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Research Publications


17. Serum free testosterone levels associated with anal human papillomavirus types 16/18 in a cohort of men who have sex with men.

Hsu H, Brown T, Li X, Young S, Cranston RD, D'Souza G, Jacobson LP, Martínez-Maza O, Seaberg EC, Detels R, Wiley DJ.

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 76.2ngdL(-1) (s.d. 57.1; median 69.0ngdL(-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.

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