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  • The authors have previously hypothesized that

    2018-10-26

    The authors have previously hypothesized that CHC that changes to the vestibular mucosa induced by CHCs are a potential cause of vestibulodynia [11]. Herein, we describe our treatment approach to and clinical outcomes in premenopausal women with vestibulodynia who presented to a vulvar pain clinic while currently taking CHCs.
    Methods After obtaining approval from the Anne Arundel Medical Center Institutional Review Board, the database for The Center for Vulvovaginal Disorders was utilized to identify 50 consecutive premenopausal women with vestibulodynia who were using CHCs at the time they presented for care. All women had previously had pain‐free intercourse and had subsequently developed vestibular pain (i.e., secondary vestibulodynia). As is our standard practice, all patients were asked to discontinue CHCs, and patients were asked to apply a compounded preparation of topical estradiol 0.03% and BV6 Supplier 0.01% to the vestibule twice daily. Testosterone was used in treatment as a recent study examining the impact of vaginal testosterone alone on vaginal atrophy demonstrated improvement in vaginal atrophy symptoms [12]. Patients who had other causes of vestibular pain such as pelvic floor muscle hypertonus, infection, and vulvar dermatoses were excluded from this review; thus, only patients in whom CHCs were the only identifiable cause of their vestibular pain were included. Data abstracted included age, average time taking CHCs, baseline and posttreatment vestibular pain scores, SHBG, and calculated free testosterone levels as well as treatment time (in weeks). Vestibular pain was assessed using a moist cotton swab. If the vestibular pain in a given patient varied at different locations on the vestibule, the highest score was used when calculating the average pre‐ and postvestibular pain scores. Descriptive statistics and t‐tests were applied as appropriate.
    Discussion The potential for negative side effects from CHCs on female sexuality in general is a subject of debate. Perhaps the most widely studied aspect of female sexuality as it relates to CHC use is libido. To date, studies have yielded conflicting results with some studies showing improvement, others a decrease in, and others showing no effect on female desire with CHC use [13]. Interestingly, the proposed explanation of decreased libido in CHC users is the same as what we are hypothesizing causes vestibular pain: elevated SHBG and decrease calculated free testosterone levels. Although several studies have shown that CHCs increase a woman\'s risk of developing vestibulodynia, other studies have not demonstrated this effect [14,15]. Unfortunately, these studies did not control for the type of CHC used or length of use. Although some studies have assessed hormone receptor expression in the vulvar vestibule and found no difference between women with vestibulodynia and pain‐free controls, CHC use was not controlled for [16]. Nevertheless, thousands of women suffer from vestibular pain and are seeking relief. Although there are undoubtedly many causes of vestibular pain, this study provides further evidence to support a hormonally mediated cause, specifically one induced by CHCs. This study has demonstrated that women with vestibulodynia who have no other identifiable cause of their pain that began while taking CHCs are effectively treated by discontinuing the CHCs combined with the application topical hormone therapy. Furthermore, subjective improvement is accompanied by normalization of calculated free testosterone and SHBG values. Panzer et al. found that in women with sexual dysfunction, SHBG levels in women who discontinued CHCs did not decrease to values of women who never used CHCs [17]. Although the present study noted a marked decrease in SHBG levels, it is unknown if the patients decreased to their baseline level. The hypothesis put forth by Panzer et al. suggesting that prolonged exposure to the synthetic estrogens in CHCs induced gene imprinting and increased gene expression of SHBG in the liver is an interesting one and merits further investigation.