17. Serum free testosterone levels associated with anal human papillomavirus types 16/18 in a cohort of men who have sex with men
Hilary Hsu A , Todd Brown B , Xiuhong Li C , Stephen Young D , Ross D. Cranston E , Gypsyamber D’Souza C , Lisa P. Jacobson C , Otoniel Martínez-Maza F G , Eric C. Seaberg C , Roger Detels G and Dorothy J. Wiley AA UCLA School of Nursing, Los Angeles, CA, USA.
B Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
C Johns Hopkins University, Bloomberg School of Public Health, Baltimore, MD, USA.
D Tricore Reference Laboratories, University of New Mexico, Albuquerque, NM, USA.
E University of Pittsburgh, Pittsburgh, PA, USA.
F UCLA AIDS Institute and David Geffen UCLA School of Medicine, Los Angeles, CA, USA.
G UCLA Jonathan and Karen Fielding School of Public Health, Los Angeles, CA, USA.
Sexual Health 10(6) 578-578 https://doi.org/10.1071/SHv10n6ab17
Published: 22 November 2013
Abstract
Background: Human papillomavirus (HPV) types 16/18 are significant causes of female cervical cancers and likely cause most anal cancers. Oestrogen influences HPV-related cervical malignancies; however, the role of testosterone in anal HPV16/18 infections is unknown. Methods: 340 men who have sex with men (MSM) enrolled in the Multicenter AIDS Cohort Study were tested for serum free testosterone (SFT) and, ~24 months later, anal HPV16/18-DNA. Poisson regression with robust error variance analyses estimated prevalence ratios for HPV16/18 infections with the following exposures: log10-transformed SFT, exogenous and supraphysiological testosterone measures, race, age, self-reported number of anal receptive intercourse partnerships ≤24 months before testing, enrolment period, body mass index, hepatitis C infection, tobacco and alcohol, HIV infection, and CD4+ T-cell counts among the HIV-infected. Stratified-tabular analyses also evaluated blood draw timing (AM/PM), study site, and time on study. Results: 89% (304/340) of men provided complete data for all covariates. On average, men were White (263/304), 60 years old (s.d. 5.3; median 60.1 years) with 76.2 ng dL–1 (s.d. 57.1; median 69.0 ng dL–1) SFT, and 43% (132/304) were HIV infected; 25% (75/304) tested HPV16/18-DNA positive. The fully adjusted model suggests each half-log10 increase of SFT is associated with a 1.69-fold (95% confidence interval (CI): 1.08, 2.64) higher HPV16/18 prevalence. Compared with HIV-uninfected men, HPV16/18 prevalence was 1.81-fold higher (95% CI: 1.08, 3.03) for HIV-infected men with ≤500 CD4+ T-cells mm–3. No other covariates were significantly associated with HPV16/18 prevalence. Conclusions: Higher free testosterone is associated with increased HPV16/18 prevalence in MSM, independent of sexual behaviour and other potential confounders. The mechanisms underlying this association remain unclear and warrant further study.
