Vulvovaginal atrophy (VVA) is a major consequence of menopause and related loss of the estrogenic effect on the vaginal epithelium. For many decades, the ideal therapeutic approach was to use systemic estrogen, which was very effective. Local treatment with vaginal estrogen (creams, tablets, and rings) is effective to the same extent. But, on the other hand, the downside of systemic hormone therapy (risks for breast cancer, cardiovascular and thromboembolic events, perhaps some cognitive decline) became a major issue after the first release of data from the Women’s Health Initiative (WHI) trial in 2002, and changed both patients’ preferences and prescription habits. The uncertainty about estrogen resulted in two changes concerning the treatment of VVA. The first has been to lower the dosage of local estrogen preparations, still maintaining a good clinical response and symptom relief, but keeping serum estrogen levels well below premenopausal levels. The other was to promote non-estrogenic and non-hormonal therapies, either by using marketed products, or by developing new drug formulations. Among the recently approved medications is prasterone – an intravaginal DHEA preparation [1,2]. In a 52-week-long study which showed a significant improvement in vaginal dryness and irritation/itching, and in pain during sexual activity, the authors commented that ‘The treatments currently used against VVA are essentially intravaginal and oral estrogen; however, as indicated by the black box on the estrogen information leaflets, there are risks. In fact, even at the lowest dose and dosing regimen, all intravaginal estrogen preparations increase serum estrogens above the normal postmenopausal range or above the threshold of no biological activity with the accompanying risk of systemic effects’ . Is this statement supported by hard clinical data?
Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
Solihull Hospital, Birmingham, UK
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