Genitourinary Syndrome of Menopause

Etiology

Estrogen plays a crucial role in maintaining the normal anatomy and physiology of the urogenital system. Estrogen receptors are present in the vagina, vulva, urethra, and bladder trigone, where they respond to estrogen stimulation by maintaining normal blood flow, tissue thickness, rugosity, elasticity, and moisture of epithelial surfaces. During the reproductive years, the vagina is rich in glycogen, which is converted by the normal flora, lactobacilli, into lactic acid. This process creates an acidic environment in the vagina, with a pH ranging from 3.5 to 5.0, allowing lactobacilli to continue to thrive and protect the vaginal and urinary tracts from infections. After menopause, the quantity of lactobacilli decreases, leading to an increase in the vaginal pH and the development of GSM.[2] 

Additionally, sexual activity promotes epithelial turnover and enhances vaginal lubrication. A decline in estrogen levels during menopause causes urogenital atrophy. As estrogen production decreases, secretions diminish, and the genitourinary tissues become atrophic, leading to the symptoms associated with GSM. Other causes of GSM include lactation, hypothalamic amenorrhea, and antiestrogen medications used in the treatment of uterine fibroids, endometriosis, and breast cancer.[4][5]

Epidemiology

GSM is a prevalent concern among the postmenopausal population. Study results indicate that while roughly 15% of women experience symptoms of vaginal atrophy before menopause, approximately 40% to 54% of postmenopausal individuals report bothersome symptoms. Menopause causes a dramatic 95% reduction in estrogen production, resulting in 75% of women experiencing vaginal dryness, 40% reporting pain during intercourse, and 30% to 40% experiencing urinary urgency and frequency. Despite these symptoms, more than 50% of affected patients are not using any treatments to alleviate their discomfort.[6] The symptoms of GSM are progressive when left untreated.[7] The end stages consist of labial adhesions resulting in complete vulvovaginal obliteration, which can lead to severe urological complications that require surgical repair.[8]

Approximately 70% of patients with signs and symptoms of GSM do not discuss their concerns with healthcare professionals.[9] Many patients feel reluctant or embarrassed to discuss or seek treatment, believing these symptoms are a normal part of aging. Cultural, religious, and societal beliefs also influence their willingness to discuss these quality-of-life issues. Additionally, many patients are unaware of available treatment options. As a result, less than 25% of affected women receive appropriate care. Clinicians often do not screen for symptoms of GSM. This omission leads to underdiagnosis and undertreatment of this condition.[2]

GSM most commonly arises from conditions that lead to a diminished estrogen state, eg, natural menopause, where the ovaries cease estradiol production, resulting in a 95% decline in estradiol levels from premenopausal levels. However, GSM can also occur in individuals with other conditions associated with low estrogen, including those who have undergone surgical menopause following bilateral oophorectomy, primary ovarian insufficiency, chemotherapy, hypothalamic amenorrhea, or are breastfeeding. Additional risk factors include ovarian failure due to radiation or arterial embolization, hypothalamic-pituitary disorders, and the use of antiestrogen medications, eg, leuprolide or gonadotropin-releasing hormone antagonists, often prescribed for endometriosis. Breast cancer survivors, particularly, are at increased risk due to treatments (eg, chemotherapy or aromatase inhibitors), which can contribute to the early onset of GSM symptoms.[4][10][11]

Pathophysiology

Estrogen serves a fundamental role in preserving the normal anatomy, physiology, and function of the lower genitourinary tract. Adequate estrogenic stimulation supports healthy blood flow to the vaginal tissues, maintains a balanced vaginal microbiome, and preserves the thickness, elasticity, hydration, and structural integrity of the vaginal epithelium by sustaining collagen production. Estrogen also promotes the continuous maturation and exfoliation of vaginal epithelial cells, increasing glycogen availability within the superficial epithelial layers. Normal vaginal flora, particularly lactobacilli, metabolize glycogen into lactic acid, maintaining the vagina's characteristic acidic environment with a pH generally ranging from 3.5 to 5.0. This acidic milieu promotes continued lactobacilli growth while providing an important defense against pathogenic microorganisms, thereby protecting both the vaginal and lower urinary tracts from infection.[11][12]

Declining estrogen concentrations disrupt each component of this tightly regulated physiologic process. Reduced epithelial maturation leads to diminished glycogen stores, causing a progressive decline in lactobacilli populations and a corresponding reduction in lactic acid production. As vaginal acidity decreases, the vaginal pH rises above 5, creating a less favorable environment for protective organisms and allowing colonization by pathogenic bacteria. Simultaneously, the vaginal epithelium becomes thinner, less elastic, and increasingly atrophic, with reduced collagen content, diminished vascularity, decreased lubrication, and reduced vaginal secretions. Collectively, these structural and biochemical alterations compromise the integrity of the vaginal mucosa, increase tissue fragility, and substantially elevate the risk of recurrent vaginal infections, urinary tract infections, irritation, and other genitourinary complications associated with GSM.[11][12]

For many years, estrogen received recognition as the principal hormone responsible for maintaining vaginal health and function. Emerging evidence, however, has expanded understanding of urogenital physiology by demonstrating an important role for androgens in preserving tissue integrity and function. Vaginal tissues express androgen receptors that contribute to maintaining vaginal contractility, supporting tissue repair, and reducing local inflammation following receptor activation. Following menopause, circulating estrogen concentrations decline substantially, whereas dehydroepiandrosterone (DHEA), a weak androgen produced primarily by the adrenal glands, becomes the predominant endogenous sex steroid precursor. Within the vaginal tissues, local enzymes convert DHEA into both estrogens and androgens, allowing continued intracrine hormone production despite low circulating estrogen levels.[13][14]

Recognition of this intracrine hormonal pathway has broadened therapeutic strategies for GSM beyond estrogen replacement alone. Local vaginal DHEA therapy capitalizes on the ability of vaginal tissues to convert DHEA into active estrogens and androgens within the target tissue, providing symptom relief while minimizing systemic hormone exposure. Growing evidence supporting the physiologic contributions of both estrogen and androgen signaling has led to increased interest in local androgen-based therapies as an additional treatment option for appropriately selected patients with GSM.[13][14]

History and Physical

Clinical History

Diagnosis of genitourinary syndrome of menopause (GSM) remains primarily clinical and relies on a comprehensive patient history combined with a thorough physical examination rather than laboratory testing. Because no single laboratory study confirms the diagnosis, routine testing generally serves no role unless needed to exclude alternative conditions. A careful evaluation begins with identifying the patient's presenting symptoms, which commonly include genital dryness, burning, irritation, and discomfort. Many patients also report dyspareunia, reduced vaginal lubrication, pain during sexual intercourse, dysuria, urinary urgency, frequency, and recurrent urinary tract infections. These symptoms frequently overlap with those of vulvovaginal infections, urinary tract infections, sexually transmitted infections, and other genitourinary disorders, often leading to delayed diagnosis or inappropriate treatment if GSM is not considered. For this reason, obtaining a detailed history remains one of the most important components of the diagnostic evaluation.[2]

The clinical interview should extend beyond the chief complaint and include a detailed sexual history, as patients often hesitate to discuss vaginal discomfort, painful intercourse, or sexual dysfunction unless specifically asked. Questions regarding sexual activity, changes in sexual habits, and symptoms occurring during or after intercourse help distinguish GSM from infectious and inflammatory conditions while identifying factors contributing to symptom progression. As estrogen deficiency advances, thinning and fragility of the vaginal mucosa frequently make intercourse increasingly painful, causing many individuals to reduce or avoid sexual activity. Reduced sexual activity further decreases epithelial turnover and vaginal lubrication, perpetuating the cycle of progressive atrophy and worsening symptoms.[11][12][15]

A complete history should also include obstetric and gynecologic history, menstrual and menopausal history, prior pelvic surgeries, current and previous medications, use of antiestrogen therapies, history of breast or gynecologic malignancy, and exposure to local irritants, eg, scented hygiene products or topical agents. Clinicians should specifically inquire about hallmark symptoms of GSM because many patients mistakenly attribute these changes to normal aging and may not volunteer their concerns during routine visits. Early symptoms commonly begin with diminished vaginal lubrication during sexual activity and gradually progress to persistent vaginal dryness, dyspareunia, postcoital bleeding, dysuria, and discomfort during everyday activities. Declining estrogen levels also alter the vaginal microbiome by reducing lactobacilli and increasing vaginal pH, creating an environment that predisposes patients to recurrent urinary tract infections and other genitourinary symptoms. Unlike vasomotor symptoms, which often improve over time, GSM follows a progressive course without appropriate treatment, making early recognition and intervention essential to preserving urogenital health and quality of life.[2]

Physical Examination

Physical examination often reveals characteristic anatomical and physiologic changes involving the vulva, vagina, and lower urinary tract. External genital examination may demonstrate fusion of the labia majora or labia minora, introital stenosis, labial and clitoral atrophy, phimosis of the clitoral prepuce, and urethral abnormalities, including caruncles, polyps, eversion, or prolapse. Increased exposure and thinning of the urethral meatus also make the tissue more susceptible to mechanical irritation and urinary symptoms.[1]

Vaginal examination may reveal marked tissue fragility and friability, loss of normal rugae, petechiae, fissures, ulcerations, decreased elasticity, diminished lubrication and secretions, and a shortened, narrowed, poorly distensible vaginal canal. Progressive thinning and regression of the labia minora, retraction of the vaginal introitus, and involution of the hymenal carunculae frequently contribute to dyspareunia and impaired sexual function. Histologic changes associated with GSM include thinning of the vaginal epithelium, reduced collagen content, hyalinization of connective tissue, and decreased elastin production, all of which reduce tissue resilience and elasticity. Because of these structural changes, pelvic and speculum examinations may cause significant discomfort, pain, or bleeding.[2] 

Classic examination findings of vulvovaginal atrophy include pale, dry, smooth, and shiny vaginal epithelium with loss of normal moisture and elasticity. Inflammatory changes may also be present, including patchy erythema, petechiae, increased visibility of subepithelial blood vessels, mucosal friability, contact bleeding, and a thin, white, odorless vaginal discharge.[16] Recognition of these characteristic clinical findings, together with a comprehensive history and targeted physical examination, allows clinicians to establish the diagnosis of GSM while avoiding unnecessary laboratory testing and facilitating timely initiation of appropriate therapy.

Evaluation

Although GSM remains a clinical diagnosis established through patient history and physical examination, selected laboratory studies may assist in excluding alternative causes of genitourinary symptoms when the diagnosis remains uncertain. Urinalysis and urine culture may help evaluate suspected urinary tract infections, while sexually transmitted infection testing and vaginal pathogen testing may prove useful when infectious vaginitis or cervicitis remains part of the differential diagnosis. Such studies serve primarily to rule out competing diagnoses rather than confirm GSM and generally provide little value in establishing the diagnosis itself.[17]

Measurement of serum estradiol concentrations also offers limited diagnostic utility. Current laboratory assays lack sufficient sensitivity to accurately reflect the low circulating estrogen concentrations characteristic of menopause and do not reliably correlate with the presence or severity of GSM symptoms. Consequently, serum estrogen testing should not guide the diagnosis of GSM in routine clinical practice.[17]

Although unnecessary for diagnosis, certain objective findings frequently accompany GSM and reflect the underlying physiologic effects of estrogen deficiency. Vaginal pH commonly exceeds 5.0 in the absence of infection or abnormal vaginal discharge because declining estrogen concentrations reduce glycogen production within vaginal epithelial cells. Diminished glycogen availability decreases lactobacilli populations and lowers lactic acid production, resulting in a less acidic vaginal environment. Concurrent epithelial atrophy produces a progressive shift in cellular composition, characterized by declining numbers of mature superficial epithelial cells and increasing proportions of immature basal and parabasal cells.[2]

One measurable manifestation of these epithelial changes involves the vaginal maturation index (VMI), a cytologic assessment derived from microscopic evaluation of vaginal epithelial cells.[6] The VMI quantifies the relative proportions of epithelial cell maturation and reflects the degree of estrogenic stimulation within the vaginal mucosa. The following 3 major epithelial cell populations contribute to the index:

• Parabasal cells represent the least mature epithelial cells and become increasingly predominant during states of estrogen deficiency.
• Intermediate cells demonstrate moderate maturation and typically occupy an intermediate proportion of the vaginal epithelium.
• Superficial cells represent the most mature epithelial cells and predominate when estrogen exposure remains adequate.[18]

During early menopause, the VMI typically demonstrates approximately 30% intermediate cells, 5% superficial cells, and 65% parabasal cells. Progressive vulvovaginal atrophy produces an even greater predominance of parabasal cells, and advanced disease may eventually demonstrate almost exclusively parabasal cells on microscopic examination. One characteristic finding associated with GSM includes fewer than 5% superficial cells on the VMI, reflecting marked estrogen deprivation and impaired epithelial maturation.[6]

Despite the physiologic information provided by vaginal pH measurement and the VMI, routine use of either assessment remains unnecessary in everyday clinical practice. Neither test consistently correlates with symptom severity, and neither provides sufficient diagnostic value to replace a careful clinical history and physical examination. Some patients with severe symptoms may demonstrate only modest changes in vaginal pH or VMI, whereas others with marked laboratory abnormalities may report relatively mild symptoms. Consequently, laboratory measurements should complement rather than direct clinical decision-making.[2]

Recognizing the limited clinical value of these objective measurements, The Menopause Society clarified in 2020 that vaginal pH testing, the VMI, and other laboratory assessments do not constitute essential components of GSM diagnosis.[1] Instead, greater emphasis falls on symptom recognition, targeted history-taking, and comprehensive physical examination.

Although laboratory testing remains unnecessary for diagnosis, validated symptom assessment tools may improve recognition of GSM and facilitate longitudinal monitoring. The Day-to-Day Impact of Vaginal Aging (DIVA) questionnaire provides a brief yet comprehensive screening instrument that evaluates the effect of vulvovaginal symptoms on daily functioning, sexual health, emotional well-being, and quality of life. Incorporation of the DIVA questionnaire during annual wellness examinations or when postmenopausal patients present with vulvovaginal or lower urinary tract complaints may improve identification of GSM and promote earlier intervention.[19]

Another commonly used assessment instrument, the Vaginal Health Index (VHI), provides a standardized clinical evaluation of vaginal health by assessing vaginal secretions, pH, elasticity, hydration, and the condition of the vaginal epithelial mucosa during physical examination. VHI scores range from 5 to 25, with lower scores reflecting more severe vaginal atrophy and poorer overall vaginal health. Although neither the DIVA questionnaire nor the VHI independently establishes the diagnosis, both tools can support symptom assessment, monitor treatment response over time, and facilitate a more comprehensive evaluation of patients with GSM.[20]

Treatment / Management

GSM can be managed with various treatment modalities aimed at alleviating symptoms. These treatments are generally classified as nonhormonal or hormonal. Below is an overview of the available treatments, including vaginal moisturizers, lubricants, vaginal estrogens, DHEA, systemic hormone replacement therapy, and ospemifene, an oral selective estrogen receptor modulator with both estrogen agonist and antagonist properties.[2] Patients with breast cancer deserve special mention as treatment of GSM presents a challenge due to the need to balance effective symptom management with the avoidance of some estrogen-based therapies that could potentially exacerbate cancer risk.(B3)

Nonhormonal Treatments

Nonhormonal treatments, eg, vaginal and topical moisturizers and lubricants, are considered the first-line therapy for GSM. Lubricants provide short-term relief, particularly for vaginal dryness during intercourse, while moisturizers offer longer-lasting effects and can be used daily or several times per week. Patients are also encouraged to engage in regular, safe sexual activity, as this helps maintain the health and integrity of the vaginal epithelium and flora.

The use of moisturizers, lubricants, and regular sexual activity promotes vaginal health by supporting epithelial integrity and maintaining a balanced vaginal flora. The World Health Organization (WHO) recommends that personal moisturizers and lubricants have an osmolarity of less than 1200 mOsm/kg, as hyperosmolar products can be toxic to epithelial cells, potentially causing irritation and further compromising vaginal health.[2](B3)

Local Estrogen Therapy 

This therapeutic option comes in many forms. These forms include vaginal creams, intravaginal tablets or capsules for more accurate dosing of estrogen, and a vaginal ring that releases small amounts of estrogen daily. All preparations are similarly effective in alleviating vaginal atrophy symptoms. Low-dose local estrogen therapy has not been shown to increase total systemic estrogen levels. Thus, vaginal estrogen allows for an excellent safety profile demonstrating a minimal to no increased risk of endometrial hyperplasia in healthy people.[11][21]

Patients usually have an improvement in symptoms after 2 to 4 weeks of local estrogen treatment.[22] However, some individuals may take 1 to 3 months to experience reduced symptoms. When urinary symptoms are present, vaginal estrogen is recommended. Progestin use and routine endometrial surveillance are not necessary for women using local estrogen therapy. However, any vaginal bleeding after menopause does require an investigation.[2](B3)

As with all medication regimens, the risks and benefits should be discussed with patients before initiating any hormonal therapy. Local estrogen therapy has not been shown to increase circulating estrogen concentrations; it may be used in most patients to treat GSM. One contraindication for vaginal estrogen therapy is undiagnosed vaginal or uterine bleeding.[2](B3)

Vaginal Dehydroepiandrosterone

DHEA comes in a low-dose vaginal insert that can be used daily for the treatment of dyspareunia from GSM. The vaginal mucosa transforms DHEA into estradiol and androgens. Daily use showed few adverse effects and improvement of GSM symptoms in menopausal women.[2](B3)

Systemic Hormonal Therapy 

Systemic hormonal therapy becomes necessary for patients experiencing more widespread menopausal symptoms, eg, night sweats and hot flashes, in addition to vaginal atrophy. For patients with these systemic symptoms, hormone replacement therapy (HRT), including estrogen-progestin combinations or estrogen alone in patients who have had a hysterectomy, offers significant symptomatic improvement. Systemic HRT can promote the growth and revascularization of the vaginal epithelium, normalize vaginal pH, and increase lubrication. HRT can be administered systemically through oral or transdermal replacement. With an intact uterus, progesterone must be added to protect the endometrium. Study results indicate that systemic HRT alleviates symptoms of GSM in approximately 75% of cases, while local therapy is effective in 80% to 90% of cases. Although both therapies have comparable adverse events, local therapy is generally considered safer. In cases where moderate to severe vasomotor symptoms are also present, systemic hormonal therapy may be a particularly effective option.[2](B3)

Ospemifene

Ospemifene is a selective estrogen receptor modulator (SERM) and an oral product approved for the treatment of GSM. This treatment is beneficial for patients with a history of hormone-sensitive cancer. SERMs can have a positive effect on the vaginal epithelium while having minimal to no impact on estrogen-dependent organs. Vasomotor symptoms are the most common adverse effect. Using ospemifene reduced the frequency of recurrent urinary tract infections and improved symptoms and examination findings in GSM. Ospemifene is an estrogen agonist/antagonist, and its use at 60 mg daily has not been shown to increase endometrial cancer, venous thromboembolism, breast cancer, or breast cancer recurrence.[2] (B3)

Additional Treatment Modalities 

Many other modalities are available to manage GSM, offering new options for symptom relief and improved patient outcomes. Pelvic floor physical therapy may also be used in combination with local estrogen therapy.[2] If anatomical vulvovaginal changes occur, vaginal dilators may be of use. This option is reserved for women who cannot take estrogen therapy and have failed moisturizers and lubricants. Dilators have been shown to improve vaginal function.[23] (B3)

More recent treatment modalities for GSM include laser and radiofrequency therapy. Laser therapy induces collagen formation by causing microtrauma in the tissue and can promote revascularization, helping restore vaginal moisture and elasticity. However, the safety and efficacy are uncertain.[20][24][25][26][27] Studies are underway to evaluate energy-based devices, including lasers (eg, fractional carbon dioxide and erbium-YAG) and radio-frequency devices, but none are currently approved specifically for treating GSM.(A1)

Herbal products and hyaluronic acid products are ineffective for GSM treatment.[2] Longer and larger studies are needed, looking at vaginal testosterone, as it currently does not have sufficient data to recommend its use for GSM. Other proposed treatments for GSM include the active ingredient of the medicinal plant Ammi visnaga, or toothpick weed, a member of the carrot family, which causes vasodilation.[28] Bovine colostrum cream, prenylflavonoids, phytoestrogens, and aloe vera extract have all been considered alternative treatments, but more research is necessary before recommending any of these options.[20](B3)

Treating Symptoms in Breast Cancer Patients

Patients with a personal history of breast cancer present several challenges related to GSM management. In patients who have had breast cancer, vaginal estrogen therapy for GSM is contraindicated per the Federal Drug Administration. However, the American College of Obstetricians and Gynecologists (ACOG) has endorsed its use and recommends it when nonhormonal therapy does not yield satisfactory results. In a cohort study by McVicker, results indicate no evidence of an increase in mortality in breast cancer patients who used vaginal estrogen. These findings support vaginal estrogen therapy use for GSM in patients with breast cancer.[29] Low-dose vaginal estrogen, which has minimal systemic absorption, may be a reasonable option for treating GSM in patients with a history of breast cancer, without evidence of increased recurrence or mortality. However, long-term safety data remain limited, especially for patients using aromatase inhibitors.[7](A1)

Vaginal DHEA has a cautionary label for use in patients with breast cancer because estrogen is a metabolite of DHEA, although it is not considered contraindicated. As a selective estrogen receptor modulator (SERM) derived from a tamoxifen metabolite, ospemifene exerts weak antiestrogenic effects in breast tissue. Clinical trials have not demonstrated an increased risk of breast cancer or other breast-related safety issues in users. However, real-world evidence regarding its effectiveness and tolerability in breast cancer survivors remains limited.[30](B2)

The absence of head-to-head trials comparing vaginal estrogen formulations in breast cancer survivors underscores the need for research to better guide individualized treatment decisions. Recent FDA labeling updates, including the clearer distinctions between low-dose vaginal estrogen and systemic hormone therapy, further align regulatory guidance with existing evidence and represent progress toward more evidence-based labeling. In parallel, clinical guidance from organizations, eg, ACOG and The Menopause Society, remains more nuanced, reflecting individualized risk assessment and shared decision-making.[31]

Differential Diagnosis

The differential diagnosis of GSM is essential for distinguishing it from other conditions with overlapping symptoms. Accurate diagnosis involves a thorough patient history, physical examination, and appropriate diagnostic tests to differentiate GSM from other conditions. Associated signs and symptoms of GSM overlap with those of many other gynecologic, urologic, and systemic conditions, making it more difficult for a clinician to attribute symptoms solely to atrophy. Although these differential diagnoses must be ruled out, their presence does not exclude the additional diagnosis of GSM. Recurring symptoms or infections may be secondary to ongoing atrophy. Understanding these distinctions is crucial for implementing effective, targeted treatments and improving patient outcomes.

The differential diagnoses of GSM include the following:

• Allergic conditions
  • Contact dermatitis
  • Desquamative inflammatory vaginitis
• Inflammatory conditions
  • Lichen sclerosis
  • Erosive lichen planus
  • Cicatricial pemphigoid
• Infections
  • Vulvovaginal candidiasis
  • Bacterial vaginosis
  • Trichomoniasis 
  • Herpes simplex virus
  • Chlamydia
  • Gonorrhea
  • Urinary tract infection
• Trauma
• Foreign bodies
• Malignancy
• Vulvodynia
• Vestibulodynia
• Chronic pelvic pain
• Provoked pelvic floor hypertonia (previously called vaginismus)
• Other medical conditions
  • Diabetes
  • Lupus erythematosus
  • Crohn disease
• Psychological disorders [2][5]

Toxicity and Adverse Effect Management

In 2025, the FDA initiated a major revision of menopausal hormone therapy labeling, removing long-standing boxed warnings related to breast cancer, cardiovascular disease, and dementia from most estrogen-containing products. The updated guidance distinguishes low-dose vaginal estrogen as a locally acting therapy with minimal systemic absorption and a safety profile distinct from systemic hormone therapy, while retaining boxed warnings only for specific risks, eg, endometrial cancer in systemic estrogen-alone regimens.

Prognosis

Patients with GSM can achieve significant symptomatic relief with treatment if the condition is diagnosed and discussed. Patients who do not undergo treatment will, unfortunately, continue to experience ongoing and progressive symptoms, which can increase frustration and lead to poor sexual lifestyles, recurrent infections, and a decreased quality of life. Clinicians can alleviate many distressing genitourinary symptoms and enhance the sexual health and quality of life of postmenopausal patients by educating them about, diagnosing, and effectively managing GSM. The choice of therapy should be based on the severity of symptoms, the efficacy and safety of available treatments for the individual patient, and the patient's preferences.[2]

Nonprescription, nonhormonal therapies often provide adequate relief for many patients with mild symptoms. For those with moderate to severe GSM, effective treatment options as noted above include low-dose vaginal estrogens, vaginal DHEA, systemic estrogen therapy, and ospemifene. When using low-dose vaginal estrogen, DHEA, or ospemifene, the addition of progesterone is not necessary; however, long-term endometrial safety beyond 1 year has not been established in clinical trials for some of these treatment modalities.[2]

Complications

GSM can lead to several complications if left untreated or undertreated. These complications include chronic vaginal dryness, recurrent urinary tract infections, and painful sexual intercourse, which can significantly impact an individual's quality of life. Additionally, GSM may cause urinary incontinence, increased susceptibility to vaginal infections, and overall discomfort in daily activities.

The physical symptoms may also lead to emotional and psychological distress, including reduced self-esteem and intimacy issues. About half of the partners are aware of their significant other’s GSM symptoms. Vaginal discomfort is associated with decreased sexual desire in men, while women often choose to avoid sexual activity due to fear of experiencing pain.[32] Early recognition and appropriate treatment are crucial to prevent these complications and improve overall well-being.