BACKGROUND: HIV-infected women need highly effective contraception to reduce unintended pregnancies and mother-to-child HIV transmission. Previous studies report conflicting results regarding the effect of hormonal contraception on HIV disease progression. METHODS: HIV-infected women in Uganda and Zimbabwe were recruited immediately after seroconversion; CD4 testing and clinical examinations were conducted quarterly. The study end point was time to AIDS (two successive CD4 200 cells/mm or less or World Health Organization advanced Stage 3 or Stage 4 disease). We used marginal structural Cox survival models to estimate the effect of cumulative exposure to depot-medroxyprogesterone acetate and oral contraceptives on time to AIDS. RESULTS: Three hundred three HIV-infected women contributed 1408 person-years. One hundred eleven women (37%) developed AIDS. Cumulative probability of AIDS was 50% at 7 years and did not vary by country. AIDS incidence was 6.6, 9.3, and 8.8 per 100 person-years for depot-medroxyprogesterone acetate, oral contraceptive, and nonhormonal users. Neither depot-medroxyprogesterone acetate (adjusted hazard ratio, 0.90; 95% confidence interval, 0.76-1.08) nor oral contraceptives ( adjusted hazard ratio, 1.07; 95% confidence interval, 0.89-1.29) were associated with HIV disease progression. Alternative exposure definitions of hormonal contraception use during the year before AIDS or at the time of HIV infection produced similar results. Sexually transmitted infection symptoms were associated with faster progression, whereas young age at HIV infection (18-24 years) was associated with slower progression. Adding baseline CD4 level and set point viral load to models did not change the hormonal contraception results, but Subtype D infection became associated with disease progression. CONCLUSION: Hormonal contraceptive use was not associated with more rapid HIV disease progression, but older age, sexually transmitted infection symptoms, and Subtype D infection were.
BACKGROUND:HIV-infectedwomen need highly effective contraception to reduce unintended pregnancies and mother-to-childHIV transmission. Previous studies report conflicting results regarding the effect of hormonal contraception on HIV disease progression. METHODS:HIV-infectedwomen in Uganda and Zimbabwe were recruited immediately after seroconversion; CD4 testing and clinical examinations were conducted quarterly. The study end point was time to AIDS (two successive CD4 200 cells/mm or less or World Health Organization advanced Stage 3 or Stage 4 disease). We used marginal structural Cox survival models to estimate the effect of cumulative exposure to depot-medroxyprogesterone acetate and oral contraceptives on time to AIDS. RESULTS: Three hundred three HIV-infectedwomen contributed 1408 person-years. One hundred eleven women (37%) developed AIDS. Cumulative probability of AIDS was 50% at 7 years and did not vary by country. AIDS incidence was 6.6, 9.3, and 8.8 per 100 person-years for depot-medroxyprogesterone acetate, oral contraceptive, and nonhormonal users. Neither depot-medroxyprogesterone acetate (adjusted hazard ratio, 0.90; 95% confidence interval, 0.76-1.08) nor oral contraceptives ( adjusted hazard ratio, 1.07; 95% confidence interval, 0.89-1.29) were associated with HIV disease progression. Alternative exposure definitions of hormonal contraception use during the year before AIDS or at the time of HIV infection produced similar results. Sexually transmitted infection symptoms were associated with faster progression, whereas young age at HIV infection (18-24 years) was associated with slower progression. Adding baseline CD4 level and set point viral load to models did not change the hormonal contraception results, but Subtype D infection became associated with disease progression. CONCLUSION: Hormonal contraceptive use was not associated with more rapid HIV disease progression, but older age, sexually transmitted infection symptoms, and Subtype D infection were.
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