Genitourinary syndrome of menopause: Common problem, effective treatments

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After menopause, about half of all women experience genital, sexual, and urinary symptoms associated with decreases in estrogen, termed genitourinary syndrome of menopause. First-line therapies are nonhormonal vaginal lubricants and moisturizers. For persistent symptoms, prescription estrogen in cream and ring formulations is effective.


  • Practitioners can use the patient’s most bothersome symptom and her vaginal pH level to assess clinical responses to therapy.
  • The diagnosis is based on clinical signs and symptoms from the medical history and physical examination.
  • If the symptoms are not bothersome to the patient, the syndrome does not require treatment.



For many women, the postmenopausal loss of estrogen is associated with uncomfortable genitourinary symptoms, collectively referred to as the genitourinary syndrome of menopause (GSM). But despite the prevalence of GSM and the availability of treatments, most women do not seek relief.

This article reviews the syndrome and offers advice on how to talk about it with patients and what treatment options to consider.


The term GSM and its definition were approved by the North American Menopause Society and the International Society for the Study of Women’s Sexual Health in 2014.1 It replaces older terms such as vulvovaginal atrophy, urogenital atrophy, and atrophic vaginitis.

GSM refers collectively to the symptoms associated with estrogen loss after menopause that adversely affect the vulvovaginal area and lower urinary tract. The most common symptoms are vulvovaginal dryness, burning, or irritation; sexual pain from inadequate lubrication; and urinary urgency, dysuria, or recurrent urinary tract infection.1,2

The definition notes that symptoms are self-reported as bothersome and are not the result of another disorder. Symptoms may be chronic and progressive, are not likely to resolve without treatment (pharmacologic or nonpharmacologic), and can have a significant negative impact on a woman’s quality of life and sexual health.1,2


From 40% to 60% of postmenopausal women experience GSM, but few seek treatment.3 Nevertheless, most postmenopausal women remain sexually active. In a 2008 survey of 94,000 postmenopausal women ages 50 to 79, 52% reported that they had been sexually active with a partner in the past year.4 However, 45% of postmenopausal women experienced unpleasant vaginal symptoms, according to a 2012 international survey of 3,520 postmenopausal women ages 55 to 65.5 In this survey, most respondents (75%) felt that vaginal symptoms had a negative impact on their life, but only 4% connected their symptoms to the vulvovaginal atrophy that resulted from loss of estrogen after menopause. Moreover, almost half were unaware of management options.5

These findings were supported by a 2013 survey of more than 3,000 US women who reported unpleasant vulvar and vaginal symptoms.6 From 60% to 85% noted negative sexual consequences from vulvovaginal symptoms, 47% felt their relationship suffered, and 27% felt it had a negative impact on their general enjoyment of life. In this study, 24% attributed their symptoms to menopause and 12% to hormonal changes. Although 56% had discussed GSM symptoms with a healthcare provider, only 40% were using GSM-specific topical treatments, mostly over-the-counter preparations.

Male partners of symptomatic women also note adverse emotional and physical effects.7 In an online survey of 4,100 men and 4,100 women ages 55 to 65, 52% to 78% of men and 58% to 64% of women expressed the negative effects of vulvovaginal symptoms on intimacy, libido, and sexual pain.

GSM is a progressive disorder. Women may note symptoms many years before menopause or have no symptoms until several years after menopause. One study found the prevalence of GSM to be 4% during perimenopause, rising after menopause to 25% after 1 year and to 47% after 3 years.8

Although distressing symptoms occur mostly after menopause, they may be seen in women of any age who experience a hypo­estrogenic state, even if it is transient. Causes of this include premature ovarian failure, hypothalamic amenorrhea, and hyperprolactinemia. In addition, some treatments such as gonadotropin-releasing hormone agonists and aromatase inhibitors may cause vulvovaginal and lower urinary tract symptoms. Chemotherapy, radiation, and surgical removal of ovaries may also precipitate symptoms. The abrupt onset of menopause that may occur with these treatments is often associated with significantly greater sexual dysfunction and negative impact on quality of life. Cigarette smoking also leads to lower estrogen levels, which may contribute to GSM.


The genitourinary system develops from common embryologic tissue, the basis for the functional and clinical connection. Estrogen maintains the epithelium of the vagina, vulva, urethra, and bladder trigone via estrogen receptors present throughout these tissues.9

Premenopausal changes

Histologically, the estrogen-exposed vagina of a premenopausal woman is lined by glycogen-rich, stratified squamous epithelium, with underlying supportive fibromuscular layers. The epithelium is composed of superficial, intermediate, and parabasal cellular layers. In the presence of estrogen, the superficial and intermediate cellular levels predominate, with few parabasal cells.

Glycogen acts as a substrate for lactobacilli, producing organic acids, primarily lactate, that help maintain an acidic pH of 2.8 to 4.0. The low pH helps protect against pathologic shifts in the microbiome. Estrogen also maintains the collagen content of the epithelium, maintains acid mucopolysaccharides and hyaluronic acid, and optimizes vaginal blood flow. These effects result in optimal epithelial thickness and elasticity, moisture, vaginal secretions, and lubrication.10

Postmenopausal changes

Low levels of estrogen after menopause result in adverse anatomic, physiologic, and clinical changes in vaginal tissue. Effects of hypoestrogenism include the loss of collagen and adipose, leading to decreased elasticity and vaginal mucosal thinning. Vascular flow is decreased. The epithelial cytology transitions to a predominance of parabasal cells and a decrease in superficial and intermediate cells. Eccrine and apocrine glands become attenuated. These changes result in decreased vaginal secretions, diminished or delayed lubrication with sexual stimulation, friability of the vaginal vault, and vaginal dryness.11

Additionally, without estrogen, glycogen content is diminished, leading to decreased lactic acid production and a rise in vaginal pH to greater than 5. As the pH rises, Lactobacillus colonization decreases, leading to a further decrease in glycogen metabolism and to propagation of an elevated vaginal pH. The loss of vaginal acidity makes the vagina more susceptible to pathologic bacteria, including those found in the bowel and skin, sexually transmitted infections, and bacterial vaginosis.12

Other affected tissues. Anatomic effects of estrogen loss are not limited to the vagina. The epithelium, connective tissue, and smooth muscle of the vulva, vagina, urethra, and bladder trigone are also affected. The labia minora become thinner and regress, the introitus retracts, and narrowing and stricture of the vaginal canal and introitus may result. In some women, the urethral meatus becomes prominent relative to the introitus and more vulnerable to physical irritation, infection, and trauma.

Clinically, estrogen-related changes are usually responsible for vaginal dryness, irritation, burning, and superficial or deep dyspareunia. Urinary frequency, urgency, and incontinence also may develop.


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