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Inflammatory Dermatoses of the Vulva

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Inflammatory Dermatoses of the Vulva Frequently Encountered Vulvar Lesions Lauren Hammock, MD Pathology Consultants, PC NO Disclosures Inflammatory Dermatoses – Benign but self-limited/treatable – Benign with potential for dyplasia/malignancy – Punch biopsy—best if at least 3-4 mm punch Infections Neoplastic—melanocytic lesions – Shave biopsy ok Inflammatory Dermatoses Wide spectrum – Incidental and innocuous to chronic, disabling, refractory to therapy – Usually present with itching, stinging, dysparunia; may be fissured/ulcerated HPV often blamed for symptoms – Finding of nonspecific vulvar acetowhitening prompts biopsy by practitioner – May be overdiagnosed by pathologist as HPV (mimics of koilocytes) Study of 144 patients by Fischer et al in 1995 (Br J Obstet Gynaecol) – Dermatitis is most common cause of chronic vulvar symptoms – 23% of patients in the study also diagnosed with HPV – 50% of the pts with histologic dx of HPV also had evidence of spongiotic dermatitis. Conclusion – HPV should not be regarded as a cause of vulvar symptoms HPV not treatable non-surgically; spongiotic dermatitis usually responds to topical corticosteroids. Vulvar skin – Labia majora Subcutaneous tissue much looser; considerable edema can form – Labia minora Similar to a mucus membrane Surface epithelial features of epidermis Sebaceous glands in lateral walls Vulvar dermatoses may be accurately diagnosed using criteria and classification schemes applied to skin from other sites Classification – International Society for the Study of Vulvovaginal Disease – Comprised of gynecologists, pathologists, dermatologists – Meet every 5 years to evaluate terminology, classification, and approach to clinical diagnoses of vulva. – Lynch et al: J Low Genit Tract Dis. 2012 Oct;16(4):339-44. 2011 ISSVD Terminology and classification of vulvar dermatological disorders: an approach to clinical diagnosis. Spongiotic Dermatitis Term referring to several entities with similar symptoms, histology and treatment (ie. topical corticosteroids). – Irritant contact dermatitis Direct toxicity of a substance without an allergic component Particular predilection for vulva given area of increased friction, overheating due to occlusive clothes and physical activity May be due to medications, douches, lubricants, contraceptives (esp. spermicides) – Allergic contact dermatitis Response to allergen to which there has been previous exposure; ie. benzocaine, meds, scented products; will occur within 12 to 48 hrs post exposure – Seborrheic dermatitis Common in genitocrural folds (flexural areas); may respond to ketoconazole therapy due to association with P. ovale – Atopic dermatitis (‘eczema’) Patients will have eczema elsewhere on skin Lichen Simplex Chronicus Chronic rubbing of pruritic lesions results in thickened skin Clinical findings – Ill-defined hyperkeratotic lesions with lichenification and hyperpigmentation – Mucosa: gray-white; may be better localized Histology – Chronic eczematous dermatitis – May overlie other dermatitides, ie. LS or candidiasis; may also mask dysplasia/neoplasia. LSC changes are often superimposed on many other pathologic disorders – Beware of a more worrisome underlying process such as lichen sclerosus or squamous cell carcinoma. – Biopsy (punch); consider multiple biopsies if large area Carlson, et al observed lichen simplex chronicus either overlying or adjacent to lesions of lichen sclerosus in 82% of LS cases studied Candida colonizes vulva in 20% of women – 5% may suffer repeated bouts of vulvar candidiasis – Less common than vaginal candidiasis Florid dermatitis is often present – Likely role for hypersensitivity Some patients with longstanding symptoms of itchy, moist and erythematous lesions with negative cultures and biopsy results likely have low numbers of organisms – Dramatic response to antifungals Herpes genitalis (HSV 2) Transmitted by close contact with an asymptomatic or symptomatic individual – Asymptomatic viral shedding Latency in sensory nerve ganglia – 50-80% suffer recurrences within 1 year Menstruation is common trigger Paresthesia, burning may precede visible lesion – Systemic symptoms common in primary infection Candidal superinfection common – Erythematous papules>>vesicles>>ulcers Risk factor for HIV acquisition Papulosquamous Dermatoses Psoriasis and lichen planus are the most common lesions with vulvar involvement Clinically present as cutaneous papules or thick, scaly plaques – Labia majora Dry and scaly lesions – Intertriginous areas Smooth, moist, erythematous lesions without scale Lichen planus Common entity of unknown etiology, ? cell- mediated immune mechanism Pruritic, violaceous, flat-topped papules and plaques with fine, white striae Vulvar lesions usually part of a generalized eruption that may also involve vagina, cervix – Inner, keratinized vulvar skin – May heal with post-inflammatory hyperpigmentation – Found in roughly half of 37 women with LP in one series (Lewis, et al; Br J Dermatol, 1996) Sclerosing Dermatoses: Lichen Sclerosus Female anogenital area is most commonly affected area – 11% of women with lichen sclerosus anogenital lesions also have extragenital lesions (Meyrick et al, Br J Dermatol 1988) – Most women with extragenital involvement will have concurrent vulvar involvement. – May occur in children – May be asymptomatic or present with itching, burning, dyspareunia; Extent of lesions does not correlate with symptoms Clinical findings – Variable Pallor and ecchymosis on milder end of spectrum Severe end of spectrum: Loss of distinction between labia majora and labia minora, with sclerosis of the introitus in a “figure-of-eight” pattern that may involve the perianal region Progression>>pinhole-shaped opening posteriorly Vaginal and cervical involvement does not occur Etiology unknown – Thought to be autoimmune; some familial associations Changes of LS frequently found in association with SCC of the vulva – Carlson, et al in a study of 39 cases of vulvar SCC showed LS in surrounding skin in 65% (Hum Pathol 1998) Conclusion: SCC more likely to develop in older women with longstanding, established LS than in younger women with HPV related VIN Also showed loss of p53 in keratinocytes from LS lesions in that group, thus postulating a role for p53 in pathogenesis LS>>>Differentiated VIN>>>SCC Differentiated VIN Precursor lesion to vulvar squamous cell carcinoma – Occurs in setting of longstanding lichen sclerosus (important to treat LS early before sclerotic changes) – Often looks clinically like lichen simplex chronicus – Hyperkeratosis, acanthosis, basal layer atypia, dyskeratosis, dysmaturation, mitoses – Should be treated as VIN3/CIS with excision/partial vulvectomy Melanocytic Lesions Most common are genital nevi (macules or papules) and benign melanotic macules (macule) Genital nevi are ‘special site’ nevi (nipple line, acral) and therefore have significant overlap histologically with dysplastic nevi – Biopsy should include entirety of epidermal component; get around it! Deep part not as important – Consider excisional biopsy first time around if possible If a particularly ‘dysplastic-appearing’ genital nevus extends to margin, pathologist will usually recommend re-excision to ensure complete removal – If marked atypia, some dysplastic nevi over time may progress to melanoma (vast majority do not) – Will likely recur; recurrent nevi may have histologic overlap with melanoma; if biopsied, may get called melanoma (esp if scar from previous biopsy not in the sampled area)>>>much bigger excision than necessary. If questions regarding path report or biopsy: – Please call Pathology Consultants 541-984-8256 to speak with pathologist List of services: www.pathconsultants.com .
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