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Treatment of Moderate to Severe Dyspareunia with Intravaginal Prasterone Therapy: a Review

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Treatment of Moderate to Severe Dyspareunia with Intravaginal Prasterone Therapy: a Review Climacteric ISSN: 1369-7137 (Print) 1473-0804 (Online) Journal homepage: https://www.tandfonline.com/loi/icmt20 Treatment of moderate to severe dyspareunia with intravaginal prasterone therapy: a review D. J. Portman, S. R. Goldstein & R. Kagan To cite this article: D. J. Portman, S. R. Goldstein & R. Kagan (2019) Treatment of moderate to severe dyspareunia with intravaginal prasterone therapy: a review, Climacteric, 22:1, 65-72, DOI: 10.1080/13697137.2018.1535583 To link to this article: https://doi.org/10.1080/13697137.2018.1535583 © 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group View supplementary material Published online: 17 Dec 2018. Submit your article to this journal Article views: 575 View Crossmark data Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=icmt20 CLIMACTERIC 2019, VOL. 22, NO. 1, 65–72 https://doi.org/10.1080/13697137.2018.1535583 REVIEW Treatment of moderate to severe dyspareunia with intravaginal prasterone therapy: a review D. J. Portmana,b, S. R. Goldsteinc and R. Kagand,e aColumbus Center for Women’s Health Research, Columbus, OH, USA; bSermonix Pharmaceuticals, Columbus, OH, USA; cDepartment of Obstetrics and Gynecology, New York University School of Medicine, New York, NY, USA; dDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco, CA, USA; eSutter East Bay Medical Foundation, Berkeley, CA, USA ABSTRACT ARTICLE HISTORY The loss of sex steroids (e.g. estradiol, dehydroepiandrosterone [DHEA], progesterone) that causes Received 11 May 2018 menopause commonly affects a woman’s general health and produces bothersome physical changes Revised 25 September 2018 that may interfere with normal sexual and genitourinary functioning. Although both over-the-counter Accepted 30 September 2018 and prescription treatments are available, there remains a large unmet need, as less than 10% of Published online 17 Decem- ber 2018 women are treated. Adrenal DHEA and its sulfate are the most abundant steroids in humans. Here we review the development of intravaginal prasterone, the synthetic equivalent to endogenous DHEA. KEYWORDS Prasterone is approved by the US Food and Drug Administration for the treatment of moderate to Dehydroepiandrosterone; severe dyspareunia, a symptom of vulvar and vaginal atrophy, due to menopause. Prasterone has been genitourinary syndrome of shown to decrease the pain associated with dyspareunia, and to improve vaginal pH, as well as superfi- menopause; dyspareunia; cial and parabasal cell counts, while maintaining serum hormone levels within the range of those seen prasterone; menopause; in normal postmenopausal women. Unlike other menopausal prescription therapies, intravaginal pras- vulvovaginal atrophy terone does not carry a boxed warning, thus allowing the clinician and patient to engage in meaning- ful and reassuring discussion around a new approach that treats this common, debilitating condition. Introduction including epithelium thinning, altered appearance and func- tion of smooth muscle cells, increased density of connective Menopause is associated with an arrest of the ovarian syn- tissue, and fewer blood vessels8,9. Changes in vaginal flora thesis of estrogen, progesterone, and dehydroepiandroster- associated with the loss of superficial cells, glycogen, and lac- one (DHEA), and its sulfate (DHEA-S), which are produced tobacilli result in increased pH and the increased potential primarily by the adrenal glands, but also by the ovaries for vaginal and urinary tract infections and inflammation10. (Supplementary Figure 1)1. In the first year of menopause, Decreases in vaginal blood flow and lubrication often result women lose about 80% of their estrogens. Testosterone lev- 11,12 els decline by about 50–75% from the early twenties to age in dryness and dyspareunia . In the vaginal epithelium, a 40–45 years but do not change significantly across the lack of sex steroids causes a decrease in the proportion of menopausal transition2. DHEA-S levels decline steadily with superficial cells and an increase in the proportion of imma- 13 age and are not significantly related to menopause. By age ture parabasal cells . There is also less elasticity and vulvo- 11 70 years, they are approximately 20–23% of their peak vaginal tissue is prone to petechiae, injury, and pain . value3. Most importantly, serum testosterone simply results from the uncontrolled leakage of some testosterone made Menopausal symptoms intracellularly from DHEA and is not a valid parameter of androgenic activity4. Thus, menopause itself is not associated A 2013 position statement by the North American 14 with dramatic decreases in androgens but postmenopausal Menopause Society (NAMS) cited the REal Women’s VIews women can have significantly less endogenous androgens of Treatment Options for Menopausal Vaginal ChangEs compared with younger women5. The loss of these sex ste- (REVIVE) survey in which the impact of vulvovaginal atrophy roids causes physical changes that may interfere with normal (VVA) symptoms is described in more than 3000 postmeno- sexual and genitourinary functioning in a significant number pausal women: 85% of partnered women had ‘some loss of of postmenopausal women6,7. intimacy’; 59% indicated that VVA symptoms detracted from During perimenopause, menopause, and postmenopause, enjoyment of sex; 47% indicated that VVA interfered with sex steroid-dependent tissues undergo atrophic changes their relationship; 29% reported that VVA had a negative CONTACT David J. Portman [email protected] Columbus Center for Women’s Health Research, Columbus, OH, USA; Sermonix Pharmaceuticals, 3000 East Main Street, Columbus, OH, USA Supplemental data for this article can be accessed here. ß 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way. 66 D. J. PORTMAN ET AL. effect on sleep; and 27% reported that VVA had a negative dyspareunia, but do not address declining levels of sex ste- effect on their general enjoyment of life. Despite this, only roids or anatomic changes29. Although vaginal estrogen 7% of the surveyed women indicated that their health-care therapies can restore estrogen to the vaginal tissue and can professional (HCP) initiated a discussion about VVA. reverse some atrophic changes, even low-dose estrogen In 2014, in response to a concern that the term VVA was therapies have been shown to increase serum estradiol inadequate to describe the range of menopausal urogenital above normal levels30–32. However, these products carry symptoms, the International Society for the Study of Food and Drug Administration (FDA) boxed warnings identi- Women’s Sexual Health and the NAMS proposed a new term cal to the risks associated with systemic estrogen based on – genitourinary syndrome of menopause (GSM)15. GSM is extrapolation of data from trials of either oral estrogen or defined as a collection of symptoms and signs associated combined oral estrogen–progestin therapy. Without large, with a decrease in estrogen and other sex steroids involving long-term prospective studies that confirm a safer adverse changes to the labia majora/minora, clitoris, vestibule/introi- event profile for vaginal estrogen compared to systemic tus, vagina, urethra, and bladder, including symptomatic therapies, the class label boxed warning for all estrogen- VVA15. This consensus statement also recognizes that andro- based products will remain. Thus, patient perceptions of gen receptors are widely distributed in the vestibule and safety based upon class labeling and the time needed by within its glands, with urogenital tissues responsive to andro- HCPs to convey information about these warnings are gens as well as estrogens. obstacles to acceptance and/or adherence to estrogen ther- With the decline of circulating sex steroids and precursors, apy28. The oral selective estrogen receptor modulator ospe- GSM can start in perimenopause, increase during the early mifene is another alternative for these symptoms; however, menopausal period, and further increase in the 2–3 years it carries a modified boxed warning33. after menopause. The symptoms range in severity from 16 mildly bothersome to unbearable . Unlike vasomotor symp- Compounded hormones toms, the vaginal symptoms associated with GSM do not resolve spontaneously; rather, there is a progressive and FDA-approved prescription drugs are required to demon- cumulative negative effect over time9. Long-term therapy strate safety and efficacy and to be manufactured according may be necessary to maintain urogenital health17. to current Good Manufacturing Practices to help ensure the Women spend more than one-third of their lives in the identity, strength, quality, and purity of drugs by requiring postmenopausal state. Over half of postmenopausal women adequate control of manufacturing operations. In contrast, – report experiencing GSM18 22, and more than 75% report an compounded medications are not FDA approved, have not impact on their sexual lives18. However, most postmeno- undergone rigorous testing, and do not contain labeling
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