Risk of Human Papillomavirus-Associated Cancers Among Persons With AIDS
Risk of Human Papillomavirus-Associated Cancers Among Persons With AIDS
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DOI：
10.1093/jnci/djp205
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发表时间：
2009-08-19
影响因子：
10.3
通讯作者：
Engels, Eric A.
中科院分区：
文献类型：
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作者：
Chaturvedi, Anil K.;Madeleine, Margaret M.;Engels, Eric A.
尽管艾滋病患者中与人乳头瘤病毒（HPV）相关的肛门、宫颈、口咽、阴茎、阴道和外阴癌的风险增加，但免疫抑制的病因学作用尚不清楚，这些癌症的发病趋势随着时间的推移，特别是在1996年引入高效抗逆转录病毒治疗后，方法1980年1月1日至2004年12月31日，499230例诊断为艾滋病的患者的数据与美国15个地区的癌症登记处联系在一起。与普通人群相比，原位和浸润性HPV相关癌症的风险通过使用标准化发病率比（SIR）和95%置信区间（CI）进行测量。我们通过在艾滋病发病时测量的CD 4 T细胞计数来评估艾滋病发病后4-60个月期间免疫抑制与发病率的关系。艾滋病发病后4-60个月的发病率在三个时期（1980-1989年，1990-1995年和1996-2004年）进行了比较。所有的统计学检验都是双侧的。结果在艾滋病患者中，我们观察到所有HPV相关原位癌的风险在统计学上显著升高，（宫颈癌的SIR范围为8.9，95% CI = 8.0至9.9，男性肛门癌的SIR范围为68.6，95% CI = 59.7至78.4），（口咽癌的SIR范围为1.6，95% CI = 1.2至2.1，男性肛门癌的SIR范围为34.6，95% CI = 30.8至38.8）。在1996-2004年期间，低CD 4 T细胞计数与男性浸润性肛门癌风险的统计学显著增加相关（每立方毫米100个CD 4 T细胞下降的相对风险[RR]= 1.34，95% CI = 1.08至1.66，P = 0.006）和无统计学意义的原位阴道癌或外阴癌风险增加（RR = 1.52，95%CI = 0.99 ~ 2.35，P = 0.055）和浸润性宫颈癌（RR = 1.32，95%CI = 0.96 ~ 1.80，P = 0.077）。在男性中，1996-2004年的原位和浸润性肛门癌（每10万人-年）在统计学上显著高于1990-1995年（原位癌增加61%，分别为18.3例和29.5例; RR = 1.71，95% CI = 1.24 ~ 2.35，P <0.001;浸润性癌增加104%，分别为20.7例和42.3例; RR = 2.03，95% CI = 1.54 ~ 2.68，P <0.001）。其他癌症的发病率随着时间的推移而保持稳定。结论艾滋病患者中HPV相关癌症的风险升高，并且随着免疫抑制的增加而增加。1996-2004年期间肛门癌发病率的增加表明生存期的延长可能与某些HPV相关癌症的风险增加有关。
Background Although risk of human papillomavirus (HPV)-associated cancers of the anus, cervix, oropharynx, penis, vagina, and vulva is increased among persons with AIDS, the etiologic role of immunosuppression is unclear and incidence trends for these cancers over time, particularly after the introduction of highly active antiretroviral therapy in 1996, are not well described.Methods Data on 499 230 individuals diagnosed with AIDS from January 1, 1980, through December 31, 2004, were linked with cancer registries in 15 US regions. Risk of in situ and invasive HPV-associated cancers, compared with that in the general population, was measured by use of standardized incidence ratios (SIRs) and 95% confidence intervals (CIs). We evaluated the relationship of immunosuppression with incidence during the period of 4-60 months after AIDS onset by use of CD4 T-cell counts measured at AIDS onset. Incidence during the 4-60 months after AIDS onset was compared across three periods (1980-1989, 1990-1995, and 1996-2004). All statistical tests were two-sided.Results Among persons with AIDS, we observed statistically significantly elevated risk of all HPV-associated in situ ( SIRs ranged from 8.9, 95% CI = 8.0 to 9.9, for cervical cancer to 68.6, 95% CI = 59.7 to 78.4, for anal cancer among men) and invasive ( SIRs ranged from 1.6, 95% CI = 1.2 to 2.1, for oropharyngeal cancer to 34.6, 95% CI = 30.8 to 38.8, for anal cancer among men) cancers. During 1996-2004, low CD4 T-cell count was associated with statistically significantly increased risk of invasive anal cancer among men (relative risk [RR] per decline of 100 CD4 T cells per cubic millimeter = 1.34, 95% CI = 1.08 to 1.66, P = .006) and non-statistically significantly increased risk of in situ vagina or vulva cancer (RR = 1.52, 95% CI = 0.99 to 2.35, P = .055) and of invasive cervical cancer (RR = 1.32, 95% CI = 0.96 to 1.80, P = .077). Among men, incidence (per 100 000 person-years) of in situ and invasive anal cancer was statistically significantly higher during 1996-2004 than during 1990-1995 (61% increase for in situ cancers, 18.3 cases vs 29.5 cases, respectively; RR = 1.71, 95% CI = 1.24 to 2.35, P < .001; and 104% increase for invasive cancers, 20.7 cases vs 42.3 cases, respectively; RR = 2.03, 95% CI = 1.54 to 2.68, P < .001). Incidence of other cancers was stable over time.Conclusions Risk of HPV-associated cancers was elevated among persons with AIDS and increased with increasing immunosuppression. The increasing incidence for anal cancer during 1996-2004 indicates that prolonged survival may be associated with increased risk of certain HPV-associated cancers.