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Hormonal contraception decreases bacterial vaginosis but oral contraception may increase candidiasis: implications for HIV transmission

van de Wijgert, Janneke H.H.M.a,b; Verwijs, Marijn C.b,c; Turner, Abigail Norrisd; Morrison, Charles S.e

doi: 10.1097/QAD.0b013e32836290b6
Epidemiology and Social

Objective: A 2012 WHO consultation concluded that combined oral contraception (COC) does not increase HIV acquisition in women, but the evidence for depot medroxyprogesterone acetate (DMPA) is conflicting. We evaluated the effect of COC and DMPA use on the vaginal microbiome because current evidence suggests that any deviation from a ‘healthy’ vaginal microbiome increases women's susceptibility to HIV.

Methods: We conducted a systematic review and reanalysed the Hormonal Contraception and HIV Acquisition (HC-HIV) study. Vaginal microbiome outcomes included bacterial vaginosis by Nugent scoring, vaginal candidiasis by culture or KOH wet mount and microbiome compositions as characterized by molecular techniques.

Results: Our review of 36 eligible studies found that COC and DMPA use reduce bacterial vaginosis by 10–20 and 18–30%, respectively. The HC-HIV data showed that COC and DMPA use also reduce intermediate microbiota (Nugent score of 4–6) by 11% each. In contrast, COC use (but not DMPA use) may increase vaginal candidiasis. Molecular vaginal microbiome studies (n = 4) confirm that high oestrogen levels favour a vaginal microbiome composition dominated by ‘healthy’ Lactobacillus species; the effects of progesterone are less clear and not well studied.

Conclusion: DMPA use does not increase HIV risk by increasing bacterial vaginosis or vaginal candidiasis. COC use may predispose for vaginal candidiasis, but is not believed to be associated with increased HIV acquisition. However, the potential role of Candida species, and vaginal microbiome imbalances other than bacterial vaginosis or Candida species, in HIV transmission cannot yet be ruled out. Further in-depth molecular studies are needed.

aInstitute of Infection and Global Health, University of Liverpool, Liverpool, UK

bAmsterdam Institute for Global Health and Development (AIGHD) and Department of Global Health, Academic Medical Center, Amsterdam

cDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands

dDivision of Infectious Diseases, The Ohio State University, Columbus, Ohio

eClinical Sciences, Durham, North Carolina, USA.

Correspondence to Janneke H.H.M. van de Wijgert, Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Ronald Ross Building, West Derby Street, Liverpool L69 7BE, UK. Tel: +44 151 795 9613; fax: +44 151 795 5529; e-mail: j.vandewijgert@liv.ac.uk

Received 19 March, 2013

Revised 22 April, 2013

Accepted 24 April, 2013

© 2013 Lippincott Williams & Wilkins, Inc.