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Hormonal Contraceptive Use and HIV Disease Progression Among Women in Uganda and Zimbabwe

Morrison, Charles S PhD*; Chen, Pai-Lien PhD; Nankya, Immaculate MD, PhD; Rinaldi, Anne BA*; Van Der Pol, Barbara PhD§; Ma, Yun-Rong MPH; Chipato, Tsungai MD; Mugerwa, Roy MBChB; Dunbar, Megan DrPH**; Arts, Eric PhD††; Salata, Robert A MD††

JAIDS Journal of Acquired Immune Deficiency Syndromes: June 1st, 2011 - Volume 57 - Issue 2 - p 157-164
doi: 10.1097/QAI.0b013e318214ba4a
Epidemiology and Prevention

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/mm3 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.

From the Departments of *Clinical Sciences and †Biostatistics, Family Health International, Research Triangle Park, NC; ‡Joint Clinical Research Centre, Kampala, Uganda; §Behavioral Sciences Program, Indiana University School Public Health, Bloomington, IN; ‖Department of Obstetrics and Gynaecology, University of Zimbabwe, Harare, Zimbabwe; ¶Faculty of Medicine, Makerere University, Kampala, Uganda; **Women's Global Health Imperative, Research Triangle Institute, San Francisco, CA; and ††Department of Medicine, Case Western Reserve University, Cleveland, OH.

Received for publication November 1, 2010, accepted February 4, 2011.

This project has been funded with federal funds from The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Department of Health and Human Services through a contract with Family Health International (FHI) (Contract Number N01-HD-0-3310).

A portion of these data was presented previously at the XVIII International AIDS Conference (Vienna, Austria, July 18-23, 2010; abstract 7515).

C.S.M. is the study principal investigator and directed the design and implementation of the study and wrote the manuscript draft; I.N. and B.V.D.P. planned, supervised, conducted (I.N.), and did quality assurance (B.V.D.P.) for the laboratory work; P.C. and Y.M. designed and conducted the statistical analysis; A.R. monitored the study sites and performed data management; T.C., R.M., and M.D. are site principal investigators and supervised the study teams in Zimbabwe and Uganda; E.A. is the laboratory coinvestigator and designed, tested, and supervised the virology assays; R.A.S. is the study coprincipal investigator and as study clinical consultant confirmed all World Health Organization clinical Stage 3 and 4 outcomes; all authors contributed to drafts of the manuscript and approved the final manuscript.

B.V.D.P. consults for Roche Diagnostics. The other authors have no conflicts of interest to disclose.

The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services or Family Health International nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.

Correspondence to: Charles S. Morrison, PhD, Clinical Sciences Department, FHI, PO Box 13950, Research Triangle Park, NC, 27709 (e-mail:

© 2011 Lippincott Williams & Wilkins, Inc.