Duncan Katrina C, Chan Keith J, Chiu Connie G, Montaner Julio S G, Coldman Andy J, Cescon Angela, Au-Yeung Christopher G, Wiseman Sam M, Hogg Robert S, Press Natasha M
aBritish Columbia Centre for Excellence in HIV/AIDS, Faculty of Medicine, University of British Columbia bBritish Columbia Centre for Excellence in HIV/AIDS cDepartment of Surgery, St. Paul's Hospital dBritish Columbia Centre for Excellence in HIV/AIDS, Division of AIDS, University of British Columbia eBritish Columbia Cancer Agency, Vancouver fBritish Columbia Centre for Excellence in HIV/AIDS, Faculty of Health Sciences, Simon Fraser University, Burnaby gDivision of Infectious Diseases, University of British Columbia, Vancouver, British Columbia, Canada.
AIDS. 2015 Jan 28;29(3):305-11. doi: 10.1097/QAD.0000000000000537.
Antiretrovirals do not prevent anal intraepithelial neoplasia. However, the influence of antiretrovirals in the natural history of invasive anal cancer is less clear. The objective is to investigate the impact of antiretrovirals in the time to the development of anal cancer in HIV-positive MSM.
A retrospective analysis of cases of anal cancer in a cohort of HIV-positive MSM receiving antiretrovirals between 1988 and 2008.
Time from first CD4 cell count or HIV RNA viral load test to anal cancer diagnosis was analysed using Cox regression and Kaplan-Meier curves. Anal cancer cases treated in the era prior to HAART (<1996) were compared with those treated later (1996-2008).
Anal cancer cases (n = 37) were compared with a cohort of 1654 HIV-positive MSM on antiretrovirals. Antiretrovirals were started in the pre-HAART era by 70% of cancer cases, and median CD4 cell count nadir was 70 cells/μl (10-130). Time to development of anal cancer was shorter for cases treated during the pre-HAART era [adjusted hazard ratio (AHR) 3.04, 95% confidence interval (95% CI) 1.48-6.24, P = 0.002], with a CD4 cell count nadir less than 100 cells/μl (AHR 2.21, 95% CI 1.06-4.62, P = 0.035) and longer duration of CD4 cell count less than 100 cells/μl (AHR 1.33, 95% CI 1.11-1.58, P = 0.002).
Results show that severe immunosuppression and starting therapy pre-HAART are associated with an increased risk of anal cancer. HIV-positive MSM initiating antiretrovirals during the HAART era (1996-2008) had a longer time to the development of anal cancer than those treated pre-HAART. Our results suggest that early use of HAART may delay progression to anal cancer.
抗逆转录病毒药物不能预防肛门上皮内瘤变。然而,抗逆转录病毒药物对浸润性肛门癌自然史的影响尚不清楚。目的是研究抗逆转录病毒药物对HIV阳性男男性接触者发生肛门癌时间的影响。
对1988年至2008年间接受抗逆转录病毒药物治疗的HIV阳性男男性接触者队列中的肛门癌病例进行回顾性分析。
使用Cox回归和Kaplan-Meier曲线分析从首次CD4细胞计数或HIV RNA病毒载量检测到肛门癌诊断的时间。将HAART时代之前(<1996年)治疗的肛门癌病例与之后(1996 - 2008年)治疗的病例进行比较。
将37例肛门癌病例与1654例接受抗逆转录病毒药物治疗的HIV阳性男男性接触者队列进行比较。70%的癌症病例在HAART时代之前开始使用抗逆转录病毒药物,CD4细胞计数最低点的中位数为70个/μl(10 - 130)。HAART时代之前治疗的病例发生肛门癌的时间较短[调整后风险比(AHR)3.04,95%置信区间(95%CI)1.48 - 6.24,P = 0.002],CD4细胞计数最低点低于100个/μl(AHR 2.21,95%CI 1.06 - 4.62,P = 0.035),且CD4细胞计数低于100个/μl的持续时间较长(AHR 1.33,95%CI 1.11 - 1.58,P = 0.002)。
结果表明,严重免疫抑制和在HAART时代之前开始治疗与肛门癌风险增加相关。在HAART时代(1996 - 2008年)开始使用抗逆转录病毒药物的HIV阳性男男性接触者发生肛门癌的时间比HAART时代之前治疗的患者更长。我们的结果表明,早期使用HAART可能会延迟进展为肛门癌。