIR），3.8；95%置信区间（CI），3.6 - 4.1），在艾滋病发病后4 - 27个月也升高（n = 393例；SIR，2.9；95%CI，2.6 - 3.2）。在艾滋病发病后4 - 27个月，所有人口亚组的风险均显著升高，在年轻的艾滋病患者中尤其高（15 - 29岁年龄组的SIR为10.4；30 - 39岁年龄组为6.3；40 - 49岁年龄组为3.7）。肺癌通常在晚期出现。风险与艾滋病时的CD4细胞计数无关（Ptrend = 0.36）。在合理的吸烟假设下，观察到的发病率在40 - 49岁和50 - 59岁的艾滋病男性（观察值/预测值分别为5.03和1.43）以及40 - 49岁的艾滋病女性（观察值/预测值为1.88）中显著高于预测值，但在年龄较大的艾滋病患者中并非如此。
艾滋病患者的肺癌风险大幅升高。吸烟不能完全解释观察到的风险升高，尤其是在年轻成年人中，这表明还有其他协同因素在起作用。
