Hormonal Contraceptive Use by HIV-infected Women

Network: 2007, Vol. 24, No. 1

Does Hormonal Contraception Increase HIV Infectivity?

Whether hormonal contraceptive use by HIV-infected women increases their risk of infecting sexual partners remains unknown.

Studies addressing this question are limited. Only two such studies have been prospective, and the results of cross-sectional studies of HIV shedding from the genital tract (thought to be a marker of increased infectiousness) are conflicting,¹ perhaps due to relatively small study samples.²

How to determine a woman's HIV infectiousness also is unclear. First, the amount of HIV genital shedding necessary to increase infectiousness is unknown. Also, questions remain about the best technique for detecting HIV in genital tract secretions.

Likewise, no consensus exists on what indicators best reflect the risk of HIV infectivity. Various researchers have measured:

1. cervical shedding of HIV-1 DNA (a marker of HIV-infected cells)
2. cervical shedding of HIV-1 RNA (a measure of cell-free virus and possible viral replication)
3. vaginal shedding of HIV
4. the presence in cervicovaginal fluid of inflammatory cells, which are thought to be associated with higher HIV loads

But the relative impact of HIV-1 DNA versus HIV-1 RNA shedding on the infectivity of a woman to her partner is uncertain. Also, the significance of vaginal versus cervical HIV shedding is unknown.

Prospective studies

The only prospective study of the direct effect of hormonal contraceptive use on genital tract shedding of HIV, conducted in 2004 among 213 HIV-infected family planning clients in Mombasa, Kenya, detected a significant but modest increase in cervical shedding of HIV-1 DNA after initiation of hormonal contraceptives. However, this increase was noted for hormonal contraceptive use overall; increases were not significant when women were divided into groups based on individual forms of hormonal contraception, including depot-medroxyprogesterone acetate (DMPA), high-dose oral contraceptive pills, low-dose oral contraceptive pills, and progestin-only contraceptive pills.³ This study also found that the increase in cervical shedding of HIV-1 DNA associated with hormonal contraceptive use overall was not accompanied by an increase in cervical shedding of HIV-1 RNA. Study authors offered the possible explanation that hormonal contraceptive use attracts infected cells to the genital mucosa (evidenced by increased HIV-1 DNA) but does not increase local viral replication in the mucosa (which increased HIV-1 RNA would reflect).

Another prospective study, conducted in 2005 among 967 U.S. women (654 of whom were HIV-infected), found that progesterone-based contraceptives appeared to raise the number of cervicovaginal inflammatory cells. The presence of these cells is assumed to be associated with increased HIV-1 viral load in genital secretions, but those viral loads were not measured. Another limitation of the study was the small number of participants using pro-gesterone contraception: 38 HIV-infected women used DMPA and 48 used levonorgestrel implants. As a result, the analysis had little statistical power.⁴

Expected in 2007 are preliminary results from a third prospective study, which is being conducted by FHI researchers and colleagues in Zimbabwe and Uganda. Funded by the U.S. National Institute of Child Health and Human Development, the study is examining the effect of combined oral contraceptive and DMPA use on cervical shedding of HIV-1 RNA among approximately 200 women with early HIV infection. Cervical shedding by these women will be compared with shedding by HIV-infected women not using hormonal contraception.

Another question with few answers at present is whether any association exists between an HIV-infected woman's hormonal contraceptive use and her acquisition of sexually transmitted infections that could enhance HIV shedding. Evidence to date — albeit, mostly from HIV-uninfected women — suggests a possible increased risk of acquiring chlamydial infection associated with both the use of oral contraceptives⁵ and DMPA.⁶ It is likely that chlamydial infection in women increases genital shedding of HIV.⁷

On the other hand, some evidence suggests that if a woman does not use contraception and experiences an unintended pregnancy, pregnancy itself may promote increased HIV shedding.⁸

— Kim Best

References

1. Clemetson DB, Moss BG, Willerford DM, et al. Detection of HIV DNA in cervical and vaginal secretions. Prevalence and correlates among women in Nairobi, Kenya. JAMA 1993;269(22):2860-64; Kreiss J, Willerford DM, Hensel M, et al. Association between cervical inflammation and cervical shedding of human immunodeficiency virus DNA. J Infect Dis 1994;170(6):1597-601; Ghys PD, Fransen K, Diallo MO, et al. The associations between cervicovaginal HIV shedding, sexually transmitted diseases and immunosuppression in female sex workers in Abidjan, Côte d'Ivoire. AIDS 1997;11(12):F86-93; Mostad SB, Overbaugh J, DeVange DM, et al. Hormonal contraception, vitamin A deficiency, and other risk factors for shedding of HIV-1 cells from the cervix and vagina. Lancet 1997:350(9082):922-27; Kovacs A, Wasserman S, Burns D, et al. Determinants of HIV-1 shedding in the genital tract of women. Lancet 2001;358(9293):1593-1601.
2. Stephenson J. Systematic review of hormonal contraception and risk of HIV transmission: when to resist meta-analysis. AIDS 1998;12(6):545-53.
3. Wang CC, McClelland RS, Overbaugh J, et al. The effect of hormonal contraception on genital tract shedding of HIV-1. AIDS 2004;18(2):205-9.
4. Ghanem KG, Shah N, Klein RS, et al. Influence of sex hormones, HIV status, and concomitant sexually transmitted infection on cervicovaginal inflammation. J Infect Dis 2005;191(3):358-66.
5. Louv WC, Austin H, Perlman J, et al. Oral contraceptive use and the risk of chlamydial and gonococcal infections. Am J Obstet Gynecol 1989;160(2):396-402; Avonts D, Sercu M, Heyerick P, et al. Incidence of uncomplicated genital infections in women using oral contraception or an intrauterine device: a prospective study. Sex Transm Dis 1990;17(1):23-29; Baeten JM, Nyange PM, Richardson BA, et al. Hormonal contraception and risk of sexually transmitted disease acquisition: results from a prospective study. Am J Obstet Gynecol 2001;185(2):380-85; Morrison CS, Bright P, Wong EL, et al. Hormonal contraceptive use, cervical ectopy, and the acquisition of cervical infections. Sex Transm Dis 2004;31(9):561-67; Cottingham J, Hunter D. Chlamydia trachomatis and oral contraceptive use: a quantitative review. Genitourin Med 1992;68(4):209-16.
6. Baeten; Morrison; Lavreys L, Chohan V, Overbaugh J, et al. Hormonal contraception and risk of cervical infections among HIV-1-seropositive Kenyan women. AIDS 2004;18(16):2179-84.
7. Lavreys; Ghys; McClelland RS, Wang CC, Mandaliya K, et al. Treatment of cervicitis is associated with decreased cervical shedding of HIV-1. AIDS 2001;15(1):105-10.
8. Kreiss; Mostad; Ghys; John GC, Nduati RW, Mbori-Ngacha D, et al. Genital shedding of human immunodeficiency virus type 1 DNA during pregnancy: association with immunosuppression, abnormal cervical or vaginal discharge, and severe vitamin A deficiency. J Infect Dis 1997;175(1):57-62; Rotchford K, Strum AW, Wilkinson D. Effect of coinfection with STDs and of STD treatment on HIV shedding in genital tract secretions. Sex Transm Dis 2000;27(5):243-48; Kilmarx P, Mock P, Levine W. Effect of Chlamydia trachomatis coinfection on HIV shedding in genital tract secretions. Sex Transm Dis 2001;28(6):347-48.

Does Hormonal Contraception Speed HIV Progression?

Does the use of hormonal contraception during the early stages of HIV infection affect disease progression? Likewise, does its use during the later stages of infection affect disease progression?

These questions cannot be answered yet. The only evidence so far that hormonal contraceptive use might affect HIV disease progression comes from a prospective study conducted among sex workers in Mombasa, Kenya.¹ This evidence suggests that using hormonal contraception at the time of infection — before women know that they are infected — may accelerate HIV-related deterioration of the immune system and thus speed the natural course of the infection.

If other studies confirm this finding, it could provide additional incentive for hormonal contraceptive users who are at high risk of HIV infection to also use condoms consistently for HIV prevention. It could also lead to changes in recommendations for hormonal contraceptive use by women at high risk of HIV infection. To date, however, the evidence of such a risk is considered insufficient to warrant any restrictions on hormonal contraceptive use by women with HIV/AIDS or women at high risk of infection.

Analyses consider viral set point, viral diversity

The association between hormonal contraceptive use and clinical progression of HIV has not been studied directly. But the research in Kenya showed associations between hormonal contraceptive use and two strong predictors of HIV disease progression, AIDS, and death: low CD4+ cell counts and high viral set point. CD4+ cells are immune system cells that are destroyed by HIV as the virus replicates. CD4+ count (the number of functioning CD4+ cells per liter of blood) indicates the strength of an infected person's immune system and whether antiretroviral treatment is needed. Viral set point is the level of HIV in the blood (viral load) after the immune system's initial response to the virus, generally three or four months after a person is infected.

In the Kenya study, researchers found that median viral set point was significantly higher among women using the injectable contraceptive depot-medroxyprogesterone acetate (DMPA) at the estimated time of HIV infection than it was among women using no hormonal contraception at that time. This difference between the two groups of women persisted during follow-up (median of 34 months). However, continuing use of DMPA did not appear to further increase viral load.

Overall, study participants' use of oral contraceptive pills was not associated with higher viral set points.² But in a subset of 156 HIV-infected sex workers (82 of whom used any hormonal contraception), use of either oral contraceptives or DMPA at the time of HIV infection was associated with acquiring genetically diverse virus populations from one partner. The women who had acquired these genetically diverse virus populations also had significantly higher viral set points and significantly lower CD4+ counts four to 24 months after infection than did those with only one strain of the virus.³

The study results suggest that greater viral genetic diversity in early HIV infection could be a mechanism by which hormonal contraception affects viral load and, ultimately, disease progression, says Dr. Ludo Lavreys, former field director of the HIV research site of the University of Washington/University of Nairobi in Mombasa.

Research on the possible relationship between hormonal contraception and HIV disease progression is hampered by the same methodological challenges facing studies of hormonal contraceptive use and the risk of HIV acquisition or transmission (see Why This Study Is Unique and  Does Hormonal Contraception Increase HIV Infectivity). One strength of the Kenya analyses is that researchers were able to estimate the dates of HIV infection with some precision because data were drawn from a larger prospective study of women who were HIV-negative at enrollment and were subsequently tested each month for HIV.

But findings from this research among Kenyan sex workers may not apply to other populations, and they have not been confirmed by other studies.⁴ For example, data from the large, FHI-led, prospective study of hormonal contraceptive use and HIV acquisition (see Hormonal Contraception and HIV Acquisition) and a sub-study of 186 women with primary HIV infection found that hormonal contraceptive use at the time of HIV infection was not significantly associated with a higher HIV viral set point. This data was collected primarily from family planning clients in Uganda and Zimbabwe.⁵ Further research among other populations in different geographic areas is needed to clarify the relationship between hormonal contraceptive use and HIV disease progression.

The limited evidence from Kenya suggests that any impact hormonal contraceptive use may have on HIV disease progression occurs during the early stages of the infection. But as part of their continuing research in Kenya, scientists from the University of Nairobi, Coast Provincial General Hospital in Mombasa, and the University of Washington at Seattle plan to evaluate the relationship between hormonal contraceptive use and HIV disease progression during the later, chronic stage of HIV infection. The study in Uganda and Zimbabwe will also explore whether hormonal contraception affects disease progression over time.

— Kathleen Henry Shears

References

1. Sagar M, Lavreys L, Baeten J, et al. Infection with multiple human immunodeficiency virus type 1 variants is associated with faster disease progression. J Virol 2003;77(23):12921-26.
2. Lavreys L, Baeten J, Kreiss JK, et al. Injectable contraceptive use and genital ulcer disease during the early phase of HIV-1. J Infect Dis 2004;189(2):303-11.
3. Sagar M, Lavreys L, Baeten J, et al. Identification of modifiable factors that affect the genetic diversity of the transmitted HIV-1 population. AIDS 2004;18(4):615-19; Baeten J, Lavreys L, Sagar M, et al. Effect of contraceptive methods on natural history of HIV: studies from the Mombasa cohort. J Acquir Immune Defic Syndr 2005;38(Suppl 1):18-20.
4. Cejtin HE, Jacobson L, Springer G, et al. Effect of hormonal contraceptive use on plasma HIV-1 RNA levels among HIV-infected women. AIDS 2003;17(11):1702-4.
5. Morrison C, Kwok C, Chen P, et al. Predictors of viral setpoint among African women with primary HIV-1 infection [abstract]. XVIth International Conference on AIDS, Toronto, Canada, August 13-18, 2006.

Does Pregnancy Speed HIV Progression?

Whether pregnancy affects the course of HIV infection is an important question for HIV-infected women interested in using hormonal contraception. Such women need to weigh the potential — but still unproven — risk of accelerated progression to AIDS among hormonal contraceptive users (see Does Hormonal Contraception Speed HIV Progression) against the risk of an unintended pregnancy resulting from reliance on a less effective contraceptive method.

Because pregnancy itself is thought to suppress immunity, concerns have been raised that pregnancy in HIV-infected women could hasten HIV-related deterioration of the immune system.¹ But the evidence to date suggests that pregnancy does not have such an effect, at least in the short term.²

Early reports of pregnancy in HIV-infected women seemed to support the hypothesis that pregnancy accelerates HIV disease progression. However, these studies involved small numbers of women and lacked control groups or the ability to adjust for other factors known to influence disease progression, such as disease stage or time of HIV exposure.³ A systematic review of studies published from 1983 to 1996 on pregnancy's effect on HIV progression and survival found a weak association between HIV disease progression and pregnancy in HIV-infected women, but it concluded that the potential for study bias was too great to draw definitive conclusions.⁴

A study published in 2000 was able to control for many potential confounding factors, including time since seroconversion (when virus can be detected in the blood), which occurs about three months after HIV infection. This study, which followed 365 HIV-infected French women — 241 of whom were pregnant — detected no increased risk of HIV progression during pregnancy.⁵ Like other prospective studies with similar findings,⁶ the French study involved mostly women who had not yet developed symptoms of HIV disease. Therefore, the possibility of increased risk of disease progression among pregnant women with more advanced HIV infection could not be ruled out.

Several studies from developing countries also suggest that pregnancy does not increase the risk of disease progression. In a study among HIV-infected women in Haiti, no statistically significant difference was observed in the rate of progression to AIDS or death between 44 pregnant women and 96 nonpregnant women.⁷ And two studies in sub-Saharan Africa — one among 823 pregnant Kenyan women and another that included 229 pregnant women in Malawi — detected no statistically significant differences in immune status between HIV-positive and HIV-negative women during pregnancy.⁸

"Of course, more rigorous studies are needed," says Dr. Marleen Temmerman, principal investigator of the Kenya study and professor of obstetrics and gynecology at the University of Ghent in Belgium. "But most studies in Europe, the United States, and Africa did not show an impact on disease progression, so if there is any impact at all, it will be a very minimal one."

— Kathleen Henry Shears

References

1. Vimercati A, Greco P, Lopalco PL, et al. Immunological markers in HIV-infected pregnant and non-pregnant women. Eur J Obstet Gynecol Reprod Biol 2000;90(1):37-41.
2. Watts H. Effect of pregnancy. J Acquir Immune Defic Syndr 2005;38(Suppl 1):36-37.
3. Scott GB, Fischl MA, Klimas N, et al. Mothers of infants with the acquired immunodeficiency syndrome. JAMA 1985;253(3):363-66; Minkoff H, Ragt RH, Landesman S, et al. Pneumocystis carinii pneumonia associated with acquired immunodeficiency syndrome in pregnancy: a report of three maternal deaths. Obstet Gynecol 1986;67(2):284; Minkoff H, Nanda D, Menez R, et al. Pregnancies resulting in infants with acquired immunodeficiency syndrome or AIDS-related complex: follow-up of mothers, children, and subsequently born siblings. Obstet Gynecol 1987;69(3 Part 1):288-91; Koonin LM, Ellerbrock RV, Atrash HK, et al. Pregnancy-associated deaths due to AIDS in the United States. JAMA 1989;261(10):1306-9; Lindgren A, Anzen B, Bohlin AB, et al. HIV and childbearing: clinical outcome and aspects of mother to infant transmission. AIDS 1991;5(9):1111-16.
4. French R, Brocklehurst P. The effect of pregnancy on survival in women infected with HIV: a systematic review of the literature and meta-analysis. Br J Obstet Gynaecol 1998;105(8):827-35.
5. Saada M, Le Chenadec J, Berrebi A, et al. Pregnancy and progression to AIDS: results of the French prospective cohorts. AIDS 2000;14(15):2355-60.
6. Hocke C, Morlat P, Chene G, et al. Prospective cohort study of the effect of pregnancy on the progression of human immunodeficiency virus infection. The Groupe d'Epidemiologie Clinique du SIDA en Aquitaine. Obstet Gynecol 1995;86(6):886-91; Weisser M, Rudin C, Battlegay M, et al. Does pregnancy influence the course of HIV infection? Evidence from two large Swiss cohort studies. J Acquir Immune Defic Syndr 1998;17(5):404-10; Burns DN, Landesman S, Minkoff H, et al. The influence of pregnancy on human immunodeficiency virus type 1 infection: antepartum and postpartum changes in human immunodeficiency virus type 1 viral load. Am J Obstet Gynecol 1998;178(2):355-59; Brettle RP, Raab GM, Ross A, et al. HIV infection in women: immunological markers and the influence of pregnancy. AIDS 1995;9(10):1177-84.
7. Deschamps M, Pape J, Desvarieux M, et al. A prospective study of HIV-seropositive asymptomatic women of childbearing age in a developing country. J Acquir Immune Defic Syndr 1993;6(5):446-51.
8. Temmerman M, Nagelkerke N, Bwayo J, et al. HIV-1 and immunological changes during pregnancy: a comparison between HIV-1 seropositive and HIV-1 seronegative women in Nairobi, Kenya. AIDS 1995;9(9):1057-60; Miotti P, Liomba G, Dallabetta GA, et al. T-lymphocyte subsets during and after pregnancy: analysis in human immunodeficiency virus type-1-infected and uninfected Malawian mothers. J Infect Dis 1992;165(6):1116-19.

Contraceptive Options for HIV-infected Women

Women with HIV have a right to decide whether they want to become pregnant and bear children. But if an HIV-infected woman chooses not to have children, or wants to space her family, she should be able to make informed, voluntary decisions about contraception and then receive her method of choice. Such use of contraception by HIV-infected women is an important way to reduce HIV-positive births.

HIV-infected women can use most contraceptive methods safely. While weighing the advantages and disadvantages of various methods, however, a woman living with HIV must consider the effects of each method on her own health, risk of infecting others with HIV, and response to HIV/AIDS treatment. Thus, counselors should help each HIV-infected woman assess her contraceptive needs, review all the contraceptive options available to her, and determine whether she and her partner will be able to use a particular method or combination of methods safely, correctly, and consistently.¹

Hormonal methods

The World Health Organization (WHO) recommends that HIV-infected women can safely use hormonal contraceptives — including combined oral contraceptives (COCs), the injectables depot-medroxyprogesterone acetate (DMPA) and norethisterone enanthate (NET-EN), and implants such as Norplant. Yet, questions remain about the effects of hormonal contraception on a woman's HIV infectiousness (see Does Hormonal Contraception Increase HIV Infectivity) and disease progression (see Does Hormonal Contraception Speed HIV Progression) and about the consequences of interactions between these methods and antiretroviral (ARV) drugs (see How Does HIV Therapy Affect Hormonal Contraception?, How Does Hormonal Contraception Affect HIV Therapy?, and COC-ARV Drug Interactions).

Condoms

Male and female condoms are the only contraceptive methods that can prevent the transmission of sexually transmitted infections (STIs), including HIV. Male condoms can be 97 percent effective in preventing pregnancy if used correctly and consistently; as typically used, they are about 86 percent effective.² Likewise, male condom use reduces HIV incidence by 80 percent to 97 percent, but only if condoms are used correctly during each act of sexual intercourse with an infected partner.³

Female condoms can be 95 percent effective for pregnancy prevention if used correctly and consistently; as typically used, they are about 79 percent effective.⁴ No clinical trial has assessed whether female condoms protect against HIV. But estimates based on studies of pregnancy prevention and evidence from laboratory and epidemiological studies of the female condom's ability to protect against STI pathogens suggest that when used correctly and consistently, the device is likely to be about as effective as a male condom in reducing the risk of HIV and other STIs.⁵ Consistent condom use can protect an already HIV-infected woman against re-infection with another strain of HIV or from acquiring STIs such as gonorrhea and chlamydial infection. It can also reduce the risk of an HIV-infected woman transmitting the virus to an uninfected partner.⁶ Even when a woman is unlikely to infect others with HIV because her own infection is controlled by ARV therapy, she should be encouraged to use condoms because treatment may not completely eliminate her risk of infecting others.⁷

Since condoms as they are typically used are not as effective in preventing pregnancy as are many other contraceptive methods,⁸ HIV-infected women who do not want to become pregnant should consider using a more effective form of contraception while using condoms for STI protection. Some studies suggest that women with HIV who use more effective contraceptives, such as oral contraceptives or an intrauterine device (IUD), are less likely to use condoms consistently or at all, even with an uninfected partner.⁹ One U.S. study, however, found that condom use remained consistent among women using condoms and another method simultaneously for dual protection against both infection and pregnancy. Consistency of condom use was reduced only among women who alternated the two methods; for example, using a condom as a backup method after a missed pill.¹⁰

Another dual protection option — consistent use of condoms alone — is unpopular with providers because they fear its adoption would increase pregnancy rates. One way to address this concern would be to ensure access to emergency contraception as a backup method of contraception.¹¹

IUDs

A highly effective yet reversible nonhormonal contraceptive method became more available to HIV-infected women in 2004, when WHO removed most of its previously recommended restrictions on use of the IUD by women with HIV. Those restrictions, based on theoretical concerns about increased risk of pelvic inflammatory disease and HIV infectivity, were lifted after studies demonstrated that complications of IUD use are no more common among HIV-infected IUD users than they are among uninfected IUD users¹² and that IUD use does not appear to increase HIV infectivity.¹³ These findings suggest that appropriately selected HIV-infected women with regular access to medical services can use IUDs safely.

Under the revised WHO guidelines, most HIV-infected women generally can initiate and use IUDs and the levonorgestrel-releasing intrauterine system, and IUD users who become infected with HIV may continue using the device. The only exceptions are for insertions among women who have developed AIDS and are not receiving ARV drugs or women with AIDS who are not responding well to ARV treatment. IUD initiation is not recommended for such women because their suppressed immune systems can make them more vulnerable at the time of IUD insertion to infections that could lead to pelvic inflammatory disease. However, HIV-infected IUD users who develop AIDS may generally continue using the device.¹⁴

Sterilization

The stigma associated with HIV and fear of coming in contact with the blood of HIV-infected women have resulted in some surgeons not wanting to perform sterilizations on such women. However, sterilization offers couples a safe, highly effective, permanent method of contraception. It may be a good option for HIV-positive women and their partners who have decided to forgo or end childbearing, and it raises no particular health concerns for HIV-infected women. If a woman has an AIDS-related illness, however, female sterilization should be postponed until her condition improves. HIV-discordant couples in which the man is HIV-negative and the woman is HIV-positive may want to consider male sterilization because it does not depend on the woman's health.¹⁵ Studies show a reduction in consistent condom use in couples after one partner has undergone sterilization.¹⁶ As with other methods, couples should be counseled about the importance of using condoms if they might be at risk of HIV infection. This advice is particularly important for discordant couples, to prevent the infected partner from transmitting the virus to the uninfected partner.

Other methods

Barrier methods other than condoms offer only modest protection against pregnancy and are generally not recommended for women with HIV.¹⁷ Frequent use of spermicides containing nonoxynol-9 (N-9) may increase the risk of re-infection with other strains of HIV because N-9 can disrupt the lining of the vagina, making it more vulnerable to infection.¹⁸ Studies have also shown that N-9 offers no protection against STIs.¹⁹

Diaphragms and cervical caps are not recommended for women with HIV or AIDS and women at high risk of HIV infection because they are usually used with spermicides containing N-9. Studies are under way to determine whether diaphragms offer any protection against STIs and HIV. A protective effect is considered possible because these barrier methods may block entry of pathogens to the cervix, which is the site of infection with gonorrhea and chlamydia and may be more susceptible than the vagina is to HIV infection.²⁰

Pregnancy rates of 1 percent to 9 percent with perfect use and 25 percent with typical use are seen for fertility awareness-based methods (natural family planning). These methods require abstaining from sex or using barrier methods only during the fertile days of the menstrual cycle in order to prevent pregnancy.²¹ But protected sex throughout the menstrual cycle — even during nonfertile periods — is necessary to prevent HIV transmission to a partner. Therefore, sexually active HIV-infected women and their partners should use male or female condoms consistently throughout the woman's menstrual cycle.

The use of breastfeeding as a temporary method of contraception (the lactational amenorrhea method) is highly effective in preventing pregnancy for up to six months postpartum in nonmenstruating women who are fully or nearly fully breastfeeding.²² HIV-infected women who are able to use safe breast milk alternatives to avoid transmitting the virus to their children do not benefit from lactational amenorrhea and will resume ovulating sooner than breastfeeding women. Their future contraceptive needs should be discussed during pregnancy or early in the postpartum period.²³

In summary, HIV-infected women face few restrictions on their use of modern contraceptive methods. Furthermore, use of effective contraception can play a key role in preventing HIV-positive births.

— Kathleen Henry Shears

References

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