Department of Orthopedic Surgery, Washington University School of Medicine, St. Louis, MO.
Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, MO.
J Acquir Immune Defic Syndr. 2018 Aug 15;78(5):499-504. doi: 10.1097/QAI.0000000000001719.
Cutaneous melanoma incidence may be modestly elevated in people with HIV (PWH) vs. people without HIV. However, little is known about the relationship of immunosuppression, HIV replication, and antiretroviral therapy (ART) with melanoma risk.
PWH of white race in the North American AIDS Cohort Collaboration on Research and Design were included. A standardized incidence ratio was calculated comparing risk with the white general population, standardizing by age, sex, and calendar period. Associations between melanoma incidence and current, lagged, and cumulative measures of CD4 count, HIV RNA level, and ART use were estimated with Cox regression, adjusting for established risk factors such as age and annual residential ultraviolet B (UVB) exposure.
Eighty melanomas were diagnosed among 33,934 white PWH (incidence = 40.75 per 100,000 person-years). Incidence was not elevated compared with the general population [standardized incidence ratio = 1.15, 95% confidence interval (95% CI) = 0.91 to 1.43]. Higher melanoma incidence was associated with older age [adjusted hazard ratio (aHR) per decade increase = 1.50, 95% CI = 1.20 to 1.89] and higher UVB exposure (aHR for exposure ≥35 vs. <35 mW/m = 1.62, 95% CI = 0.99 to 2.65). Current, lagged, and cumulative CD4 and HIV RNA were not associated with melanoma incidence. Melanoma incidence was higher among people ART-treated for a larger proportion of time in the previous 720 days (aHR per 10% increase = 1.16, 95% CI = 1.03 to 1.30).
These results suggest that HIV-induced immune dysfunction does not influence melanoma development. The association between ART and melanoma risk may be due to increased skin surveillance among PWH engaged in clinical care. Associations with age and UVB confirmed those established in the general population.
与未感染 HIV 的人群相比，HIV 感染者（PWH）的皮肤黑色素瘤发病率可能略有升高。然而，人们对免疫抑制、HIV 复制和抗逆转录病毒治疗（ART）与黑色素瘤风险之间的关系知之甚少。
纳入了北美艾滋病队列协作研究与设计中的白种人 PWH。通过比较年龄、性别和日历期标准化后的白人普通人群的风险，计算风险比。采用 Cox 回归估计黑色素瘤发病率与当前、滞后和累积的 CD4 计数、HIV RNA 水平和 ART 使用的关系，调整了年龄和每年居住紫外线 B（UVB）暴露等已知危险因素。
在 33934 名白人 PWH 中诊断出 80 例黑色素瘤（发病率为 40.75/100000 人年）。发病率与普通人群相比并未升高[标准化发病率比=1.15，95%置信区间（95%CI）=0.91 至 1.43]。较高的黑色素瘤发病率与年龄较大有关[每增加 10 岁的调整后的危险比（aHR）=1.50，95%CI=1.20 至 1.89]和较高的 UVB 暴露有关[aHR 为暴露≥35 与<35 mW/m=1.62，95%CI=0.99 至 2.65]。当前、滞后和累积的 CD4 和 HIV RNA 与黑色素瘤发病率无关。在过去 720 天内接受 ART 治疗时间比例较大的人群中，黑色素瘤发病率更高[aHR 每增加 10%=1.16，95%CI=1.03 至 1.30]。
这些结果表明，HIV 引起的免疫功能障碍不会影响黑色素瘤的发生。ART 与黑色素瘤风险之间的关联可能是由于参与临床护理的 PWH 进行了更多的皮肤监测。与年龄和 UVB 的关联证实了在普通人群中建立的关联。
