Male Fertility and Reproductive Health
ßand IVF in a series of 29 seropositive women (66 cycles). They compared their results with an age-matched group of uninfected women and with their overall uninfected population. Higher cancellation rates and lower pregnancy rates were observed when the overall population was considered, but these differences disappeared when using an age-matched group.
also found a clinical pregnancy rate of 16.2% among infected patients (n=50), which was half that of a group of age-matched uninfected patients (37.5%). When they restricted their analysis to cycles with oocyte donation, these differences disappeared (36 versus 44% of patients). These authors therefore concluded that poor IVF results in HIV-positive women may be due to reduced ovarian response. Ovarian resistance to hyperstimulation may be involved in this effect because a greater number of units of gonadotrophins were needed to adequately stimulate these patients. As stated before, this resistance may reflect underlying subclinical and subanalytical hypogonadism and superovulation may be a useful functional stress test on the ovary.
Coll et al.61 Finally, Guibert et al.62 observed increased FSH levels on the third day of
the cycle in a population of 80 HIV-positive patients compared with a control group of similar age (n=70), and concluded that HIV infection accelerates ovarian reserve depletion. On the other hand, when selecting women below 42 years of age with normal basal FISH and inhibin levels, no difference in ovarian response was observed between HIV-positive and HIV-negative patients (n=14 for each group). The authors at the Luigi Sacco Biomedical Institute concluded from these results that IVF is not influenced by HIV infection in patients with a normal ovarian reserve. The discrepancies in the results between studies may be explained by heterogeneities in the populations studied. Differences in the matching processes and lack of power of the various studies are other possible explanations.
Pelvic inflammatory disease has been shown to reduce ovarian stimulation due to direct damage to the ovaries, follicle loss or
1.
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2. Minkoff H, et al., N Engl J Med, 2000;342:1748–50. 3. Englert Y, et al., Hum Reprod, 2001;16:1309–15. 4. Bujan L, et al., Fertil Steril, 2004;82:857–62. 5. Garrido N, et al., Hum Reprod, 2004;19:2581–6. 6. Semprini AE, et al., Curr Opin Obstet Gynecol, 2004;16:257–62.
7. Coll O, et al., AIDS, 2002;16(Suppl. 2):S1–S18. 8. Brettle RP, et al., AIDS, 1995;9:1177–84. 9. Saada M, et al., AIDS, 2000;14:2355–60. 10.
24.
mechanical alterations in follicle development. This may result from adherences or a deficiency in ovarian vascularisation.63,64
For instance,
a significantly higher prevalence of serum immunoglobulin G (IgG) antibodies to Chlamydia trachomatis was observed in poor responders, suggesting a possible detrimental effect of C. trachomatis on subsequent ovarian function.64
This may explain a tendency
towards reduced ovarian response among HIV-positive patients. Conclusion
Reproductive counselling for individuals with HIV might motivate them to ask for reproductive care in order to limit the risk of infecting uninfected partners, or of superinfection if the partner is also infected. By offering reproductive care to men infected with HIV, it is possible to strengthen the message that, by protecting their partners from becoming infected through unprotected sex, they could in the future become the healthy mother of an uninfected child. For uninfected women with an infected partner, the optimal solution remains protecting themselves from becoming infected to avoid perinatal transmission of HIV. For women who are HIV-1-positive, the problem remains the risk of vertical transmission. Significant progress has been made in this area, but additional research into the mechanisms of vertical transmission of HIV is still needed. n
Valeria Savasi is a Researcher in the Department of Obstetrics and Gynaecology at the Luigi Sacco Biomedical Institute of the University of Milan Medical School, where she is Chief of a unit dedicated to the reproductive and gynaecological care of patients with infective problems. She co-ordinates the Italian collaborative study on vertical transmission of HIV and participates in a number of national and international multicentre trials. Dr Savasi is a member of the Italian
Society of Obstetrics and Gynaecology and the European Society of Human Reproduction and Embryology (ESHRE). She graduated magna cum laude from the University of Milan Medical School in 1994 with a thesis on reproductive assistance in HIV-discordant couples. She was board-certified with honours in obstetrics and gynaecology in 2000, and completed a fellowship in foetal medicine with honours at the University of Milan Medical School in 2003.
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21. Bagasra O, et al., J Acquir Immune Defic Syndr, 1988;1: 431–5.
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Pudney J, Caveats associated with identifying HIV-1 using transmission electron microscopy. In: Alexander NJ, Gabelnick HL, Spieler JM (eds), Heterosexual Transmission of AIDS. Proceedings of the Second Contraceptive Research and Development (CONRAD) Program International Workshop, Held in Norfolk, Virginia, February 1–3, 1989, New York: Wiley-Liss, 1990;197–204.
30. Mermin JH, et al., J Infect Dis, 1991;164:769–72. 31. Van Voorhis BJ, et al., Fertil Steril, 1991;55:588–94. 32. Scofield VL, et al., AIDS, 1994;8:1733–6. 33. Dussaix E, et al., Res Virol, 1993;144:487–95. 34. Nuovo GJ, et al., Am J Pathol, 1994;144:1142–4. 35. Muciaccia B, et al., FASEB J, 1998;12:151–63. 36. Shevchuk MM, et al., J Reprod Immunol, 1998;41:69–79.
37. Ohl J, et al., Hum Reprod, 2003;18:1244–9. 38. Garrido N, et al., J Am J Obstet Gynecol, 2002;187:1121. 39. Politch JA, et al., Fertil Steril, 2004;81:440–7. 40. Marina S, et al., Fertil Steril, 1998;70:35–9. 41. Garrido N, et al., J Am J Obstet Gynecol, 2002;187:1121. 42. Meseguer M, et al., Fertil Steril, 2002;78:1199–1202. 43. Leruez-Ville M, et al., AIDS, 2002;16:2267–73. 44. Xu C, et al., AIDS Res Ther, 2005;2:9. 45. Muciaccia B, et al., Hum Reprod, 2007;22:2868–78. 46. Savasi V, et al., Hum Reprod, 2007;22:772–7. 47. Sauer MV, Reprod Biomed Online, 2005;10:135–40. 48. Peña JE, et al., Fertil Steril, 2003;80:356–62. 49. Oliviennes F, Hum Reprod, 2000;15:1663–5. 50. Garrido N, et al., Fertil Steril, 2006;86:1544–6. 51. Persico T, et al., Hum Reprod, 2006;21:1525–30. 52. Stephenson JM, et al., AIDS, 1996;10:1683–7. 53. Hinz S, et al., Gynecol Endocrinol, 2002;16:33–8. 54. Sobel JD, Clin Infect Dis, 2000;31:1225–33. 55. Clark RA, et al., J Infect Dis, 2001;184:1325–7. 56. Englert Y, et al., Hum Reprod Update, 2004;10:149–62. 57. Bertrand E, et al., AIDS, 2004;18:823–5. 58. Martinet V, et al., Hum Reprod, 2006;21:1212–7. 59. Ohl J, et al., Hum Reprod, 2005;20:3136–40. 60. Terriou P, et al., Hum Reprod, 2005;20:2838–43. 61. Coll O, et al., Human Reprod, 2005;20: abstract 0–22. 62. Guibert J, et al., Troisièmes Journées Nationales ‘Désir d’enfant et VIH’, 7/05/2004, Toulouse.
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