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Advances in Diagnosing Dyspareunia.

INTRODUCTION

Three major factors adversely affect postmenopausal female sexuality: anatomic and physiologic changes associated with aging, ovarian and adrenal hormonal insufficiency, and partnership issues. (1,2) In postmenopausal women, the lack of estrogen stimulation in vaginal and vulvar tissue commonly results in involution of these tissues--commonly referred to as vulvovaginal atrophy (VVA). In the United States, it is estimated that there are 64 million postmenopausal women and that as many as 32 million women have been found to suffer WA symptoms. (3,4) The symptoms may also occur in premenopausal women if they exhibit significant hypoestrogenemia (eg, postpartum breastfeeding women). Symptoms of WA include, but are not limited to, vaginal dryness, irritation, burning, dysuria, dyspareunia, and vaginal discharge. (5) Whereas vasomotor symptoms (VMS) associated with menopause diminish over time, WA is a chronic condition that worsens in the absence of treatment. (6) VVA symptoms can adversely affect a woman's sexual functioning, partnership issues, and her overall quality of life. (7,8,9)

WA is a component of what is now better referred to as the "genitourinary syndrome of menopause" (GSM): a constellation of signs and symptoms that are the result of hormonal (estrogen and androgen) insufficiency in the urogenital tissues. (10) The term GSM arose from a perceived need by the International Society for the Study of Women's Sexual Health and The North American Menopause Society to find a medically accurate and all-encompassing term to replace the pejorative "vulvovaginal atrophy." (10) GSM is a more accurate nosology because it refers to the entire genitourinary system and incorporates changes to the labia major/minora, clitoris, vestibule/introitus, vagina, urethra, and bladder. Signs include decreased vaginal moisture and diminished elasticity, labial resorption, pallor/erythema, loss of rugae, petechiae, fragility, urethral atrophy, and introital involution. GSM often includes genital symptoms of vaginal dryness, burning, and irritation; adverse effects on sexual function (lack of lubrication, dyspareunia, decreased libido); and urinary symptoms of urgency, dysuria, and recurrent urinary tract infection (UTI).

Dyspareunia, another prevalent component of GSM, has recently been (re)characterized by the American College of Obstetricians and Gynecologists as "a pain disorder that interferes with sexuality rather than as a sexual disorder characterized by pain." (11) In fact, a recent study of 500 postmenopausal women with vaginal discomfort identified "vaginal dryness" (85%) and "dyspareunia" (52%) as the most commonly reported complaints. (12) Over time, the vast majority of postmenopausal women will develop VVA. (13) For the syndrome to be classified as a sexual dysfunction, the symptoms must be bothersome to the patient and not better accounted for by another diagnosis, such as cancer, or other major medical or psychiatric disorder. (10,14)

Despite its frequency, GSM and the accompanying sexual dysfunction often go unrecognized, undiagnosed, and therefore untreated. This may stem from embarrassment (on the part of the patient as well as the healthcare provider [HCP]), a misperception that the symptoms are a natural consequence of aging, and/or the erroneous belief that there is no specific therapy for the condition. (15)

Data from the CLarifying Vaginal Atrophy's Impact On SEx and Relationships (CLOSER) study revealed that 28% of women did not tell their partner when they first experienced vaginal discomfort because they either associated it with growing older (52%) or were embarrassed (21 %). (16) Dr. Sheryl A. Kingsberg (page S2) highlights the lack of communication between patient and HCP as well as the apparent disconnect between GSM symptoms and hormonal changes of menopause.

PATHOPHYSIOLOGY OF THE AGING GENITOURINARY TRACT

Estrogen is a prerequisite for the normal physiology and ecosystem present in the vagina. (1,5) The lower or distal urogenital tract is derived from the embryonic urogenital sinus and is endoderm in its origin. In contrast, the upper portions of the vagina and bladder are mesodermal in origin. The vaginal vestibule is also a homologue of the urogenital sinus, whereas the labia majora is of ectodermal origin. (5) The vagina is composed of 3 layers: a superficial stratified squamous epithelium, a middle muscular layer, and an outer fibrous layer. Estrogens, progesterone, and androgens all influence maturation of the 3 types of vaginal epithelial cells: parabasal, intermediate, and superficial (FIGURE 1). The percentage of each "type" of cell is summarized in the Vaginal Maturation Index (VMI). In the presence of adequate estrogenic stimulation, there are approximately 15% or more superficial cells and less than 5% parabasal cells. Conversely, in estrogen-deficient states, there are typically less than 5% superficial cells, and there are more than 30% parabasal cells. The VMI simply represents the relative percentage of superficial, intermediate, and parabasal epithelial cells on a vaginal smear taken from the lateral vaginal wall. As will be discussed, the VMI, as well as vaginal pH, is considered a good proxy for adequate levels of circulating estradiol.

In the presence of adequate endogenous estrogen (principally estradiol), the vaginal wall is a thickly stratified squamous epithelium with a rugated surface that is rather elastic. The rich vasculature of the underlying dermis contributes to the epithelium's moisture and lubrication. The menopausal transition is characterized by diminishing levels of endogenous estrogen; an estradiol level <30 pg/mL can impact the entire lower urogenital tract rather rapidly.

Reduced estrogen levels result in distinct atrophic changes in the vulvovaginal tissues: thinning of vaginal epithelium, vaginal dryness, pruritus, loss of rugae, and loss of considerable vaginal elasticity, as well as thinning of the vaginal wall and, ultimately, shortening of the vaginal vault. (17) The vaginal epithelium becomes friable and is susceptible to injury, resulting in petechiae and occasional bleeding with minimal trauma. Once serum estradiol levels are <20 pg/mL, patients often begin to experience vulvovaginal symptoms such as dryness, irritation and dyspareunia. (6,18) Administration of exogenous hormone can stimulate estrogen receptors and usually alleviates symptoms.

Estrogen receptors have been found throughout the body. The highest concentration of these receptors in the female body is found in the homologues of the urogenital sinus shown in yellow in FIGURE 2. (1,15) Consequently, hormonal insufficiency is also associated with urinary dysfunction: thinning of urethral mucosa, atrophy of the bladder trigone, loss of muscle tone and connective tissue in the urogenital diaphragm, decreased intraurethral pressure, disordered collagen metabolism, and decreased activity of the a-adrenergic system innervating the bladder neck and urethral sphincter. (6) Symptomatic manifestations include increased urinary frequency, nocturia, urge incontinence, dysuria, and recurrent urinary tract infection (UTI), thereby authenticating a urogenital syndrome--a constellation of signs and symptoms--rather than simply VVA.

As shown by the white arrow in figure 2, the atrophy associated with diminished estrogen production is most pronounced initially in the areas with the highest density of estrogen receptors: the vaginal introitus and distal urethra. In contrast, the upper two-thirds of the vagina is spared significant atrophy initially. The vestibule loses much of its concavity and, as the introitus contracts, it begins to lose its elasticity. (1) The involution at the level of the vestibule and hymenal carunculae leads to introital stenosis, which is often associated with dyspareunia. The contraction of the distal vagina at the area of the hymen and transverse perineal membrane can lead to subsequent "reflex" vaginismus, but the pain associated with introital stenosis is at the perineum and hymenal "ring" rather than higher in the vagina at the area of the insertion of the levator muscles.

Hormonal changes also affect the vaginal microbiome across the life cycle. During the reproductive years, lactobacilli metabolize the abundant vaginal glycogen, producing lactic acid and hydrogen peroxide. This leads to the normal acidic pH in the vagina (range, 3.5-4.5) and helps maintain the normal ecosystem of the lower urogenital tract.1 The acidic pH, along with a healthy stratified squamous epithelium, affords protection against various vaginal pathogens. (5) During the menopausal transition, pH levels usually begin to rise and become more alkaline. Continued declining levels of estrogen are associated with a diminution in vaginal lactobacilli, and vaginal pH rises >5.0 within 12 months of becoming truly hypoestrogenic (defined as serum estradiol <20 pg/ mL) (1,18,19) Higher pH levels can also be associated with the overgrowth of pathogens that predispose postmenopausal women to irritation and infection in both the vagina and the bladder. (6,20)

VULVOVAGINAL ATROPHY AS A CAUSE OF DYSPAREUNIA

The diagnosis of dyspareunia associated with postmenopausal VVA is based on patient-reported symptoms of pain with sex and physical findings of VVA. (6,21) Patients may report vaginal dryness, itching, and burning; pain with sex; bleeding with intercourse or wiping; and/or urinary complaints of frequency, urgency, dysuria, or frequent UTI. It is easy to understand why many women report reduced sexual activity owing to these symptoms.

A careful physical examination should assess the appearance of the epithelium, skin color and elasticity, rugae, moisture, labial fat content, and the morphology of the vaginal introitus. (1,22) In patients with VVA, the vulvo-vaginal epithelium may appear erythematous initially and then appear pale, dry, and inelastic. (These physiologic changes are illustrated in the section "Diagnostic Considerations.") Because atrophy typically occurs insidiously, sometimes over years, the contraction of the introitus and changes in the urethra often go unnoticed at the time of the patient's annual visit. (1)

DIAGNOSTIC TOOLS

Over the years, a few indices have been developed to aid in the diagnosis of VVA. Most include both quantitative and qualitative assessments of variables associated with the pathophysiologic changes in the genitourinary tract after menopause. The Vaginal Health Index was developed to evaluate vaginal elasticity, fluid secretion, epithelial integrity, pH, and vaginal moisture (TABLE 1). (22) Another index, the VMI (discussed on page S10), indirectly assesses the level of estrogen based on the number of mature and parabasal epithelial cells on a vaginal smear. (23) Other research--for example, that of Minkin and colleagues (21)--focused on general, external, and internal physical signs of VVA. (21,22)

In a recent study of 1500 healthy, asymptomatic postmenopausal women who were seen for their annual well-woman visit, the effect of exogenous estrogen therapy in the prevention of atrophy was evaluated by a single investigator. (18) Vaginal pH and the degree of atrophy (mild, moderate, or severe) were recorded in women treated with various forms of estrogen (oral, transdermal, and injectable) versus untreated patients. (18) Eighty-six percent of the 992 patients (862 of 992) receiving estrogen therapy had no physical signs of atrophy, whereas 70% of the women not receiving estrogen therapy (353/508) had demonstrable, visible changes of urogenital atrophy (TABLE 2). Notably, among women in the "no-therapy" arm in whom the vaginal pH was >5, 85% exhibited at least "mild" atrophy. Fifteen percent of the untreated women presented with a nor mal pH and did not show signs of atrophy. Contraction and loss of elasticity at the introitus and "typical" urethral changes were consistent and prominent features of atrophy, whereas changes inside the vagina (erythema/ petechiae, loss of elasticity, vaginal shrinkage, secretions, discharge, etc.) were more variable and usually only seen among women with "moderate"-to-"severe" atrophy.

Findings from this study led to the development of the Vaginal Health Score (VHS) (TABLE 3), which is based on objective, quantifiable variables (vaginal pH and changes in the epithelium at the introitus, the urethra, and morphology of the fourchette/vestibule) rather than on variable subjective findings (moisture, secretions, and tissue friability) found in the vagina per se. In a more recent study, 20 postmenopausal patients (52-62 years of age) were evaluated for visual signs of atrophy, had vaginal pH measured, and had serum estradiol levels assayed by mass spectrometry [Freedman MA, unpublished data (2018)]. All 10 patients with a serum estradiol <10 pg/mL had a pH >5.5 and severe atrophy, whereas 5 patients in whom serum estradiol values were >10 pg/mL but <20 pg/mL had moderate-to-severe atrophy. None of the 5 whose serum estradiol was >20 pg/mL had significant atrophy on exam, but they were clearly postmenopausal. pH was also very predictive of the degree of atrophy in the previous study of the 1500 patients done by the author [Freedman MA, unpublished data (2018)], but estradiol values, when available, were obtained by radioimmunoassay, not mass spectrometry. (18) The correlation between serum estradiol, pH, and degree of atrophy has been quite consistent when all 3 parameters have been available.

DIAGNOSTIC CONSIDERATIONS

It is sometimes challenging to make an accurate diagnosis of GSM in the perimenopause and early menopausal years, particularly among women with mild symptoms. Because most women affected do not report symptoms spontaneously, including those experiencing dyspareunia, HCPs need to initiate the conversation if they observe atrophic change. Establishing the relationship of the onset of symptoms to menopause is often helpful in discussing therapy. Patients need to be made aware of the many safe and effective therapies that are available today. It also behooves clinicians to determine the impact that the symptoms have on the patient's sexual functioning and quality of life. (5,14) It should also be noted that the severity of symptoms does not always correlate with the degree of physical findings.

The most constant feature in the VHS is the correlation between vaginal pH and presence of atrophy. When the pH is >5.5, there is almost always evidence of significant atrophy; therefore, it has greater "weight" than other parameters. The 3 parameters measured in the VHS include the epithelium at the introitus, the urethra, and the morphology of the four-chette/vestibule. The epithelium at the hymenal carunculae is particularly noteworthy (figure 3), as is its color and elasticity. The urethral meatus becomes patulous and is relatively exteriorized (secondary to contraction of the surrounding tissues) and thus causes a "tunneling" or "tubular" appearance (FIGURE 4). The stratified squamous epithelium at the meatus is atrophied and exposes the transitional (columnar) epithelium of the urethra. The concavity of the fourchette/vestibule is diminished, the labia undergo involution, and the introitus contracts and becomes circular rather than oval (FIGURE 5).

Cases Illustrating the Effects of Hypoestrogenemia and Estrogen Therapy on Vulvovaginal Atrophy

Case 1 and Case 2

Both women were 64 years of age, G2P2002 (figure 6). The woman on the left (A) has been on hormone therapy for years; the woman on the right (B) stopped therapy 4 years previously. The woman on the right (B) has loss of the concavity of the vestibule, and the introitus has become circular in its contraction. The epithelium (6) shows loss of elasticity at the fourchette, whereas the epithelium (A) at the hymenal carunculae is normal and maintains its elasticity.

Case 3

This nulliparous woman was "normal"; her pH was 4.5 in (A). In (B), she demonstrates severe atrophy; pH was 5.5. The changes in the epithelium, urethra, and fourchette are "severe" after 5 years (FIGURE 3).

Case 4(a)

This woman stopped hormone therapy approximately 6 months before this visit (A) (FIGURE 7). She reinstituted topical estrogen therapy and returned in 3 months (B). In (A), the change in the atrophic epithelium is particularly apparent in the hymenal carunculae, color, and elasticity; the urethra is obvious because of the everted meatus, revealing transitional epithelium (rather that squamous epithelium), "tunneling," and exteriorization; and morphology is represented by contraction and loss of considerable concavity, labial resorption and circular dimension.

Case 4(B)

This is the same woman in Case 4(a) (FIGURE 8). She stopped, then restarted, topical hormone therapy several times over the next few years. The changes in the epithelium, urethra, and morphology were "moderate" in February 2008 and are "severe" in July 2009. This demonstrates the rapidity of atrophy as well as its responsiveness to therapy in truly hypoestrogenemic women, FIGURE 9 shows the changes once again when she discontinued her topical therapy again in 2010.

An accurate diagnosis requires elimination of other possible vulvovaginal conditions with similar symptoms. (5) The following conditions should be considered in a differential diagnosis of dyspareunia associated with WA: candidiasis, bacterial vaginosis, desquamative inflammatory vaginitis, contact dermatitis (irritant or allergic), lichen sclerosis, lichen planus, lichen simplex chronicus, and vulvar neoplasia, as well as other benign and malignant tumors, psychological causes, trauma/foreign body, and vulvodynia. (11,24)

Symptomatic WA often ensues once the serum estradiol is <20 pg/mL, and is often seen after bilateral ovariectomy, pelvic radiation therapy, chemotherapy, gonadotropin-releasing hormone therapy and premature menopause. Because of the abrupt drop in estrogen and androgen levels after bilateral salpingo-oophorectomy, patients may experience significantly greater severity of psychological, vasomotor, and somatic menopausal symptoms, including significantly more sexual dysfunction, compared to women undergoing natural menopause. (5,25)

In the study of 1500 patients referenced above [Freedman MA, unpublished data (2018)], a number of factors were found that can mitigate the degree of postmenopausal atrophy women experience. (18) In addition to the concentration of estrogen in the urogenital tissues, there are many factors that impact the degree of atrophy women experience. Some women with diabetes or cardiovascular disease, or who smoke, develop "vasculogenic insufficiency" in the pelvis and may develop GSM despite normal circulating levels of estradiol. A very significant factor in mitigating against atrophy is sexual activity, especially penetrative sex. (26) Obesity (peripheral conversion of androgen to estrogen in adipose tissue) may mollify risk and, similar to osteoporosis, genital atrophy is typically less severe and less prevalent in African-American women as well as women with intact ovaries. Vaginal births also afford some protection, in that the diameter of the introitus is less compromised as compared to nulliparous women.

CONCLUSION

Symptoms and consequences of vulvovaginal atrophy associated with menopause, including dyspareunia, are common and frequently necessitate treatment. (27) By observing the changes in the epithelium, urethra, and the morphology of the fourchette/vestibule, urogenital atrophy is easily identifiable. Distinct physical changes combined with vaginal pH measurement provide identification and quantification of VVA. Appropriate treatment requires accurate diagnosis, which, in turn, necessitates open and objective dialogue with all perimenopausal and postmenopausal patients, irrespective of symptoms.

Murray A. Freedman, MS, MD

Clinical Professor of Obstetrics and Gynecology

Medical College of Georgia

Augusta, GA

Disclosure:

Consulting Fees: AMAG Pharmaceuticals; Commercial Interest Speakers Bureau: Valeant Pharmaceuticals; Contracted Research: Procter and Gamble

REFERENCES

(1.) Freedman M. Vaginal pH, estrogen and genital atrophy. Menopause Manage. 2008; 17(4):9-13.

(2.) Freedman MA. Partnership issues and sexuality. Clin Obstet Gynecol. 2009;52(4):656-665.

(3.) Kingsberg SA, Wysocki S, Magnus L, Krychman ML. Vulvar and vaginal atrophy in postmenopausal women: findings from the REVIVE (REal Women's Views of Treatment Options for Menopausal Vaginal ChangEs) Survey. J Sex Med. 2013;10(7):1790-1799.

(4.) Santoro N, Komi J. Prevalence and impact of vaginal symptoms among postmenopausal women. J Sex Med. 2009;6(8):2133-2142.

(5.) The North American Menopause Society. Management of symptomatic vulvovaginal atrophy: 2013 position statement of The North American Menopause Society. Menopause. 2013;20(9):888-902.

(6.) Minkin MJ. Postmenopausal vulvovaginal atrophy: communication and care. The Clinical Advisor. 2013;16(10):59-65.

(7.) Freedman MA. Quality of life and menopause: the role of estrogen. J Womens Health (Larchmt). 2002;11 (8):703-718.

(8.) Freedman M. Perceptions of dyspareunia in postmenopausal women with vulvar and vaginal atrophy: findings from the REVIVE survey. Womens Health (Lond). 2014;10(4):445-454.

(9.) DiBonaventuraM, Luo X, Moffatt M,et al. The association between vulvovaginal atrophy symptoms and quality of life among postmenopausal women in the United States and Western Europe. J Womens Health (Larchmt). 2015;24(9):713-722.

(10.) Portman DJ, Gass ML; Vulvovaginal Atrophy Terminology Consensus Conference Panel. Genitourinary syndrome of menopause: new terminology for vulvovaginal atrophy from the International Society for the Study of Women's Sexual Health and the North American Menopause Society. Menopause. 2014;21 (10):1063-1068.

(11.) American College of Obstetricians and Gynecologists Committee on Practice Bulletins-Gynecology. ACOG Practice Bulletin Number 119: Female sexual dysfunction. Obstet Gynecol. 2011;117(4):996-1007.

(12.) Simon JA, Kokot-Kierepa M, Goldstein J, Nappi RE. Vaginal health in the United States: results from the Vaginal Health: Insights, Views & Attitudes survey. Menopause. 2013;20(10):1043-1048.

(13.) Freedman MA, Nolan TE. Genital atrophy: an inevitable consequence of estrogen deficiency. The Female Patient. 1996;21:62-66.

(14.) Goldstein I. Recognizing and treating urogenital atrophy in postmenopausal women. J Womens Health (Larchmt). 2010;19(3):425432.

(15.) Gandhi J, Chen A, Dagur G, et al. Genitourinary syndrome of menopause: an overview of clinical manifestations, pathophysiology, etiology, evaluation, and management. Am J Obstet Gynecol. 2016;215(6):704-711.

(16.) Nappi RE, Kingsberg S, Maamari R, Simon J. The CLOSER (Clarifying Vaginal Atrophy's Impact On Sex and Relationships) survey: implications of vaginal discomfort in postmenopausal women and in male partners. J Sex Med. 2013;10(9):2232-2241.

(17.) Lobo RA. Treatment of the Postmenopausal Woman: Basic and Clinical Aspects. New York, NY: Raven Press; 1994.

(18.) Freedman MA. Genitourinary syndrome of menopause: physical characteristics and prevalence. Poster (#P-21 presented at NAMS Annual Meeting, Orlando FL: October 2016. Available at http:// www.menopause.org/docs/default-source/2016-doc/scientificposter-abstracts.pdf. Accessed February 14,2018.

(19.) Panda S, Das A, Singh AS, Pala S. Vaginal pH: a marker for menopause. J Midlife Health. 2014;5(1):34-37.

(20.) Brotman RM, Shardell MD, Gajer P, et al. Association between the vaginal microbiota, menopause status, and signs of vulvovaginal atrophy. Menopause. 2014;21 (5):450-458.

(21.) Minkin MJ, Guess MK. Diagnosis and treatment of the non-sex-related symptoms of vulvovaginal atrophy. The Female Patient. 2012;37:33-41.

(22.) Bachmann G, Stern L, Ramos J. Female sexual function. In: Gynecology and Obstetrics CD-ROM. Philadelphia, PA: Lippincott Williams & Wilkins; 2008: Chapter 99. Available at www.glowm.com/ resources/glowm/cd/pages/v6/v6c099.html. Accessed February 14,2018.

(23.) Nilsson K, Risberg B, Heimer G. The vaginal epithelium in the postmenopause--cytology, histology and pH as methods of assessment. Maturitas. 1995;21 (1):51 -56.

(24.) MacBride MB, Rhodes DJ, Shuster LT. Vulvovaginal atrophy. Mayo ClinProc. 2010;85(1):87-94.

(25.) Benshushan A, Rojansky N, Chaviv M, et al. Climacteric symptoms in women undergoing risk-reducing bilateral salpingo-oophorectomy. Climacteric. 2009;12(5):404-409.

(26.) Leiblum S, Bachmann G, Kemmann E, et al. Vaginal atrophy in the postmenopausal woman. The importance of sexual activity and hormones. JAMA. 1983;249(16):2195-2198.

(27.) Sturdee DW, Panay N; International Menopause Society Writing Group. Recommendations for the management of postmenopausal vaginal atrophy. Climacteric. 2010;13(6):509-522.

Caption: FIGURE 1 Vaginal Maturation Index (1)

Caption: FIGURE 2 Estrogen-receptor concentration in select adult genital tissues (1)

Caption: FIGURE 3 Morphological and color changes

Caption: FIGURE 4 Morphology, urethral changes, and epithelial changes

Caption: FIGURE 5 Progression of atrophy (1)

Caption: FIGURE 6 Case 1 and Case 2

Caption: FIGURE 7 Case 4a

Caption: FIGURE 8 Case 4(b)

Caption: FIGURE 9 Case 4b (continued)
TABLE 1 Vaginal Health Index (22)

               1                 2                  3

Elasticity     None Poor                            Fair

Fluid volume   None              Scant amount,      Superficial
(pooling of                      vault not          amount, vault
secretions)                      entirely covered   entirely covered

pH             >6.1              5.6-6.0            5.1-5.5

Epithelial     Petechiae noted   Bleeds with        Bleeds with
integrity      before contact    light contact      scraping

Moisture       None, surface     None, surface      Minimal
(coating)      inflamed          not inflamed

               4                 5

Elasticity     Good              Excellent

Fluid volume   Moderate amount   Normal amount
(pooling of    of dryness        (fully saturates
secretions)    (small areas      on cotton-tip
               of dryness on     applicator)
               cotton-tip
               applicator)

pH             4.7-5.0           <4.6

Epithelial     Not friable,      Normal
integrity      thin epithelium

Moisture       Moderate          Normal
(coating)

TABLE 2 Vaginal pH and atrophy (18)

Therapy                       Atrophy              No atrophy

Estrogen therapy (n=992)      14.1%                85.9% (862 of 992)

No estrogen therapy (n=508)   69.5% (353 of 508)   30.1%

No estrogen                   85.1% (434 of 508)   --
therapy + pH >5 (n=434)

TABLE 3 Vaginal Health Score *

Atrophic change            Minimal   Moderate   Severe

PH                           <5       5-5.5      >5.5
                             -/+        2         4

Introital morphology                    1         2
  Fourchette ([dagger])       -         +         +
  Labia                       -         +         +
  Involution                  -         +         +

Urethra                                 1         2

  Meatus                      -         +         ++
  Tunneling/tubular           -         +         ++
  Externalized                -         +         ++

Epithelium                              1         2

  Rugation                    -         +         ++
  Color/moisture              -         +         ++
  Elasticity                  -         +         ++

* Freedman, unpublished data (2012).

([dagger]) Contour/contraction.

The introital morphology, urethra, and epithelium
are each given a score of 1 or 2, depending on whether
it reveals "moderate" or "severe"change, respectively.
In order for a category to receive a 1 or 2 score, however,
2 of the 3 changes under that category must be affected.
Because of its importance and objectivity, pH is weighted
more heavily. The numerical scoring system allows for
quantitative assessment of the progression (or regression
with therapy) of urogenital atrophy. With "severe" atrophy,
scores are usually [greater than or equal to] 8, whereas
"moderate"atrophy scores are usually [less than or equal to] 6.
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Date:May 1, 2018
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