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AIDS:
doi: 10.1097/QAD.0b013e32836290b6
Epidemiology and Social

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

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Abstract

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.

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins

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