Chronic vulvar itch: diagnostic and therapeutic challenges Katarina Trčko 1 ✉ 1 Department of Dermatology, Maribor University Medical Center, Maribor, Slovenia. 123 2025;34:123-131 doi: 10.15570/actaapa.2025.25 Introduction Vulvar pruritus is a common symptom that can cause physi- cal discomfort and emotional distress. It is classified as acute or chronic, with the distinction based on a duration of less than or more than 6 weeks, respectively (1). Depending on the underly- ing cause and the timeliness or effectiveness of treatment, acute vulvovaginal pruritus has the potential to progress to a chronic form (2, 3). Unlike sensations such as burning or stinging, pru- ritus is typically characterized by an urge to scratch, which can temporarily alleviate discomfort (4). Despite its prevalence, vul- var itch is often overlooked in clinical settings. Although it can significantly interfere with daily life, intimacy, and mental health, data on its overall prevalence and clinical impact are limited (5, 6). Most of the available data come from studies that focus on spe- cific underlying conditions, which makes it difficult to quantify pruritus as a distinct clinical concern (7, 8). In Europe, estimated prevalence rates of chronic vulvar pruritus range from 5% to 10%, although these figures may underestimate the true burden due to social stigma and the sensitive nature of genital symptoms, which often discourages reporting (9). Importantly, vulvar pruritus is a symptom rather than a distinct diagnosis. It can arise from a wide range of causes, including inflammatory dermatoses, infections, neoplastic processes, hormonal changes, and neuropathic dis- orders (1, 2). Without adequate treatment, persistent scratching can result in secondary skin changes, such as excoriations and lichenification (thickening of the skin), which increase the risk of further irritation or infection (10). This narrative review provides clinicians with a concise sum- mary of potential etiologies, diagnostic considerations, and ther- apeutic options, emphasizing the importance of a multidiscipli- nary and patient-centered approach. Vulvar physiology Due to several anatomical and physiological factors, the skin of the vulva is more sensitive than the skin on other parts of the body (11). Located between the urinary and digestive tracts, the vulva serves as a transition point from keratinized skin to non- keratinized mucosal surfaces (12). Its unique location means it is constantly exposed to irritants, such as perspiration, vaginal discharge, urine, and friction from skin-to-skin contact, cloth- ing, and hygiene products (13). These factors can compromise the integrity of the epidermal barrier. In the genital region, skin pH levels are typically higher than in other areas of the body and are comparable to those found in occluded, moisture-prone sites such as the axillae (14). Moreover, vulvar pH varies not only dur- ing the menstrual cycle—being more acidic in the estrogen-domi- nant mid-cycle phase and temporarily elevated during menstrua- tion—but also across different life stages. In prepubertal girls and postmenopausal women, lower estrogen levels are associated with a higher (more alkaline) pH, whereas, during puberty and the reproductive years, increased estrogen supports a more acidic environment that favors mucosal integrity and microbial balance. Elevated vulvar skin pH may activate serine proteases, disrupting the epidermal barrier and contributing to pruritus (15). The vulvar region has higher moisture levels and increased transepidermal water loss, indicating a weakened skin barrier and consequently greater moisture loss (2, 16). All these factors contribute to itchi- ness by exacerbating abnormal sensory responses in the vulvo- vaginal region, making it more susceptible to irritant and allergen penetration, and increasing the risk of local inflammation and irritation (17). The structural and functional health of vulvar tissue is strongly influenced by hormonal status, particularly estrogen levels. Es- trogen plays a central role in maintaining vulvar epithelial thick- ness, an acidic pH, and a healthy microbiota composition (18). Throughout a woman's life, hormonal fluctuations significantly impact the structure and function of the vulvar epithelium, in- cluding pH balance and microbial composition. In early child- hood, low estrogen levels result in a neutral or alkaline vulvo- vaginal pH due to the absence of lactobacilli. As estrogen levels rise during puberty, glycogen accumulates in the vulvovaginal epithelium, providing a substrate for lactobacilli. These bacteria Abstract Vulvar pruritus refers to itching affecting the skin and mucosal surfaces of the external genital and perineal regions. It is most frequently associated with infections, inflammatory skin disorders, or neoplastic conditions. Due to the distinctive anatomical and physiological features of the anogenital area, clinical manifestations in this region are often subtle or atypical, which can complicate both diagnosis and management. Because vulvar itch can be highly distressing, timely identification and appropriate intervention are crucial for improving patient quality of life. A comprehensive clinical approach is essential when evaluating pa- tients with vulvar pruritus. This includes a detailed medical history, focused physical examination, and relevant diagnostic testing. Management should involve elimination of contributing or exacerbating factors and treatment directed at the underlying cause. This review article discusses the common causes of vulvar pruritus, emphasizing the diagnostic approach and outlining current treatment strategies. The importance of an individualized patient-centered management plan is emphasized. Keywords: vulvar itch, pruritus, diagnosis, treatment, barrier function Acta Dermatovenerologica Alpina, Pannonica et Adriatica Acta Dermatovenerol APA Received: 20 June 2025 | Returned for modification: 30 July 2025 | Accepted: 31 July 2025 ✉ Corresponding author: katarina.trcko@gmail.com 124 Acta Dermatovenerol APA | 2025;34:123-131 K. Trčko ferment glycogen into lactic acid, thereby lowering the vaginal pH and promoting a protective acidic environment. During the men- strual cycle and menopause, estrogen levels fluctuate or decline, leading to an increase in pH (19). This more alkaline environment can enhance protease activity, which can potentially trigger neu- rogenic inflammation by activating protease-activated receptors on sensory neurons, keratinocytes, and endothelial cells (20). In postmenopausal women, reduced estrogen levels lead to mucosal thinning, reduced elasticity and lubrication, and increased vul- nerability to irritants. These changes weaken the skin’s protective barrier, making it more susceptible to mechanical injury, irrita- tion, and infection (19). Classification of pruritus according to etiology Various classification systems have been developed to categorize pruritus based on its underlying etiology and clinical features (21). Due to the distinct anatomical and physiological properties of vulvar skin, the causes of vulvar pruritus differ from those of other cutaneous regions and often necessitate a tailored diag- nostic approach. To facilitate differential diagnosis and guide management, vulvar pruritus can be clinically classified into the following categories: dermatological, systemic, neuropathic, psy- chogenic, mixed, and of undetermined origin (21–24). This classi- fication system emphasizes the multifactorial nature of vulvar itch and highlights the importance of comprehensive clinical evalua- tion. An overview of this classification is presented in Table 1. Common differential diagnoses of vulvar pruritus and its diagnosis Precise data on the prevalence of specific causes of chronic or recurrent vulvar pruritus are lacking; however, according to the available literature, dermatitis is the most common cause, ac- counting for more than half of cases (ranging from 54% to 64%). Other notable causes include lichen sclerosus et atrophicus (7%– 13%), chronic vulvovaginal candidiasis (approximately 10%), dysesthetic vulvodynia (approximately 9%), and psoriasis (ap- proximately 5%) (25). The differential diagnosis of vulvar pruri- tus varies significantly across different life stages. In prepubertal girls, common triggers include group A streptococcal infections, poor hygiene, irritant contact dermatitis, atopic dermatitis, pso- riasis, and lichen sclerosus. Among women of reproductive age, the condition is often associated with irritant or allergic contact dermatitis, recurrent vulvovaginal candidiasis, lichen simplex chronicus, psoriasis, lichen sclerosus, and sexually transmitted infections (STIs). In postmenopausal women, declining estrogen levels lead to atrophic vulvovaginitis and recurrent lichen sclero- sus, both of which are often accompanied by persistent itching. Recognizing the age-specific prevalence of these conditions is crit- ical for achieving timely diagnosis and effective treatment (2, 26). When evaluating a patient presenting with vulvar pruritus, it is essential to obtain a thorough medical history, including po- tential risk factors for STIs, exposure to irritants or allergens, per- sonal hygiene practices, and psychosocial stressors. The use of hormonal contraceptives—in particular, progestogen-only pills— should also be carefully considered because they can suppress endogenous estrogen levels, leading to vulvovaginal dryness and mucosal thinning and secondary itching. It is also necessary to assess the patient for specific clinical signs that may inform the diagnostic process. The clinical approach should be tailored ac- cording to symptom duration and any accompanying findings. Diagnosis may be complicated by environmental factors unique to the vulvar region, such as increased warmth, humidity, and partial occlusion, which can alter the clinical presentation of common dermatoses and obscure characteristic features such as scaling (3, 9, 13, 27, 28). In cases of acute pruritus (lasting less than 6 weeks), the primary focus should be on ruling out STI and other infectious causes. Treatment should be based on the results of these tests. If there is no improvement following the initial treatment, or if the test results are negative, clinicians should consider noninfectious causes or dermatoses. In such cases, further investigation into un- derlying dermatological conditions is indicated (3, 9). For chronic Table 1 | Proposed etiological classification of vulvar pruritus, adapted from Ständer et al (21). Category Associated disease Dermatological Inflammatory dermatoses: atopic dermatitis, irritant contact dermatitis, allergic contact dermatitis, lichen sclerosus, lichen planus, lichen simplex chronicus, psoriasis, seborrheic dermatitis, plasma cell vulvitis, dermatographism, autoimmune bullous disorders (pemphigoid, pemphigus, linear IgA disease), acantholytic dermatosis (Darier disease, Hailey–Hailey disease, papular acantholytic dyskeratosis), Fox–Fordyce disease, aphthae (idiopathic or secondary to systemic disorders such as Behçet, inflammatory bowel disease, etc.). Infectious dermatoses: fungal (Candida albicans, C. glabrata, dermatophytes), bacterial (streptococcal and staphylococcal infections, Escherichia coli, Neisseria gonorrhoeae, Chlamydia trachomatis), viral (herpes simplex virus, human papillomavirus, molluscum contagiosum, varicella zoster virus), parasitic infection (Trichomonas vaginalis), parasitic infestations: scabies, pediculosis, enterobiasis. Neoplasms: vulvar intraepithelial neoplasia (VIN), Paget’s disease, squamous cell carcinoma, melanoma. Systemic Diabetes mellitus, hepatic/renal diseases, drugs, estrogen deficiency, HIV infection, chronic hepatitis C virus infection, hyper/hypothyroidism, malignancies (leukemia, Hodkin’s disease), hematologic (iron deficiency, polycythemia rubra vera). Neuropathic Result of nerve dysfunction or damage: • Sm a l l fi ber po ly neu r op ath y (S FPN), oft en sec ond ar y t o sy s t emic c ondition s s uc h a s di a bet e s mel lit u s, vitamin B12 deficiency, amyloidosis, sarcoidosis, drugs (chemotherapy, alcohol use, etc.); • M y elop ath y and c ent r a l ner v ou s sy s t em le s ion s; • P o s therpetic it c h a s m anif e s t ation of po s therpetic neu r a lgi a; • Deg ener ati v e and infl amm at or y s p ine di se a se s (e.g., c ompr e s s ion of ner v e s or ner v e r oot s). Psychogenic/psychosomatic Delusional parasitosis, tactile hallucinations, obsessive compulsive disorders, anxiety, depression, somatoform and dissociative disorders. Mi x ed Overlapping and coexistence of several diseases. Of undetermined origin No clear underlying cause identified despite thorough evaluation: idiopathic vulvar pruritus (sensitive skin). 125 Acta Dermatovenerol APA | 2025;34:123-131 Vulvar itch pruritus lasting more than 6 weeks, infectious causes are less like- ly and underlying dermatoses are a more probable cause. Table 2 summarizes the main features of common vulvar dermatoses, including their clinical presentation and treatment approaches. Figures 1–3 present the typical morphological presentation of lichen sclerosus, highlighting its key diagnostic characteristics. Figure 4 illustrates the typical appearance of vulvar lichen planus. A biopsy is indicated when a diagnosis remains uncertain de- spite noninvasive testing and clinical examination. This is the case when neoplasia is suspected, treatment response is poor, or diagnostic uncertainty continues after therapy is completed (29). Further investigations may be required based on clinical sus- picion. Patch testing can confirm contact allergies, and skin prick tests can determine underlying atopy in patients with a history of allergic disease (30). Laboratory testing, including blood glucose and iron studies, as well as relevant immunological tests, can also support the diagnosis of systemic or metabolic conditions that may be contributing to vulvar symptoms (9). If a neuropathic origin is suspected, appropriate imaging studies should be performed (31). In cases in which a psychogenic component is considered, referral for a psychiatric evaluation may be necessary (2, 32). When evaluating a patient presenting with vulvar pruritus and pain, lichen planus is one of the key differential diagnoses to consider (9, 31). Vulvar pain may occur with or without itch- ing, and so identifying any accompanying symptoms is crucial for guiding further evaluation. If pruritus is absent, attention should be directed toward identifying the underlying cause based on the specific symptoms present. One common cause in postmenopau- sal women is genitourinary syndrome of menopause, previously known as atrophic vaginitis (32). Figure 1 | Lichen sclerosus typically presents as whitish plaques, change in the texture of the mucosa, altered vulvar architecture with the fusion of the labia minora with the interlabial sulci, clitoral phimosis, and erosions. Figure 3 | Hyperkeratotic lichen sclerosus. Figure 2 | Figure-eight involvement of vulvar lichen sclerosus. 126 Acta Dermatovenerol APA | 2025;34:123-131 K. Trčko If no itching or menopausal changes are present, clinicians must consider other vulvodynia-related or structural causes (9). Vulvodynia is a chronic pain condition of unknown origin, which is often associated with neuropathic mechanisms. Rather than be- ing considered a distinct disease entity, it is classified as a pain syndrome characterized by ongoing vulvar discomfort, such as burning, pain, stinging, or itching. These symptoms are often trig- gered by minimal stimuli, and they persist for at least 3 months without a known cause. Proposed etiological factors include peripheral nerve damage or irritation that alters pain signaling pathways from the vulva to the spinal cord, as well as increased density and hypersensitivity of vulvar nociceptive fibers. Elevated concentrations of proinflammatory mediators such as cytokines, abnormal sensory responses to environmental stimuli, possible genetic predisposition, and dysfunction of the pelvic floor mus- culature manifesting as weakness, hypertonicity, or instability have also been implicated in its pathogenesis (33, 34). In addi- tion, vulvodynia may, in certain instances, have a psychogenic origin involving a different pathophysiological mechanism to that of neuropathic pain (30). When appropriate, an interdisciplinary approach involving dermatologists, gynecologists, pain manage- ment specialists, and other relevant specialists is recommended. Disease progression and associated morbidities The risk of vulvar squamous cell carcinoma is notably elevated in women diagnosed with lichen sclerosus, with incidence estimates ranging from 1.16 to 13.67 per 1,000 person-years and reported ab- solute risks reaching up to 21.88%. In comparison, lichen planus is associated with a considerably lower and less clearly estab- lished risk, with available data suggesting an absolute risk of ap- proximately 1.16% (35). Due to the increased risk of malignancy, timely diagnosis, appropriate treatment, and regular long-term follow-up are necessary for all patients with these conditions. Vulvar pruritus can have a significant impact on quality of life. Psychological burdens include anxiety, depression, and disrupted sleep. It can also affect sexual health, often resulting in discom- fort during intercourse and reduced sexual satisfaction, which affects intimate relationships (36–38). Women with vulvar symp- toms often initially self-treat with over-the-counter (OTC) antifun- gal products, often due to embarrassment or misinterpreting their symptoms as a fungal infection. However, these products are often ineffective, delaying accurate diagnosis and management, and po- tentially worsening the underlying vulvar condition. Inappropri- ate use of OTC agents can irritate the delicate vulvar skin barrier, and it can even exacerbate inflammation and itchiness (3). Therapeutic principles in vulvar pruritus Successful management of vulvovaginal pruritus depends on more than just accurate diagnosis and disease-specific therapy; several other factors also play a role. These include educating pa- tients about the chronic nature of the condition, identifying and eliminating irritants, and using well-tolerated topical formula- tions. Realistic expectations must be set because most vulvovagi- nal conditions are chronic and treatment usually aims to control symptoms rather than provide a definitive cure. Basic supportive care involves avoiding known irritants and triggers. These include fragranced hygiene products, cleansers containing emulsifiers, antimicrobial agents such as parabens, certain lubricants, and latex condoms. It is recommended that the vulva be washed once or twice a day with lukewarm water, without soap, cleansers, or detergents (2). Regular application of lipid-rich emollients or petrolatum can help restore moisture and support barrier function. Additional measures, such as wear- ing loose-fitting clothing, choosing silk or cotton underwear, and avoiding pubic hair removal can further reduce mechanical irri- tation and support skin recovery (39). Activities such as cycling should be avoided because these may worsen symptoms, and treatment for incontinence should be sought if necessary (40). Acute symptom flare-ups can be managed with cold compress- es, followed by the application of emollients to hydrate and pro- tect the skin. Disruption to sleep due to itching can be managed with sedating antihistamines (e.g., diphenhydramine or hydrox- yzine) or tricyclic antidepressants, such as amitriptyline or dox- epin (13). If vulvovaginal symptoms persist despite treatment, clinicians should consider poor adherence, contact dermatitis, resistance to topical corticosteroids, or other factors, such as physical limi- tations in applying treatment, especially in elderly or obese pa- tients. Clinicians should consider the possibility of misdiagnosis, associated candidiasis, or an emerging systemic disease, and per- form a biopsy where appropriate (13). The most commonly used topical agents according to the iden- tified etiology are outlined in Table 2. Systemic treatment is generally only considered for severe or refractory cases of vulvar pruritus, particularly when standard topical therapies have been ineffective. Systemic corticosteroids may be indicated for certain inflammatory dermatoses, such as lichen sclerosus or lichen planus, for which more aggressive im- Figure 4 | Lichen planus: sharply demarcated, intensely erythematous erosions accompanied by surrounding white epithelium and significant loss of normal vulvar architecture. 127 Acta Dermatovenerol APA | 2025;34:123-131 Vulvar itch munosuppressive treatment is required to control disease activity and alleviate pruritus. Short courses of oral corticosteroids, such as prednisolone, can provide rapid symptom relief in such cases, but they must be administered with caution because long-term use can lead to adverse effects. Appropriate tapering and moni- toring are required (40, 41). Immunosuppressive and immunomodulatory agents includ- ing methotrexate, azathioprine, cyclosporine, mycophenolate mofetil, and hydroxychloroquine may have potential roles in se- lected inflammatory vulvar conditions (44, 45). Acitretin has been shown to be effective in treating lichen sclerosus (46). Evidence- based guidelines are essential for optimizing patient outcomes and supporting clinical decision-making. In the treatment of genital psoriasis, interleukin (IL)-17 and IL- 23 inhibitors have demonstrated significant clinical efficacy (47– 49). Apremilast, a phosphodiesterase-4 inhibitor, has also shown promise, particularly in reducing pruritus and improving skin clearance (49). Dupilumab, which blocks IL-4 and IL-13 signaling, has shown consistent effectiveness in treating atopic dermatitis, including cases with genital involvement (50). Furthermore, oral Janus kinase (JAK) inhibitors, such as upadacitinib and abroci- tinib, both of which have been approved by the Food and Drug Administration for treating moderate-to-severe atopic dermatitis, have been shown to be beneficial in controlling dermatitis and alleviating lichen simplex chronicus and the associated itchiness (51, 52). Most of the systemic therapies currently used to manage vulvar dermatoses are used off-label, which reflects the limited availability of approved treatment options for this condition. This underlines the need for high-quality randomized controlled trials in the future to evaluate the efficacy and safety of these interven- tions more effectively. Neuropathic or psychogenic vulvar pruritus may benefit from neuromodulating therapies. Anticonvulsants, such as gabapentin and pregabalin, have shown efficacy in treat- ing neuropathic itch (53, 54). Tricyclic antidepressants (e.g., ami- triptyline or mirtazapine 10 to 100 mg 2 hours before bedtime) and selective serotonin reuptake inhibitors (e.g., paroxetine) possess antipruritic effects and may be considered in cases linked to cen- tral sensitization or mood disorders (13). Duloxetine, a serotonin- norepinephrine reuptake inhibitor used for neuropathic pain and anxiety, may also reduce itch intensity in psychogenic presenta- tions (54). Opioid antagonists such as naltrexone, targeting endogenous opioid pathways, have demonstrated positive outcomes in small studies (55). Topical lidocaine has been used with some success for localized neuropathic itch (13). In hypoestrogenic states, topi- cal estrogen therapy may alleviate symptoms of dryness, atrophy, and pruritus by improving mucosal integrity (56). Future perspective Targeted therapies are emerging as a potential treatment option for refractory vulvar dermatoses, particularly in cases that do not respond to conventional topical or systemic agents. Although these therapies are frequently employed off-label for vulvar dis- ease, mounting clinical experience validates their potential ef- ficacy, necessitating additional research to clarify their position within treatment protocols. Adalimumab, a tumor necrosis factor alpha inhibitor, has dem- onstrated efficacy in treating treatment-resistant lichen sclerosus and lichen planus, with reports indicating improvements in in- flammation and symptom control (57). Tildrakizumab, an IL-23 inhibitor, showed clinical effectiveness in a case series of 24 pa- tients diagnosed with vulvar lichen planus (58). Oral JAK inhibi- tors such as tofacitinib have demonstrated therapeutic success in the management of vulvar lichen planus (59). The efficacy of apremilast in the treatment of erosive lichen planus has been evaluated, and clinical trials are ongoing to study the use of deucravacitinib (a tyrosine kinase 2 inhibitor) and topical ruxolitinib in treating vulvar lichen planus (60–62). Studies have demonstrated the efficacy of baricitinib and abrocitinib in the treatment of lichen sclerosus (63–65). Conclusions Vulvar pruritus is a common, sometimes disabling symptom, with a broad and multifactorial etiology. The diagnostic process can be complex due to the anatomical and neurophysiological sensitivity of the vulvar region, as well as the overlap of symptoms. After in- fectious, neoplastic, and systemic causes have been addressed or excluded, management should focus on gentle vulvar care, elimi- nating potential irritants and reinforcing skin barrier protection. As with other chronic pruritic conditions, it is crucial to set realis- tic expectations early during treatment because symptom resolu- tion is often gradual and may require long-term follow-up. Despite growing interest in vulvar dermatoses, vulvar pruritus remains an under-researched area with much therapeutic uncertainty. Con- tinued investigation is needed to improve diagnostic accuracy and identify more effective targeted antipruritic therapies with favorable safety profiles. 128 Acta Dermatovenerol APA | 2025;34:123-131 K. Trčko Table 1 | Common vulvar dermatoses. Disease Clinical manifestations Signs/symptoms Additional diagnostic clues Treatment Irritant contact dermatitis (ICD) • Acute:* erythema, edema, vesicles, erosions, usually confined to the contact area; • Chronic:** erythema, dryness, scaling, and fissuring. • Acute: burning, stinging, pain, and skin soreness; • C hr onic: pru r it u s i s oft en a le s s pr ominent symptom than burning and pain. • Exposure to irritants; • Onset of symptoms within minutes to hours of exposure; • Chronic cumulative ICD develops gradually aft er r epe at ed e x po s u r e t o w e a k irr it ant s;** • M a y impr o v e quic k ly aft er r emo v a l of the irritant. • Avoidance of irritants; • Topical steroid, until lesions regress; • Emollients. Allergic contact dermatitis • Acute: erythema, edema, vesicles/blisters; it may extend beyond the initial site of contact, occasionally presenting in a diffuse or spreading pattern; • Chronic: lichenification, scaling, and hyperpigmentation. • Intense pruritus. • T y p ic a l ly oc c u r s 24–48 hou r s aft er exposure to allergens in sensitized individuals; • Persists or recurs upon re-exposure to the allergen; may become chronic if undiagnosed; • Patch testing is diagnostic and helps identify specific allergens. • Allergen*** identification and strict avoidance; • Topical steroid until lesions regress; • Emollients. Atopic dermatitis • Acute: erythema, edema, vesicles, erosions; • Chronic: lichenified erythematous to hyperpigmented plaques with variable scale. • Pruritus. • Early age of onset; • Chronic/relapsing history; • Personal/family history; • Typical age-specific pattern of eczema; • Atopy; • Xerosis cutis; • Elevated IgE. • Topical steroid; • Topical calcineurin inhibitors; • Emollients; • Antihistamines. Lichen sclerosus • Atrophic, white scaly patches/plaques with wrinkled or thinned appearance; • Symmetric distribution; affects labia minora, clitoris, perineal region, vestibule; • “Figure-of-eight” anogenital distribution; • Erythema, ecchymosis occasionally, hyperkeratosis is prominent; • Erosions/fissures/ecchymoses; • Advanced disease: labial resorption, burying of the clitoris, and narrowing of the introitus. • Irritation, pruritus, burning, painful sexual intercourse, dysuria, constipation in girls; • In 1% asymptomatic. • In patients of all age groups; • Mo s t c ommon in po s t menop au s a l/ perimenopausal women and prepubertal girls; • Other body parts can be involved; • M a y h a v e a f ami ly or per son a l hi s t or y of another autoimmune disease (thyroid disease, alopecia areata). • High-potency topical steroid ointment once per d a y; aft er one t o thr ee month s le s s frequently; • Life-long topical steroid maintenance dose in reduced dose (once or twice per week); • Emollients; • Second-line therapy: calcineurin inhibitors (off-label); • Continued follow-up is recommended. Lichen planus • Intense erythema involving the introitus and vagina, whitish striae, and whitish epithelium; • Well-defined and intensely erythematous erosions; • Scarring and adhesions may develop, leading to clitoral burial and potential narrowing of the introitus, with possible extension to the vaginal mucosa. • Early form: pain, severe pruritus, burning; • Late form: dyspareunia, postcoital bleeding, burning; • Rarely asymptomatic. • Oral mucosa: reticulated white patches on buccal mucosa are common; • Other mucous membranes (e.g., vaginal, anal, esophageal) may also be affected; • Vaginal involvement must be assessed using a speculum, wet mount, or biopsy; • Nail dystrophy or scarring in chronic forms; • Cutaneous lesions: flat, polygonal, purple papules (less common in vulvar-only disease); • Biopsy. • High-potency topical steroid ointment once per d a y , aft er one t o thr ee month s le s s frequently; • Life-long topical steroid maintenance dose in reduced dose (once or twice per week); • Emollients; • Second-line therapy: calcineurin inhibitors; • Systemic therapy in therapy-resistant cases;**** • Continued follow-up is recommended. 129 Acta Dermatovenerol APA | 2025;34:123-131 Vulvar itch Table 1 | Continued. Disease Clinical manifestations Signs/symptoms Additional diagnostic clues Treatment Lichen simplex chronicus (LSC) • Thickened and lichenified plaques with excoriations, erosions, hyperpigmentation, or whitish hue due to the presence of scale. • Pruritus; • Rubbing or scratching results in intense pleasure. • Primary LSC: in individuals with an atopic predisposition; • Secondary LSC develops in the context of underlying itchy vulvar pathology; • Pruritus is frequently exacerbated by heat, perspiration, physical activity, mechanical friction, and psychological stress. • Potent topical corticosteroids; • Nighttime antihistamines; • Emollients. Psoriasis • Well-demarcated erythematous plaques with/without scaling on the labia majora, may extend to the inguinal folds; • The labia minora are usually spared. • Pruritus; • Burning, irritation. • Usually accompanied by lesions in other areas (elbows, knees, scalp, nails); • F ami ly and per son a l hi s t or y i s oft en present; • M a y be the on ly m anif e s t ation in in v er se or genital psoriasis. • Topical corticosteroids (low- to mid- potency); • Calcineurin inhibitors (off-label); • Vitamin D analogs (calcipotriol); • Systemic therapy (moderate to severe or refractory cases): methotrexate, cyclosporine, acitretin, biologics. Plasma cell vulvitis • Well-demarcated, erythematous to orange-red macules/patches, involving the introitus, labia minora, or periurethral area; • Lesions may exhibit a glazed, shiny surface with punctate petechiae or telangiectasias; • Typically nonulcerative, even though erosions may occur. • Pruritus, burning, soreness, dyspareunia. • Rare dermatosis; • Fifth t o eighth dec ade s. • Topical steroids; • Topical calcineurin inhibitors (off-label); • Imiquimod (off-label); • Surgical excision; • Cryotherapy; • Carbon dioxide laser ablation. Vulvar intraepithelial neoplasia (VIN) • White, red, brown, or skin-colored papules, plaques, macules, nodules, or thickened areas; • Solitary or multifocal; • Ar e a s t u rn whit e aft er app lic ation of 5% acetic acid (helps in lesion detection); • Erosions more common in differentiated VIN • • Pruritus (most frequent); • Burning, pain, or tenderness; • Dyspareunia; • Irritation or discomfort; • Some cases are asymptomatic, discovered incidentally during routine examination. • Usual-type VIN (uVIN): typically multifocal; associated with human papillomavirus (HPV ) inf ection; oft en oc c u r s in y ou ng er women; lesions may be warty or basaloid; • Differentiated VIN (dVIN): usually unifocal; oc c u r s in o lder w omen, oft en in the background of lichen sclerosus; lesions ar e oft en s u btle, er ythem at ou s, or er oded plaques; higher risk of progression to invasive carcinoma; • Biopsy is essential to confirm diagnosis. • Usual-type VIN (HPV-related): imiquimod; laser ablation; surgical excision; • Differentiated VIN (HPV-unrelated): surgical excision is mandatory due to high malignant potential. Extramammary Paget’s disease • Sharply defined erythematous plaques with whitish scaling and a moist or exudative surface; • The labia majora are most frequently involved, with possible extension to adjacent areas, such as the perineum, perianal region, or inner thighs. • Persistent pruritus; • Burning, pain; • Potentially asymptomatic. • Postmenopausal women; • Slo w gr o w ing, oft en mi sdi agno sed a s chronic eczema; • Biopsy is essential to confirm diagnosis. • Extensive workup to rule out underlying adenocarcinoma; • W ide loc a l e x c i s ion or Mo h s mic r ogr ap hic surgery; • Radiation, laser therapy, and topical therapies (imiquimod); • Follow-up. 130 Acta Dermatovenerol APA | 2025;34:123-131 K. Trčko Table 1 | Continued. Disease Clinical manifestations Signs/symptoms Additional diagnostic clues Treatment Candidiasis • Vulvar edema and erythema; • Vaginal discharge may be absent or present as thick, white, and clumpy with minimal odor—but in some cases it can appear thin, watery, and nonspecific. • Pruritus (most frequent); • Burning, soreness, irritation; • Dysuria, dyspareunia; • Infections with Candida glabrata or other non-albicans species usually resent with mild or minimal signs. • Symptoms frequently worsening before menstruation; • Predisposing factors: diabetes mellitus; treatment with sodium glucose cotransporter 2 inhibitors; use of broad-spectrum antibiotics; increased estrogen levels (e.g., during pregnancy or postmenopausal estrogen therapy); immunosuppression. • Ac ut e: or a l fluc on az o le 150 mg or a l ly gi v en onc e or tw ic e (72 hou r s aft er the fir s t do se) or topical clotrimazole preparations; • C hr onic: or a l fluc on az o le 150 mg f or tw o to three sequential doses, 72 hours apart, followed by maintenance fluconazole 150 mg or a l ly onc e a w eek f or at le a s t 6 months; • C. glabrata : int r a v agin a l bor ic ac id 600 mg daily for 14 days; • C. krusei: intravaginal clotrimazole, miconazole for 7 to 14 days; • All other non-albicans Candida: conventional dose fluconazole; • Pregnancy: topical clotrimazole or miconazole for 7 days. *St r ong irr it ant s: so lv ent s, drug s (5-fluor ou r ac i l , podop h yl lot o x in, t r ic h lor o ac etic ac id). **Cumulative irritants: sweat, urine, feces, semen, vaginal secretions, diapers, perfumes, washcloths, sponges, deodorants, detergents, soaps, cleansers, powders, douches, perfumes, bubble baths, bath oils or salts, depilatory creams, adult or baby wipes, topical antibacterial and antifungal medications, over-the-counter creams, condoms, spermicides, diaphragms, lubricants. ***Common contact allergens: topical anesthetics, (e.g., benzocaine), fragrances (e.g., fragrance mix-I and II, Balsam of Peru, cinnamic alcohol), preservatives (in creams, prescription creams, hygiene products), topical medications (corticosteroids, antibiotics, antimycotics, antiseptics), clothing with azo dyes. ****Methot r e x at e, m y c op heno l at e mof eti l , sy s t emic c or tic o s t er oid s, h y dr o x y c h lor oquine, ac it r etin, minocy c line, cy c lo s por ine. 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