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  53rd ICAAC Interscience Conference on
Antimicrobial Agents and Chemotherapy
September 10-13, 2013, Denver CO
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One in 5 HIV+ Women in Spanish Group Has Anal Dysplasia, Predicted by Warts
  53rd ICAAC, September 10-13, 2013, Denver
Mark Mascolini
One in 5 women in a Spanish HIV cohort had anal dysplasia, a possible anal cancer precursor, and anal or genital warts raised chances of anal dysplasia more than 11 times [1]. In contrast, two thirds of HIV-positive men who have sex with men (MSM) in the same cohort had anal dysplasia. Yet the investigators believe the 21% anal dysplasia rate in women justifies routine screening for abnormal anal cells in women with HIV.
Human papillomavirus (HPV) infection causes both cervical cancer (an AIDS cancer) and anal cancer (a non-AIDS cancer). Abundant research indicates that people with HIV infection have higher rates of anal HPV infection, anal dysplasia, and anal cancer than the general population. But much of this work focuses on MSM. Less is known about anal dysplasia and anal cancer rates in women with HIV and how their rates compare with men. In contrast, much work has focused on cervical dysplasia and cancer in women with HIV.
To analyze prevalence and predictors of anal dysplasia (abnormal anal cells that may be a harbinger of anal cancer), researchers at a university hospital in Granada, Spain conducted a cross-sectional study of HIV-positive women and HIV-positive MSM cared for in the infectious disease unit at some time between December 2008 and December 2012. Consecutive patients were enrolled in a dysplastic lesion screening program and gave two anal mucosal samples--one for PCR of HPV and another for anal cytology. Women also gave samples for cervical cytology. All participants in this cross-sectional study provided information on epidemiologic variables, sexual behavior, and clinical variables including antiretroviral therapy, CD4 count, and viral load.
The 148 study participants included 45 women (30%) and 103 men. Women and men were statistically similar in average viral load (4.1 and 3.7 log10 copies/mL), current CD4 count (692 and 646), and antiretroviral-naive status (6.7% and 14.6%, P = 0.176). But women differed from men in average age (42.8 versus 36.2, P = 0.0001), condom use rate (53.3% versus 69.6%, P= 0.011), anal intercourse rate (22.2% versus 100%, P = 0.0001), median HIV duration (165 versus 49.5 months, P = 0.0001), nadir CD4 count (223.7 versus 387.5, P = 0.001), median months of antiretroviral therapy (113 versus 35, P = 0.0001), treatment for sexually transmitted infections besides syphilis (4.4% versus 49.5%, P = 0.0001), chronic HCV infection (26.7% versus 3.8%, P = 0.0001), and current smoking (71.1% versus 48.5%, P = 0.01).
More than three quarters of anal swabs from women (78.5%) had normal cytologic results, compared with about one third from men (32.9%), a highly significant difference (P = 0.0001). Rates of low-grade squamous intraepithelial lesions (LSIL) were lower in women than men (19.1% versus 53.5%), as were rates of high-grade squamous intraepithelial lesions (HSIL) (0% versus 5.3%) and atypical squamous cells of undetermined significance (ASCUS) (2.4% versus 5.3%).
A significantly lower proportion of women than men tested positive for low-risk HPV (22.7% versus 70.5%), high-risk (cancer-causing) HPV (34.1% versus 85.4%), median number of low-risk HPV types (0 versus 1), and median number of high-risk HPV types (0 versus 1) (P = 0.0001 for all comparisons). HPV-16, the prime cause of anal cancer and cervical cancer, could be detected in 4.5% of women and 27% of men (P = 0.002).
In univariate analysis, anal infections with low- or high-risk HPV and number of low- or high-risk HPV types were associated with risk of anal dysplasia in women. There were trends toward such an association with a history of anal or genital warts, higher HIV load, and lower CD4 count.
Multivariate analysis determined that a history of anal or genital warts raised chances of anal dysplasia more than 11 times in these women (adjusted odds ratio 11.5, 95% confidence interval 1.04 to 127.6, P = 0.046). In the same analysis, infection with low- or high-risk HPV and number of low- or high-risk HPV genotypes were not associated with chances of anal dysplasia.
The researchers proposed that, although anal dysplasia and HPV rates were much lower in these HIV-positive women than in HIV-positive MSM from the same cohort, rates in women are high enough to justify screening for anal dysplasia in women with HIV. The 22%-versus-100% female-versus-male anal intercourse rates probably contributed substantially to higher prevalence of anal HPV and anal dysplasia in men than women.
In the United States, a 2001-2003 comparison of 470 HIV-positive women and 185 HIV-negative women in the Women's Interagency HIV Study found that women with HIV had higher rates of low-grade anal intraepithelial neoplasia (AIN) (12% versus 5%) and high-grade AIN (9% versus 1%) [2]. Independent predictors of low-grade AIN in HIV-positive women were younger age, history of receptive anal intercourse, HPV infection, and cervical HPV infection. Anal HPV infection was the only independent predictor of high-grade AIN.
1. Hidalgo Tenorio C, Rivero Rodriguez M, Gil Anguita C, et al. Is HPV anal dysplasia in HIV patients a matter of sexual behaviour or gender? 53rd ICAAC. September 10-13, 2013. Denver. Abstract H-1270.
2. Hessol NA, Holly EA, Efird JT, et al. Anal intraepithelial neoplasia in a multisite study of HIV-infected and high-risk HIV-uninfected women. AIDS. 2009;23:59-70. http://www.natap.org/2008/HIV/121508_02.htm