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Vaginal Fissure That Heals With Cortisone but Opens Up Again

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  • Journal List
  • Mayo Clin Proc
  • v.85(one); 2010 Jan
  • PMC2800285

Mayo Clin Proc. 2010 Jan; 85(ane): 87–94.

Vulvovaginal Atrophy

Abstract

Vulvovaginal atrophy (VVA) is a common and underreported condition associated with decreased estrogenization of the vaginal tissue. Symptoms include dryness, irritation, soreness, and dyspareunia with urinary frequency, urgency, and urge incontinence. It can occur at any time in a woman's life cycle, although more than commonly in the postmenopausal phase, during which the prevalence is close to fifty%. Clinical findings include the presence of stake and dry vulvovaginal mucosa with petechiae. Vaginal rugae disappear, and the cervix may become flush with the vaginal wall. A vaginal pH of iv.6 or more supports the diagnosis of VVA. Even while taking systemic estrogen, x% to twenty% of women may still accept residual VVA symptoms. Breast cancer treatment increases the prevalence of VVA considering the surgical, endocrine, and chemotherapeutic agents used in its treatment tin can cause or exacerbate VVA. Local estrogen treatment for this group of women remains controversial.

AI = aromatase inhibitor; CI = confidence interval; ER = estrogen receptor; HT = hormone therapy; SERM = selective ER modulator; VMI = vaginal maturation index; VVA = vulvovaginal cloudburst

Vulvovaginal atrophy (VVA) is a common condition, particularly in postmenopausal women. Vaginal atrophy, atrophic vaginitis, and urogenital atrophy are other terms used to describe this constellation of symptoms associated with decreased estrogenization of the vulvovaginal tissue. Although handling with topical estrogen is constructive in alleviating symptoms, women oft practice not written report symptoms and thus go untreated.1,2

Mutual symptoms include vaginal dryness, irritation, postcoital bleeding, and soreness. These symptoms may exist associated with vaginal discharge and dyspareunia. Urinary symptoms associated with VVA include frequency, urgency, and urge incontinence.

PREVALENCE

Vulvovaginal atrophy can occur at any time in a woman's life cycle, although information technology is more than mutual in the postmenopausal phase, a time of hypoestrogenism. Other causes of a hypoestrogenic state include lactation, various breast cancer treatments, and use of certain medications. In situations other than menopause, VVA may resolve spontaneously when estrogen levels are restored.

Numerous retrospective studies take evaluated the prevalence of symptoms of VVA (Table 1).iii-ten Although these studies differ in type of symptoms elicited, study design, and study population, they provide a range of estimates of VVA prevalence. They all used cocky-reported symptoms of vaginal dryness to make up one's mind the prevalence of VVA. In full general, the prevalence ranged from well-nigh four% in the early premenopausal groups to 47% in the late postmenopausal group.

TABLE 1.

Studies Assessing Prevalence of Vaginal Dryness

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The prevalence of VVA in some subgroups of women can be much higher. In a accomplice of breast cancer survivors, vaginal dryness was nowadays in 23.4% of the premenopausal patients and in 61.5% of the postmenopausal patients.8

PHYSIOLOGY

Vulvovaginal cloudburst occurs under conditions of hypoestrogenism. In the premenopausal country, estradiol levels fluctuate from ten to 800 pg/mL (to catechumen to pmol/L, multiply past three.671),11 depending on when measured during the cycle. In the postmenopausal state, estradiol levels are typically less than 30 pg/mL. Afterward menopause, circulating estradiol derives from estrone, which is peripherally converted in adipose tissue from adrenal androstenedione.

The vaginal epithelium is a stratified squamous epithelium, which until menopause is moist and thick with rugae. At menopause, with declining levels of estrogen, the vaginal epithelium thins. Fewer epithelial cells result in less exfoliation of cells into the vagina. As epithelial cells exfoliate and die, they release glycogen, which is hydrolyzed to glucose. Glucose, in plow, is broken downward into lactic acid by the action of lactobacillus, a normal vaginal commensal organism. Without this cascade, the pH in the vagina rises, resulting in a loss of lactobacilli and an overgrowth of other bacteria, including group B streptococcus, staphylococci, coliforms, and diphtheroids12 (Figure 1). These bacteria tin crusade symptomatic vaginal infections and inflammation. After menopause, the elasticity of the vagina is reduced and connective tissue increases.13 A decline in estrogen level causes a decrease in vaginal blood flow and a subtract in vaginal lubrication. These changes can exist reversed by the use of estrogens.14,15

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Proposed cascade-of-effects machinery for vulvovaginal atrophy.

The effects of endogenous estrogens on vulvovaginal tissues are mediated through estrogen receptors (ERs) α and β, establish at sites throughout the urogenital area, including the vagina, vulva, labia, urethra, and float trigone. These sites, in turn, regulate transcription at specific areas on the DNA.16

SYMPTOMS

The initial symptom is often lack of lubrication during intercourse. Somewhen, persistent vaginal dryness may occur. Thinning of the epithelial lining may also cause pruritus, soreness, and a stinging hurting in the vaginal and vulvar area, which, in turn, may further contribute to dyspareunia. Vaginal spotting, due to small tears in the vaginal epithelium, may also occur. Women with VVA may report a thin yellow or grey watery discharge secondary to the rise in pH that accompanies VVA.17

Women with VVA oftentimes report symptoms such as urgency, frequency, nocturia, and urge incontinence. Urinalysis may prove microscopic hematuria. Recurrent urinary tract infections can also result. Stress incontinence is commonly constitute in this historic period group of women, but electric current evidence suggests it is non directly attributable to VVA.18

Women practice not always report their symptoms of VVA. They are more than likely to report vaginal discharge and urinary urgency merely are less likely to written report vaginal itching, soreness, or dyspareunia. Women may not study symptoms considering they are self-treating, feel the symptoms are not important enough, or are embarassed.xix

CLINICAL FINDINGS

Clinical findings include atrophy of the labia majora and vaginal introitus. The labia minora may recede. Vulvar and vaginal mucosae may appear stake, shiny, and dry; if there is inflammation, they may appear reddened or pale with petechiae. Vaginal rugae disappear, and the cervix may become flush with the vaginal wall. Vaginal shortening and narrowing tend to occur.20

A thin watery yellowish vaginal discharge may exist observed. A urethral caruncle, a minor, soft, smooth friable cherry-red outgrowth along the border of the urethra, may develop.

CLINICAL TESTS

The diagnosis of VVA is a clinical ane. All the same, 2 tests may be used to support the diagnosis: a vaginal pH and a vaginal maturation index (VMI). To assess pH, a piece of litmus paper is placed on the lateral vaginal wall until moistened. A pH of 4.6 or greater indicates VVA, bold the patient does not have bacterial vaginosis. Premenopausal women without VVA typically have a pH of 4.5 or less.12

The VMI (Figure 2) is the benchmark standard for VVA confirmation just is generally non used or needed in clinical practice. This examination assesses the relative proportion of parabasal, intermediate, and superficial vaginal epithelial jail cell types. In premenopausal women, greater than xv% superficial cells would be considered normal; however, in postmenopausal women with VVA, the typical proportion would be less than v%.

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Photomicrographs of superficial and intermediate cells (top) and atrophic cells (bottom). (Papanicolaou stain; original magnification x20). Courtesy of the Mayo Cytopathology Laboratory.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis includes other conditions that cause chronic vaginal and vulvar itching, belch, or hurting (eg, vaginal infections, irritants, and vulvovaginal dermatoses). Vaginal infections can be caused by leaner, viruses, protozoa, and fungi. The iii most common vaginal infections are Candida vulvovaginitis, bacterial vaginosis, and trichomoniasis. Bacterial vaginosis may result from atrophic changes in the vagina. Irritants that tin can crusade chronic vaginal itch include perfumes, whatever locally applied lubricant or moisturizer, and soaps. Vulvovaginal dermatoses, including lichen sclerosus, lichen planus, and lichen simplex chronicus, may crusade like symptoms.21 Cancer and precancerous lesions, including vulvar intraepithelial tumour, vulvar cancer, and extramammary Paget disease, are in the differential diagnosis of any localized areas of redness, thickening, or ulceration (Table 2 ). Biopsy should be performed if a malignancy is suspected or if the diagnosis is unclear.

TABLE 2.

Differential Diagnosis for Symptoms of Vulvovaginal Atrophy

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Treatment

Nonhormonal Treatments

Current over-the-counter treatments include nonhormonal vaginal moisturizers for VVA symptoms and lubricants for dyspareunia. Vaginal moisturizers, which are h2o based, are bachelor every bit liquids, gels, or ovules inserted every few days. Vaginal moisturizers tin can be safely used long term, only they need to exist used regularly for optimal upshot.

Vaginal lubricants are shorter acting than moisturizers and are applied at the time of sexual activity to reduce dyspareunia. They tin be either water or silicone based, with the water-based products being the well-nigh widely available. They are applied to the vaginal opening and/or to the penis and often require repeated application during sexual practice. Silicone-based lubricants require application of only a very minor amount and last longer; however, they can interfere with erectile function in male partners. The choice of lubricant may depend on individual preferences and product availability.

Hormonal Treatments

On the basis of an evidence-based review of clinical trials examining bachelor low-dose vaginal estrogen preparations for the treatment of VVA in postmenopausal women, The Northward American Menopause Club (NAMS) 2007 position argument noted that "the choice of therapy should be guided by clinical experience and patient preference."22 NAMS also stated it is generally unnecessary to prescribe a progestogen in combination with low-dose vaginal estrogen to prevent endometrial hyperplasia or cancer.

On the basis of a meta-analysis of 19 randomized clinical trials involving 4162 postmenopausal women, the 2006 Cochrane Database of Systematic Reviews concluded that vaginal estrogen is an effective handling for VVA23 and that all forms, whether foam, band, or tablet, appeared to relieve symptoms more effectively than nonhormonal gels and placebo. Differences observed between the treatments were in participant preferences.

Therefore, for symptomatic vaginal atrophy that does non respond to self-care measures, estrogen treatment is the standard of care, typically with vaginally administered local estrogens. Prescription vaginal estrogens are available as either estradiol or conjugated estrogens. In some countries outside the The states, vaginal estriol is too available.

SYSTEMIC ABSORPTION OF VAGINAL HORMONAL PREPARATIONS

An important concern about treatment safety relates to the extent of systemic absorption of vaginal estrogens. The determination from several studies comparing different doses of estradiol vaginal tablets24,25 or different vaginal estrogen preparations (conjugated estrogens and estradiol vaginal tablets)26 is that systemic absorption occurs, but to a limited extent. Labrie et al26 showed that levels of estradiol increased on average from a baseline (pretreatment) level of 3 pg/mL to 17 pg/mL on day vii of handling for both estradiol vaginal tablets (25 μg) and conjugated estrogen cream (0.625 mg). Nilsson and Heimer24 showed that, although plasma estradiol concentration diminished by the 14th day of daily treatment with ten or 25 μg of vaginal estradiol, it was withal statistically significantly higher than pretreatment levels. Some bear witness shows that estradiol levels diminish over fourth dimension when vaginal estrogens are used consistently.24,25

Although vaginal estrogens applied every bit a cream, vaginal tablets, or a low-dose vaginal ring are systemically captivated, the rise in serum estrogen levels appears to remain well below premenopausal levels. Nonetheless, this may exist of concern to women with a history of chest or other hormonally sensitive cancers

PRACTICAL ISSUES

Because all low-dose vaginal estrogens appear comparable in efficacy for the treatment of VVA, the choice of estrogen formulation is determined by the clinician and by each woman'south preferences. Estrogen creams are currently the to the lowest degree costly and most widely used but require commitment to regular utilize for sustained outcome. Dosing vaginal creams can be confusing because the dose of active estrogen cream is specified in milligrams, the dose of base of operations cream in grams, and applicator book in proportions. A simplified approach to dosing is provided in Table 3. The estradiol tablet is preferred by some to avert the messiness of cream. The estradiol ring is long interim and requires less sustained effort to employ; withal, it requires dexterity to insert and remove and needs to be replaced every 3 months. The presence of a cystocele or rectocele may crusade ring displacement.

Tabular array iii.

Vaginal Estrogen Products

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SYSTEMIC ESTROGEN AGENTS AND VVA

Systemic estrogen therapy, in the form of patches, oral agents, or a higher-dose vaginal band, is sometimes used for VVA, particularly when the patient besides has hot flashes. However, x% to xx% of women may have residual VVA symptoms fifty-fifty while taking systemic estrogen.27 These women will require administration of local vaginal estrogens lone or forth with systemic therapy for relief of VVA symptoms.

Two studies have shown that oral hormone therapy (HT) may worsen symptoms of urinary incontinence. The Heart and Estrogen-Progestin Replacement Study establish a college risk of both urge (odds ratio, 1.5; 95% confidence interval [CI], 1.2-1.8; P<.001) and stress incontinence (odds ratio, 1.7; 95% CI, 1.5-2.1; P<.001) in the hormone-treated group vs the placebo group throughout the treatment menstruation.28

It has been suggested that urge incontinence worsened with HT because progesterone was a component. However, in the Women's Health Initiative, 3 treatment groups were evaluated for urge incontinence (conjugated estrogens solitary, conjugated estrogens with progesterone, and placebo). Women given conjugated estrogens lonely were at increased risk of developing urge incontinence compared with those receiving placebo (relative risk, 1.32; 95% CI, 1.ten-1.58), whereas the women given combination conjugated estrogens with progesterone were not (relative risk, 1.15; 95% CI, 0.99-1.34).29 Thus, whether oral HT adversely affects urge urinary incontinence remains unclear.

Chest CANCER AND VVA

Currently, more than 2 meg women in the United states have a history of breast cancer. In chest cancer survivors, the estimated prevalence of vaginal atrophy, by symptom report, ranges from 23% to 61%.viii Prescribing even very low-dose localized estrogen treatments for these patients can cause business organization because of the potential for systemic absorption.

Business organisation about the provision of any course of estrogen, either systemic or local, to breast cancer survivors contributes to the high incidence of VVA in women with breast cancer. Discontinuation of HT may trigger the onset of VVA symptoms.

Many surgical, endocrine, and chemotherapeutic treatments for breast cancer can cause or exacerbate VVA.10,xxx-37 Tamoxifen acts as an estrogen adversary or agonist depending on the target organ and menopausal status. In premenopausal women, tamoxifen may cause VVA by acting every bit an estrogen adversary and blocking the naturally high levels of endogenous estrogen. In postmenopausal women, however, information technology acts as an estrogen agonist on the urogenital tract.38

Raloxifene does non announced to accept an consequence on the urogenital area in either premenopausal or postmenopausal women. Davies et al35 found no significant differences in incidence of VVA when comparison databases of postmenopausal women treated with raloxifene vs placebo.

Aromatase inhibitors (AIs) are prescribed as adjuvant systemic therapy to women with ER+ breast cancer. In the ATAC (Arimidex, Tamoxifen, Alone or in Combination) written report, designed to compare outcomes in postmenopausal breast cancer survivors taking tamoxifen, anastrozole (an AI), or a combination of both, Cella et alx demonstrated that vaginal dryness was more than common in the group taking anastrozole than in the group taking tamoxifen (18.five% vs 9.1%). Dyspareunia was also more mutual in the anastrozole grouping (17.3% vs 8.1%).x

Chemotherapy itself can result in vaginal dryness and dyspareunia. In a randomized clinical trial comparing loftier-dose chemotherapy with standard-dose chemotherapy for breast cancer survivors, followed by radiotherapy and tamoxifen in all patients, more patients in the high-dose chemotherapy group experienced persistent vaginal dryness.37

Chemotherapeutic agents used in the handling of chest cancer can likewise cause VVA because of chemotherapy-induced ovarian failure. Premenopausal women account for 25% of all diagnosed breast cancer cases and are more likely to need systemic chemotherapy. The risk of permanent chemotherapy-induced ovarian failure is more common in women older than 40 years (49%-100%) than in those younger than twoscore years (21%-71%).39

Premenopausal women with hormone-sensitive (ER+) advanced breast cancer may be offered gonadotropin-releasing hormone agonists to induce a temporary menopause through suppression of ovarian function, with VVA as a potential agin result.forty Loftier-take a chance premenopausal women who are BRCA1/2+ sometimes cull bilateral oophorectomy, which in turn increases their likelihood of developing VVA.

Whether breast cancer survivors with VVA tin can be safely treated with low-dose vaginal estrogens remains controversial. Kendall et al41 addressed this question when they followed up 7 breast cancer survivors taking AIs to suppress estrogen levels. These women took 25-μg vaginal tablets of estradiol daily for 2 weeks and then twice weekly for astringent symptoms of VVA. After ii weeks of handling, mean serum estradiol levels increased from a pretreatment value of 1.four pg/mL or less to 19.6 pg/mL. The estrogen levels had decreased to less than 9.v pg/mL by 4 weeks of therapy in almost women, just only two women had pretreatment estradiol levels at calendar week 7. If third-generation AIs decrease the levels of circulating estrogens more earlier-generation AIs and at the same fourth dimension amend survival, Kendall et al41 hypothesized that a small-scale increase in circulating estradiol could worsen survival outcomes.

COMPLEMENTARY AND Culling MEDICINE

Complementary and alternative medicine products take been extensively studied in the treatment of hot flashes, simply less information is available on their apply in VVA. One report found that Vitamin Due east and phytoestrogen applied locally as a gel improved the symptoms of VVA.42 An evaluation of VVA was undertaken in a cross-sectional report of 60 women, one-half of whom had taken 1,25-dihydroxyvitamin D (0.five μg/d of calcitriol) orally for at least 1 year and half of whom had not. The prevalence of vaginal atrophy was significantly higher in the group who did not utilize vitamin D, equally measured by VMI and symptoms.43

In a separate study, soy supplementation for the treatment of VVA was investigated. Phytoestrogens such as soy demark to ERs in the vagina and float. A randomized controlled trial evaluating dietary supplementation with 12 to 20 mg/d of soy showed no improvement in VMI.44

Currently, well-established effective complementary and alternative medicine treatments for VVA are lacking.

Future STUDIES

Future studies will go along to explore the utilise of even lower doses of vaginal estrogens. The efficacy and safety of ten-μg vaginal tablets of depression-dose estradiol for the treatment of VVA were evaluated in a 2009 study; after 12 weeks of therapy, significant improvements in symptoms, pH, and VMI were observed, with no adverse effects.45 In a contempo report comparing treatment with 25 μg of estradiol, 10 μg of estradiol, and placebo, Bachmann et al46 constitute that both active groups experienced improvement in vaginal cloudburst symptoms, vaginal pH, and VMI, with greater improvements seen for the higher dose.

Interest in vaginal estriol products is stiff considering of the inverse relationship with breast cancer take a chance at a population level. Studies take shown that estriol improves symptoms of VVA and reduces the incidence of urinary tract infection. Exogenous estriol administration does not alter serum estradiol or follicle-stimulating hormone levels.47-l

Studies are currently under manner to evaluate newer selective ER modulators (SERMs), which specifically target urovaginal health without compromising chest health.51

Because moisturizers and lubricants likewise play a function in the treatment of VVA, better delivery systems for these nonhormonal vaginal treatments will likely be developed in the time to come.

Conclusion

Vulvovaginal atrophy, a mutual and frequently underreported condition, occurs in women who feel hypoestrogenic states. Systemic treatment, when prescribed for menopausal symptoms, may non be sufficient to control VVA. Local estrogens include creams, tablets, and rings, all of which are equally effective. Thus, patient preference volition guide the selection. A growing number of women are at risk of developing VVA because of decreased use of systemic HT and increased use of SERMs, AIs, and chemotherapy in women with a history of breast cancer, for whom the prophylactic of even low-dose vaginal estrogens has not been established.

Hereafter research on VVA will likely explore the use of much lower doses of vaginal estrogens, seek to develop newer delivery systems for nonhormonal therapy, and develop SERMs that preferentially target urogenital tissues.

Supplementary Material

Notes

On completion of this article, you should be able to (1) recognize the common symptoms and signs of vulvovaginal cloudburst, (2) evaluate the part of tests used in its identification, and (3) recommend effective handling options.

CME Questions Most Vulvovaginal Cloudburst

  1. A 58-year-old adult female, who has been taking oral hormone therapy (HT) for successful control of hot flashes and night sweats, reports vaginal itching, burning, and dyspareunia. Clinical examination reveals a stake shiny vulva and petechiae in the vagina, consistent with vulvovaginal atrophy (VVA).

    Which one of the following treatments would be almost constructive for managing this patient's symptoms?

    1. Increase her current dose of oral HT

    2. Decrease her current dose of oral HT, and recommend initiation of vaginal estrogen applied twice weekly and vaginal lubricant applied at time of intercourse

    3. Continue current dose of oral HT, and recommend initiation of vaginal estrogen applied twice weekly and vaginal lubricant applied at fourth dimension of intercourse

    4. Substitute transdermal patch estrogen for oral estrogen and recommend initiation of vaginal lubricant applied at time of intercourse

    5. Continue current dose of oral HT and advise employ of vaginal lubricant at fourth dimension of intercourse

  2. A 65-yr-erstwhile postmenopausal woman who is not taking HT therapy reports new-onset vaginal itching, burning, and dyspareunia. Clinical examination reveals a generalized stake shiny vulva and a white raised area on the vulva.

    Which one of the following would be the all-time recommendation for this patient?

    1. Apply low-dose estrogen cream to the vulvovaginal area

    2. Apply depression-dose estrogen foam to the vulvovaginal area and hydrocortisone cream to the whitened area

    3. Utilise hydrocortisone cream to the whitened surface area

    4. Perform biopsy of the whitened area

    5. Administer 1 dose of fluconazole (150 mg) orally, followed by awarding of low-dose estrogen cream to the vulvovaginal surface area

  3. A 58-twelvemonth-old adult female, who has been taking oral HT for successful command of hot flashes and night sweats, reports vaginal itching, burning, and dyspareunia. Clinical test reveals a pale shiny vulva and petechiae in the vagina, consistent with VVA.

    Which i of the following tests is necessary to make the diagnosis?

    1. pH of the vaginal mucosa

    2. No test required

    3. Urinalysis

    4. Vaginal maturation alphabetize (VMI)

    5. Vaginal culture

  4. Which 1 of the following is not associated with VVA?

    1. Lactation

    2. Premenopausal utilise of tamoxifen

    3. Postmenopausal use of tamoxifen

    4. Premenopausal use of chemotherapeutic agents

    5. Postmenopausal utilize of chemotherapeutic agents

  5. Which one of the following medications would be virtually probable to cause VVA in a postmenopausal woman?

    1. Raloxifene

    2. Tamoxifen

    3. Exemestane

    4. Systemic estradiol

    5. Medroxyprogesterone

This activeness was designated for 1 AMA PRA Category 1 Credit(s).™

Because the Curtailed Review for Clinicians contributions are at present a CME activeness, the answers to the questions will no longer be published in the print journal. For CME credit and the answers, see the link on our Web site at mayoclinicproceedings.com.

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Articles from Mayo Clinic Proceedings are provided here courtesy of The Mayo Foundation for Medical Education and Research

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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2800285/

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