Scratching the Surface: A Comprehensive Guide to Understanding and Managing Vulvovaginal Itching

Definition of Terms

The terms “vulvitis,” “vaginitis,” and “vulvovaginitis” are sometimes used interchangeably to describe inflammation in the lower genital tract [10]; similarly, the literature also often uses vulvar pruritus, vaginal pruritus, and vulvovaginal pruritus interchangeably. Therefore, it is important to clarify the meaning of these terms. The vulva is the general external genitalia, while the vagina refers to the internal canal [11], and “vulvovaginal pruritus” is a broader term encompassing both the vulvar and vaginal regions. Clearly distinguishing these terms is crucial to accurately identify the tissues involved in pruritic processes and narrow down potential causes.

Pruritus, or itching, is an unpleasant sensation temporarily relieved by scratching or rubbing the affected area [2]. Unlike pain, itching is characterized by a “need to scratch,” providing relief [11, 12]. This symptom is common in dermatological conditions and differs from irritation, which encompasses broader discomfort not necessarily alleviated by scratching [13]. Pain, involving burning or aching sensations, is distinct from itching and is not relieved through scratching [2, 8, 12]. “Vulvitis,” “vaginitis,” and “vulvovaginitis” are terms that describe inflammation of the ascribed tissues. These terms should not be used to describe pruritus that is not associated with inflammation.

Vulvovaginal pruritus can be defined as acute or chronic, distinguished by occurring for less than or more than 6 weeks, respectively [14]. Acute vulvovaginal pruritus may become chronic depending on the cause and access to effective treatment [15, 16].

Epidemiology

The exact prevalence of vulvovaginal pruritus is difficult to determine due to the broad range of conditions that can cause it [15, 17], but it is a common condition and affects most women at some point in their lives [11]. Vulvar pruritus may affect women of all ages [9, 10], and there is a notable correlation between age and the prevalence of many specific causal conditions. For instance, in one study vulvovaginitis was reported in 61.8% of gynecological issues in childhood and adolescence, with a high frequency of dermatitis in prepubertal populations [18–20]. Infectious causes such as vulvovaginal candidiasis (VVC) and trichomoniasis affect adolescent and adult women more frequently than children [8].

Age-related hormonal changes affect the vulvar anatomy, resulting in unique risk factors for vulvar pruritus for different age groups [9]. Vaginal discomfort and pruritus in children aged 2–7 years may stem from early physiological and floral changes [18]. Prepubertal girls are susceptible to conditions such as atopic and irritant dermatitis [9, 21] due to lack of estrogenization of the vagina. Additionally, proximity of the anus to the vagina and poor hygiene predisposes to the risk of inoculation with digestive bacteria and vaginal dysbiosis. Absence of labial fat pads and pubic hair as protective barriers are risk factors for dermatoses and pruritus-inducing infections in this age group [22]. In contrast, estrogen loss occurring in the postpartum or postmenopausal state or from medications results in thinning of the vaginal epithelium and reduced elasticity, increasing vulnerability to irritation and infection [23, 24].

Three primary vulvar dermatoses—lichen sclerosus, lichen planus, and lichen simplex chronicus—affect various age groups. At a vulvar specialty clinic in Oxford, UK, 20–25% of new patients presented with these conditions [25]. Lichen sclerosus can impact prepubertal and postmenopausal women [26, 27], lichen planus typically affects women aged 30–60 years [28], and lichen simplex chronicus is prevalent across all age groups [29].

Disease-specific risk factors include a family history of allergies, asthma, or eczema for lichen simplex chronicus [30]; pregnancy, coitus frequency, conditions and medications associated with hyperglycemia and glucosuria, antibiotic use, and immunosuppressive conditions for vulvovaginal candidiasis [31, 32]; sexual activity for trichomoniasis [32]; hereditary and environmental factors for atopic dermatitis; and ingestion of specific triggers for irritant contact dermatitis [33]. Other multifactorial risk factors for vulvovaginitis include obesity [16] and inflammatory bowel disease [34]. Understanding these risk factors is crucial for assessing the clinical likelihood of the various causes and management strategies of vulvar and vaginal pruritus.

Impact on Patient’s Quality of Life

Vulvovaginal itch can significantly impact emotional well-being and quality of life [35]. Patients often feel embarrassed discussing or seeking help for this issue [4, 35]. Frustration arises when over-the-counter remedies fail, and difficulty in diagnosing the cause or causes of itch can exacerbate feelings of helplessness and anxiety [4]. Concerns about severe health issues can heighten emotional stress [34]. Notably, a study by Choragudi et al. reported that pruritus in the genital region was associated with a significantly poorer quality of life compared with other body areas, highlighting the profound impact of genital itch on patients’ well-being [36]. This emotional strain may lead patients to avoid healthcare appointments, preferring over-the-counter products despite the ineffectiveness of this approach [2, 11]. Nonprescription antifungals are commonly used, often due to patients’ cognitive bias or reluctance to confront their issues directly [37]. Accumulated costs from ineffective treatments can add to financial stress [10]. Furthermore, a national inpatient sample (NIS) study found that genital pruritus is associated with longer hospital stays, higher costs, and increased odds of psychiatric hospitalization among inpatients, underscoring the severe impact on quality of life and healthcare burden [38].

Chronic itching disrupts daily life, affecting work, sleep, and social interactions [17]. It also impacts intimate relationships and sexual function. Patients report that itch is a significant concern affecting sexual relationships and mental health, contributing to embarrassment and reduced self-esteem [17, 39]. Discomfort during sexual activity is common, diminishing pleasure and satisfaction and sometimes leading to misconceptions of sexually transmitted infections (STIs) [4, 15]. The stigma associated with sexually transmitted infections can also increase reluctance to seek help [11]. Recognizing the emotional and psychological impact of vulvar itch is essential for healthcare providers, who should approach these cases with empathy and sensitivity [8].

Infectious Causes

Vulvovaginal itching of acute onset is frequently attributed to infection with fungal, bacterial, or parasitic species [15, 58]. VVC results from an overgrowth of Candida species, predominantly Candida albicans, due to disruptions in the normal vaginal flora [17]. The release of pro-inflammatory cytokines and chemokines stimulate nerve endings in the vaginal area, resulting in pruritus, edema, and erythema of the region [17, 58]. VVC is not typically acquired through contagion but rather from alterations in the environment that are favorable for fungal species, such as obliteration of the healthy vaginal microbiome defenses, moisture trapping in the inguinal region, and elevated skin surface pH, and states with lower immunological defenses such as human immunodeficiency virus (HIV) or higher glucose availability seen in pregnancy and diabetes [9, 59]. Yosipovitch et al. found that the skin surface pH in intertriginous areas, such as the inguinal region, is significantly higher in diabetic patients compared with healthy individuals, which may promote susceptibility to candidal infections [60]. This elevated pH can create an environment conducive to Candida overgrowth and infection. Tinea cruris affects the inguinal creases and labia majora, presenting with a visible rash, unlike the discharge characteristic of candidiasis [61].

In bacterial vaginosis (BV), an imbalance in the vaginal microbiota, results in the elevated pH that is more favorable for pathogenic, anaerobic bacteria such as Gardnerella vaginalis, than protective bacteria, such as Lactobacilli [62]. While BV does not typically cause inflammation, it can lead to discomfort and itching if it progresses to anaerobic vaginitis [9, 63–65]. The imbalance in the vaginal microbiome of patients with BV increases susceptibility to opportunistic or sexually transmitted infections. It can also contribute to itch by activating keratinocytes and peripheral nerve fibers, thus stimulating the release of alarmins and histamine [15]. However, itch is not a sensitive or specific sign of bacterial vaginosis [58].

Group A β-hemolytic streptococcus (GABHS) infections, more common in prepubertal females [18, 66], and other bacterial infections such as those caused by Staphylococcus aureus [9] can also cause vulvovaginal symptoms, but often affect the vulvar skin. Parasitic infections such as trichomoniasis [67], pediculosis pubis (pubic lice), Enterobius vermicularis (pinworms), and scabies can cause genital itching [61, 68]. Viral infections such as herpes simplex virus (HSV), human papillomavirus (HPV), and molluscum contagiosum may also present with vaginal itch [61].

Inflammatory Causes

Vaginal itching can often arise from inflammatory dermatological conditions, with atopic dermatitis (AD) and irritant and allergic contact dermatitis among the most common causes of vulvar itch [15]. AD affecting the vulva, also known as vulvar eczema, is a genetic disorder that compromises the skin barrier and causes itching with resulting rash formation [15]. Contact dermatitis results from external irritants or allergens [69]. Common irritants and allergens include feminine hygiene products, a warm and moist environment, fragrances, preservatives, and topical treatments [69] that trigger allergic reactions [15].

Other inflammatory causes include genital psoriasis, lichen simplex chronicus (LSC), lichen sclerosus (LS), and lichen planus (LP) [15]. In genital psoriasis, immune-mediated inflammation leads to the overproduction of skin cells, causing scaling, redness, and itching [70]. LSC is an eczematic disorder where an underlying skin condition or systemic disease leads to an intense, prolonged itch–scratch cycle and ultimate thickening of the skin [71]. The typical LS lesions are hypopigmented, pruritic areas surrounding the vaginal introitus and anus [72]. LP is a chronic inflammatory disorder affecting the skin and mucosal surfaces and can lead to itching, scarring, and atrophy of the vulvar skin [28]. Though less common, seborrheic dermatitis, plasma cell vulvitis, and Fox–Fordyce disease can also cause vulvar itching [15]. Seborrheic dermatitis affects sebum-rich areas and can cause erythematous plaques on the vulva with severe pruritus [11]. Plasma cell vulvitis is a rare condition associated with plasma cell plaques primarily within the vulvar vestibule [73]. Fox–Fordyce disease involves blocked apocrine sweat ducts and consequent inflammation of glands that can affect the vulvar skin [74].

Neoplastic Causes

Vulvar malignancies are uncommon, accounting for about 2–5% of all gynecologic cancers, and primarily include squamous cell carcinoma (SCC), basal cell carcinoma (BCC), melanoma, and extramammary Paget’s disease [75, 76]. Vulvar pruritus is rarely caused by neoplasms, but it is not an uncommon manifestation of these conditions. Up to 50–60% of patients with vulvar malignancy report moderate-to-severe itching as the first symptom [15, 17, 77]. Interestingly, one study even found a correlation between itch severity and subsequently determined cancer stage [78]. Benign neoplastic conditions such as syringomas and hidradenoma papilliferum can also present as pruritic nodules on the vulva and cause itching [79].

The pathophysiology of itch in vulvar neoplasms is often mixed, but severe itch is usually associated with eosinophilic and inflammatory mediator infiltration, which takes place in the invaded, superficial layers of the neoplastic and surrounding skin [78]. The itch sometimes even precedes the appearance of the neoplastic lesion as the skin reacts to the changes beginning to occur [78]. While malignant neoplasms may invade the neural tissues in the affected and nearby skin, this process is usually associated with pain rather than itch [78]. Of note, vulvar melanoma lesions were rarely associated with itching in one study and mostly devoid of inflammatory cells on histological examination [78]. Meanwhile, SCC was associated with both inflammatory cells on histology and itch [78]. Another study looked at symptomatology of extramammary Paget’s disease of the vulva and found itching in 95% of patients, often accompanied by eczematoid-appearing lesions and burning pain [80]. Histologically, the cells seen in vulvar Paget’s disease lesions are known to cause inflammatory changes to surrounding tissue [81].

Neuropathic Causes

Neuropathic itch is thought to occur through disruption in normal nerve signaling, which leads to abnormal pain and itch signals being transmitted to the brain [15]. Neuropathic causes of vaginal itching are linked to damage or dysfunction of nerve fibers in the vulvar region, leading to abnormal sensory experiences [15, 82]. The nerve damage results in decreased desensitizing neurotransmitter activity on the skin and hypersensitization of neurons in the central nervous system, resulting in both or either an excessive or inappropriate sensation of itch, burning, paresthesia, or other uncomfortable sensations on nondiseased skin that can be intense and difficult to treat and cause high morbidity [83, 84]. The damage may occur from many neuronal points, and neuropathology is often defined by the location of dysfunction. Examples are small fiber polyneuropathy (SFPN), myelopathy, and central nervous system (CNS) lesions [15]. Vaginal and vulvar itch could be present in cases of spinal injuries, lumbosacral spinal stenosis, or lumbosacral arthritis involving nerve or nerve root compression at the L4–S2 vertebrae as well as those with reactivation of varicella zoster [85], suggesting the role dermatomal innervation in causing pruritus of the vulvar area [15].

Sensitive skin in the genital area may contribute to the itch by exacerbating abnormal sensory responses in the vulvovaginal region. The genital skin has a thinner stratum corneum, increased hydration, and a semi-occlusive environment, making it more permeable and vulnerable to irritation and hypersensitivity [86]. These structural characteristics, combined with heightened neural innervation, may predispose individuals to exaggerated sensory experiences, including pruritus, burning, and paresthesia, which are hallmarks of neuropathic itch. Additionally, damage or dysfunction of nerve fibers in this area—whether from chronic inflammation, hormonal changes, external irritants, or underlying neuropathic conditions—can lead to increased neuronal sensitization and persistent discomfort [86]. Given the role of peripheral and central neural pathways in vulvar pruritus, the delicate nature of genital skin may amplify neuropathic mechanisms, further complicating symptom management and treatment.

An example of a cause of vulvar neuropathic itch is external insult to the skin of the genitals and surrounding tissues, such as burns, scars, and radiation exposure [87]. Damage occurs to the terminal neurons in the affected skin, which activates a skin-healing cascade [83]. In the acute stage, keratinocytes activate itch-inducing inflammatory mediators. However, in the later stages, the degeneration of GABA receptors, disinhibition of anti-pain neurotransmitters, and hypersensitization of the post-burn tissue ensues [81, 87]. Therefore, the chronic or long-term itch in post-burn, post-radiation, and scarred skin is primarily neuropathic in nature [83].

Vulvodynia is an idiopathic condition often thought to be a result of a neuropathic mechanism and is primarily classified as a chronic pain syndrome. Vulvodynia is a symptom rather than a specific disease characterized by the experience of chronic pain and discomfort in the vulva that may manifest as pain, burning, stinging, and itching sensations, particularly in response to light stimulus, and lasts at least 3 months without any identifiable cause [88, 89]. It has been reported that vulvar itch can be a symptom of small fiber polyneuropathy (SFPN), which affects the small, unmyelinated C-fibers and thinly myelinated A-delta fibers responsible for conducting pain and itch [90], and may be present in some cases of vulvodynia. Vulvodynia may also be psychogenic in origin, with a different pathophysiology than that described above [56].

Systemic Causes

Systemic conditions may present with or contribute to vulvovaginal itching [91]. This kind of itch is referred to as neurogenic, not to be mistaken with the term neuropathic. While neuropathic itch is due to nerve dysfunction or damage [82], neurogenic itch is caused by circulating molecular irritants, called pruritogens, which bind to unmyelinated C-fibers and trigger the central nervous system’s itch response [92, 93]. Both forms of itch have a different mechanism than inflammatory or infectious itch because they are not modulated by histamine [94] but rather by the nervous system [82]. Golpanian et al. points toward the pathophysiology of genital itch involving transient receptor potential (TRP) channels, such as TRPA1 and TRPV1, which play a crucial role in the transmission of itch signals in the genital region, contributing to chronic itch conditions [95].

Systemic causes often involve mixed mechanisms, with predisposition to infection, associated dermatoses, molecular irritants, and the stressors associated with illness creating a recipe for chronic itch [82]. Diabetic patients serve as an example of a population with predisposition to multiple itch etiologies. High blood sugar levels in patients can alter the vaginal environment to increase the susceptibility to infections such as vulvovaginal candidiasis [9]. Additionally, sodium–glucose cotransporter 2 (SGLT2) inhibitors are a common medication for type 2 diabetes mellitus, which increases the glucose concentrations in the urine, causing predisposition to fungal growth [31]. Finally, poorly controlled diabetes can also result in vulvar itch that is neurogenic in nature in the absence of a clinically proven fungal infection [92]. The wide variety of etiologies can lead to delayed diagnosis [31]. HIV infection, particularly when poorly controlled, is another example of a disease process that may result in multiple pruritic conditions. The weakened immune system is susceptible to diseases such as scabies, molluscum contagiosum, and candidiasis, while the virus itself may cause a neurogenic itch response [82, 96].

Hepatic and renal diseases often present with systemic pruritus and can cause vulvar itching [15, 93]. The itch is usually generalized but can be localized due to tight pants or undergarments, which can trigger preferential itch in the vulvar region [92]. Itch from chronic kidney disease (CKD) particularly occurs in association with uremia and recent dialysis [97]. CKD is also associated with increased risk for lichen simplex chronicus; low estradiol levels, which can lead to atrophic vulvitis; and small fiber polyneuropathy (SFPN) [15, 98]. Therefore, vulvar itch in patients with a suspected systemic cause should always be evaluated carefully for all potential mechanisms by which the patient may be experiencing itch.

Genetic Factors

Genodermatoses, or genetic disorders that directly affect the skin, may affect the vulvovaginal region. Darier disease is a genodermatosis caused by mutation of the ATPA2 gene on chromosome 12, responsible for a calcium pump protein [99]. This condition is inherited in an autosomal dominant fashion, but a recognized diagnosis in an immediate family member is seen in less than half of cases [99]. The condition causes itchy, hyperkeratotic papules that may affect mucosal surfaces and in rare cases may affect the vulva [100, 101]. The lesions may appear wart-like or be mistaken for acneiform conditions [99]. Most patients experience itching during lesion outbreaks, which is exacerbated by heat, sweat, and sometimes the menstrual cycle [102].

Another dyskeratosis caused by a genetic mutation is Hailey–Hailey disease [103]. A heterozygous mutation of the ATP2C1 gene causes failure of normal junction between keratinocytes, resulting in flares of vesico-bullous lesions and, over time, acanthosis [103]. These lesions often cause burning and itching and often affect flexural parts of the body and intertriginous zones [103]. While the condition is rare, vulvar involvement is common in affected women. Anal involvement is less common and may be mistaken for condylomatous disease [104]. Involvement of the vaginal mucosal is not usually seen [104].

There may be genetic predispositions for certain conditions that cause vaginal itching, although research in this area is still developing. For example, individuals with a family history of atopic dermatitis, psoriasis, LS, or other inflammatory skin conditions may be more prone to experiencing vaginal itching due to similar immune response mechanisms [17]. Personal history of recurrent VVC, defined as four or more episodes in a year, may also be linked to genetic predisposition [105]. Table 1 describes the main characteristics of vulvovaginal itch by etiology.

Differential Diagnosis

When evaluating vulvovaginal pruritus, it is essential to consider a broad differential diagnosis, encompassing infectious, inflammatory, hormonal, neoplastic, neuropathic, systemic, and psychogenic causes. Given the overlapping presentations of these conditions, a systematic approach is necessary to narrow down the most likely etiology [11]. Of note, if hormonal causes are suspected, referral to a gynecologist is warranted for further workup. If a psychogenic cause is suspected or a psychiatric condition is suspected to be an aggravating factor, psychiatric evaluation is warranted. A detailed discussion on these topics is beyond the scope of this review.

Formation of a differential is led by the timing, absence or presence of lesions, location, absence or presence of abnormal discharge, age, and other risk factors. Medical history, contacts, and other elements of history may increase clinical suspicion for causes of vaginal itch originating from certain domains.

Acute pruritus frequently arises from infectious causes, which should be strongly considered in the initial differential diagnosis. Common infectious causes that do not cause lesions and can be evaluated quickly are vulvovaginal candidiasis (VVC), bacterial vaginosis (BV), trichomoniasis (TV), chlamydia, and gonorrhea. Parasitic infestations such as public lice and pinworms should also be readily considered in patients with excoriations but no other visual lesions, particularly in children and sexually active individuals, especially those with risk factors such as contact with infected individuals or children with frequent exposure to other children. If there is suspicion for STI, HIV status should be evaluated, as affected individuals are prone to more severe or recurrent infection. If lesions are present, their appearance and associated symptoms should guide the differential diagnosis. Herpetic lesions, condylomas, molluscum contagiosum, scabies, and syphilis primary lesions all have distinctive appearances and can be confirmed with laboratory testing or biopsies.

Inflammatory dermatological conditions such as psoriasis, AD, lichen planus (LP), and contact dermatitis, frequently cause vaginal pruritus and should be on the differential for acute and chronic vulvovaginal itching due to their intermittent and relapsing and remitting nature. Psoriasis is a chronic cause of itch accompanying well-demarcated, erythematous red plaques limited to the labia majora often misdiagnosed as candida [8]. In AD, the presence of poorly defined erythematous plaques, excoriations, and a history of itching and scratching are key diagnostic clues. LP results in erosive lesions and scarring of the vulva, and there is often extragenital involvement [8]. Irritant contact dermatitis causes rapid onset burning sensations with localized vesicular plaques or scaly patches [33]. For allergic contact dermatitis, intermittent symptoms and a lack of response to standard treatments may raise suspicion for an underlying allergen, warranting further evaluation such as a patch test [33].

Atrophic dermatitis should be high on the differential for postmenopausal women with acute or chronic itch or women taking medications that modulate or suppress estrogen. Timing of itch onset in relation to hormonal medications should be considered. Another important differential to consider is GSM, a chronic, progressive condition caused by estrogen deficiency, which affects the vulvovaginal and lower urinary tract. GSM commonly presents with symptoms such as vulvovaginal dryness, burning, irritation, and pruritus, making it a potential cause of unexplained itching in postmenopausal women [112–114]. If GSM is suspected, referral to gynecology is warranted for further evaluation and management. The presence of vaginal atrophy can be assessed on physical exam [47].

Other causes of vulvovaginal pruritus should be considered when common infectious and inflammatory causes have been ruled out and the clinical picture suits another domain, especially in cases of chronic pruritus or when treatment has failed to improve symptoms. Neuropathic itching may arise from conditions such as vulvodynia, small fiber polyneuropathy (SFPN), scars and burns, postherpetic neuralgias, radiculopathies, or spinal nerve compression [115]. The presence of risk factors for neuropathy, associated burning pain or neurological symptoms, pruritus with a dermatomal distribution or in the location of previous lesions, or sensory abnormalities may be associated [115]. Nerve conduction studies, imaging with magnetic resonance imaging (MRI) of the lower spine to assess for spinal stenosis, mapping of pruritus by neural distribution, and assessment for an itch response to a nonpruritic stimulus may be used to assess for neurologic vulvovaginal pruritus. Laboratory studies that can assess for causes of SFPN include hemoglobin A1C, hepatic and renal disease panels, HIV testing, and vitamin B₁₂ level [91, 115]. However, these conditions would not likely cause itch limited only to the vulvar region [115].

Neoplasms, such as squamous cell carcinoma and syringomas, are rare causes of vaginal itch but should be considered when associated with unclear, abnormally pigmented, ulcerated, or persistent, ulcerating lesions or a history of vulvar or cervical dysplasias. Lesions are often slow-growing, painless, and multifocal. A low threshold to biopsy lesions that do not respond to treatment may prevent delayed diagnosis and dermal invasion [116]. Figure 2 provides a visualization of the diagnostic algorithm for the majority of these conditions.

Lifestyle and Environment Modifications

Several lifestyle modifications can help manage vulvovaginal itching, as the vulva is notably vulnerable to irritants [4]. Fabric choices impact comfort; wearing breathable cotton underwear, limiting panty hose, changing from moist clothing such as bathing suits and exercise clothes, and selecting loose-fitting fabrics such as silk or cotton can reduce irritation and moisture [3, 8]. Avoiding wearing underwear with sleepwear may further help, and caution with rubber items such as pessaries and condoms is advised, as they can act as sensitizers [15]. Skin care and hygiene adjustments are crucial for managing vulvar dermatoses, skin damage from wounds or radiation, and infections and to avoid exacerbation and promote healing [4]. Photoprotection, or avoiding sun exposure of wounded or inflamed skin, is highly recommended in these cases [117]. Avoiding products that may contain vulvar allergens, even in products marketed for use on the vulva for hygiene and other purposes, may prevent or help alleviate contact dermatoses [118]. Mild soaps, avoiding harsh alkaline soap products, avoiding shaving and other harsh pubic hair removal practices, and using water- or silicon-based lubrication during intercourse can also prevent and treat irritation [119]. Keeping fingernails short and gentle rubbing can mitigate the itch–scratch cycle, with some suggesting gloves during sleep to manage unconscious scratching [11]. Proper toilet habits, including gentle wiping and removing foreign bodies such as toilet paper fragments, are also important [16, 22]. Stool should be kept away from the vagina as much as possible, by wiping away from the vulva and changing young children’s diapers as frequently as possible after defecation with care to cleanse the vulva of stool afterwards [120]. Additionally, addressing psychological factors such as anxiety, depression, and stress is essential for managing pruritus and its underlying causes [121]. Given the strong interplay between psychological well-being and chronic pruritus, addressing underlying stress, anxiety, and mood disorders is essential in comprehensive vulvovaginal itch management. Cognitive behavioral therapy, mindfulness techniques, and stress-reduction strategies may help alleviate symptoms in patients with psychogenic or pruriplastic itch [57]. However, a detailed discussion on the psychological management of vulvar pruritus is beyond the scope of this review.

Topical Therapies

Topical corticosteroids are the primary symptomatic treatment for pruritus with inflammation in affected areas [11, 17]. Their efficacy and safety depend on their potency and the application site, necessitating thorough patient education on selection, frequency, and duration of use. Mid- to high-potency corticosteroids such as triamcinolone, betamethasone, and fluocinolone are commonly prescribed for short-term management of vulvovaginal inflammation and pruritus [3]. Lower-potency hydrocortisone is suitable for thinner skin and more frequently used but is less effective than other corticosteroids [3]. Ointments are preferred over creams for their superior efficacy, and intralesional triamcinolone acetonide can target specific lesions [3, 29].

For chronic management, especially maintenance therapy, topical calcineurin inhibitors such as tacrolimus and pimecrolimus are effective alternatives following initial corticosteroid control [15]. Local estrogen therapy addresses symptoms related to low estrogen levels, notably improving dryness and dyspareunia, though they may not significantly affect vulvar or vaginal itching severity if another condition is present [27, 122].

Fungal infections such as vulvovaginal candidiasis are managed with topical or oral antifungals, with efficacy varying by yeast species. Certain Candida strains are resistant to ketoconazole [123]. Terconazole, effective against C. albicans, requires a prescription [32]. Patients often initiate treatment with over-the-counter treatments, which include intravaginal imidazoles, anti-itch creams, and homeopathic options [37]. A single dose of the intravaginal imidazole 1200 mg of 2% miconazole nitrate can treat up to 80% of mild to moderate cases of vaginal candidiasis, with similar efficacy to oral fluconazole [124]. Severe cases may require two doses of oral fluconazole or intravaginal imidazoles 36 h apart [124]. Anti-itch creams containing the topical anesthetics benzocaine or resorcinol or low potency hydrocortisone 1% offer only symptomatic relief [37].

Recent studies have shown that maintaining an acidic vaginal environment can help alleviate symptoms of vaginal itching, particularly in conditions such as bacterial vaginosis. Lactic-acid-containing products have been found to support the restoration of a healthy vaginal microbiota by promoting the growth of Lactobacilli, which produce lactic acid and help maintain a low vaginal pH. This acidic environment inhibits the growth of pathogenic bacteria and reduces inflammation, thereby alleviating symptoms such as itching [125, 126]. Additionally, the use of acidic electrolyzed water with a pH close to normal vaginal levels has shown potential in inhibiting the viability of harmful bacteria such as Gardnerella spp. while having minimal effects on beneficial Lactobacillus species [127]. These findings suggest that using low-pH solutions and lactic acid gel products can be an effective strategy for reducing vaginal itch by maintaining a balanced vaginal microbiome and preventing overgrowth of pathogens.

Topical emollients such as petroleum jelly, dimethicone, and zinc oxide paste provide symptomatic relief to vulvar lesions by soothing the compromised skin barrier [33]. These are especially beneficial when itching disrupts skin integrity.

Formulations of pramoxine 1%, a topical anesthetic, in combination with a topical steroid such as hydrocortisone, is commonly used to manage pruritus associated with vulvar diseases, including conditions such as vulvar lichen sclerosus [128, 129]. This combination provides both anti-inflammatory effects from the steroid and local anesthetic effects from pramoxine, effectively reducing itch and inflammation in these sensitive areas. Additionally, topical silver sulfadiazine, known for its antimicrobial properties, has been noted to alleviate itching in cases of Candida vaginitis and other vulvar irritations by reducing inflammation and controlling fungal growth [130, 131].

Topical anesthetics such as lidocaine and pramoxine and ketamine−amitriptyline−lidocaine (KAL) also relieve itching and discomfort and can be especially useful for neuropathic vulvar itch [132]. Cooling agents such as menthol may help decrease itch by inhibiting the transient receptor potential cation channel subfamily M member 8 (TRPM8), reducing nerve excitability and providing a soothing effect [133].

Topical tofacitinib, a Janus kinase (JAK) inhibitor, has shown promise in treating inflammatory skin conditions such as vulvovaginal lichen planus, lichen simplex chronicus (LSC), and psoriatic lesions by targeting inflammatory cytokine signaling pathways involved in these diseases [134–136]. Clinical studies suggest that tofacitinib can reduce inflammatory markers and improve symptoms in resistant or severe cases, offering a valuable alternative to traditional corticosteroid therapies for managing these vulvar conditions [134]. Additionally, topical tacrolimus and pimecrolimus, both calcineurin inhibitors, are effective alternatives to corticosteroids for managing pruritus in conditions such as lichen sclerosus and LSC [137, 138]. These agents work by selectively inhibiting T-cell activation, which helps alleviate symptoms in patients unresponsive to first-line corticosteroids. Studies have shown significant improvement in symptom relief and skin appearance, with these treatments proving particularly beneficial for sensitive areas such as the vulva, where corticosteroids may pose risks of skin thinning with prolonged use [138, 139].

Systemic Treatments

When topical corticosteroids are insufficient for managing vulvovaginal pruritus, oral corticosteroids and systemic immunotherapies may be considered [140]. Oral corticosteroids, such as prednisone at 40−60 mg daily for 2−4 weeks, are aggressive measures that are effective for rapid control [15, 29, 119, 121]. Monitoring and tapering are essential to mitigate the risk of long-term complications [3].

Anticonvulsants such as gabapentin and pregabalin and tricyclic antidepressants (TCA) such as mirtazapine taken at bedtime, can be beneficial for neuropathic pruritus [141, 142]. Neuropathic and psychogenic causes of pruritus may both be treated with selective serotonin reuptake inhibitors (SSRI), and TCAs such as paroxetine and amitriptyline have also been shown to have anti-itch properties for these cases [57]. Patients with psychogenic itch associated with depression or anxiety may benefit from duloxetine, a selective norepinephrine reuptake inhibitor (SNRI) often used to treat neuropathic pain [57]. Opiate receptor antagonists have been found to enhance pruritus management for some adult women due to the role of endogenous opioids in the condition [143]. A recent study administering 50 mg of oral naltrexone, an opioid antagonist, to five patients between 24 and 54 years old with chronic vulvovaginal pruritus showed significant reduction in itching [143].

For refractory cases of inflammatory, noninfectious vulvar itching, systemic immunotherapies such as methotrexate, mycophenolate mofetil, and hydroxychloroquine are options [17].

Hydroxychloroquine therapy can sometimes cause itching, a side effect that may be more prevalent among patients with darker skin tones. This potential for increased itchiness may make hydroxychloroquine less suitable for treating these individuals [144, 145]. Methotrexate, commonly dosed at 5−7.5 mg weekly with daily folic acid (5 mg), can improve disease management, particularly when combined with topical therapies [146].

Systemic biologics may be used to treat inflammatory and autoimmune causes of vulvovaginal pruritus on the basis of their associated immunologic etiologies. Ixekizumab, a biologic targeting the IL-17A receptor, has received Food and Drug Administration (FDA) approval for the treatment of genital psoriasis and has been shown to significantly reduce itch and improve sexual activity and patients’ quality of life. In a randomized, double-blind study, patients treated with ixekizumab reported significant improvements in genital psoriasis symptoms compared to placebo [147]. Another study demonstrated that ixekizumab effectively reduced the severity of moderate-to-severe genital psoriasis, with significant improvements in both physical symptoms and health-related quality of life [148]. A recent case series has reported successful treatment of three refractory cases of lichen simplex chronicus with dupilumab, a biologic which targets and inhibits IL-4 and IL-13 [118, 149]. Tralokinumab, a competitive inhibitor of IL-13, has also shown some promise in improving genital atopic dermatitis [150]. There remains a need for further studies to confirm the reproducibility of these results. However, these novel treatments may be considered for refractory cases that have failed other standard therapies [118].

For fungal and parasitic infections, medications tend to reduce itch quite rapidly. Metronidazole is commonly used for bacterial vaginosis and trichomoniasis [32] while fungal infections are often treated with oral fluconazole [3, 151]. For bacterial vulvar infections, antibiotics are prescribed on the basis of the identified pathogen [19].

Very rarely, long-term management of vulvar itching in postmenopausal women may involve low-dose estradiol, administered orally or via transdermal application, following the failure of localized topical treatments [9, 122]. This therapy is not preferred or used often because the safety of long-term low-dose hormone therapy is inferior to that of localized treatments [27].

In rare cases, botox injections and spinal blocks have been used as treatment options for neuropathic itch, including vulvovaginal pruritus, by modulating nerve activity and reducing hypersensitization [152]. Additionally, dorsal root ganglion (DRG) stimulation, a neuromodulation technique commonly used for chronic pain, has shown potential for managing intractable neuropathic itch. This approach targets the DRG, which plays a critical role in transmitting itch signals, and can be applied as a treatment for localized vulvovaginal itch [153].

Nonpharmaceutical Therapies

Nonpharmaceutical methods can also mitigate symptoms of vulvovaginal pruritus. Tub and sitz baths can soothe symptoms by hydrating the vulvar area, but water should not be too hot. In inflammatory conditions, applying bland emollients such as petroleum jelly can help retain moisture and protect the skin [4, 11]. Cold compresses may alleviate severe itching [119]. Transcutaneous electrical nerve stimulation (TENS) and acupuncture offer potential benefits; TENS reduces itch through nerve stimulation, while acupuncture may address skin barrier imbalances [8]. Physical therapy may help with neuromuscular-related discomfort [3]. Homeopathic remedies, however, lack significant efficacy for itching [37].

Funding

None.

Conflicts of Interest

None to declare for Kayla Mashoudy. None to declare for Ana Tomlinson. None to declare for Sarah Kim. None to declare for Vanya Shivashankar. None to declare for Michelle Fletcher. Conflicts of interest for Gil Yosipovitch: Abbvie, Arcutis, Almiral, Amgen, Celldex, Escient Health, Eli Lilly, Galderma, LEO Pharma, Merck, Novartis, Pfizer, Pierre Fabre, Regeneron Pharmaceuticals, Inc., Sanofi, Vifor, GSK—advisory board member; Eli Lilly, LEO Pharma, Novartis, Pfizer, Galderma, Escient, Sanofi, Regeneron, Sanofi Celldex, Pfizer– grants/research funding; Regeneron Pharmaceuticals, Inc., Sanofi—Galderma investigator. Gil Yosipovitch is an Editorial Board member of the American Journal of Clinical Dermatology. Gil Yosipovitch was not involved in the selection of peer reviewers for the manuscript nor any of the subsequent editorial decisions.

Ethical Approval

Not applicable.

Data Availability

Not applicable.

Patient Consent to Participate/Publish

Not applicable.

Code Availability

Not applicable.

Author Contributions

Kayla Mashoudy: conceptualization, methodology, and writing—original and final draft preparation. Ana Tomlinson: material preparation and writing—original draft preparation. Sarah Kim: material preparation, writing—original draft preparation. Vanya Shivashankar: material preparation and writing—original draft preparation. Gil Yosipovitch: supervision, writing, and manuscript review. Michelle Fletcher: supervision, writing, and manuscript review. All authors read and approved the final manuscript.