| Etiology | • Persistent HPV infection (high risk serotypes) • Chronic inflammation | | --- | --- | | Risk factors | • Tobacco use • Vulvar lichen sclerosus • Immunodeficiency • Prior cervical cancer • Vulvar/cervical intraepithelial neoplasia • Lichen sclerosus | | Clinical features | • Vulvar pruritus • Vulvar plaque/ulcer • Abnormal bleeding | | Diagnosis | • Biopsy |
if the lesion is neoplastic, additional management is indicated. Patients with noninvasive disease can be treated with either medical therapy (eg, imiquimod) or laser ablative therapy
Those with invasive disease require surgery (eg, wide local excision ± lymph node dissection) and possible chemoradiation.
Most HPV infections are transient, patients with either chronic tobacco use or immunodeficiency (eg, HIV) are less likely to clear the infection, resulting in dysplastic changes.
Constant dysplastic changes over the vulvar squamous cells can result in a unifocal, erythematous friable plaque or ulcer, typically on the labia majora, that produces persistent vulvar irritation (eg, vulvar excoriations, erythema) and/or pain. Patients may also have intermittent bleeding and dyspareunia(as seen in this patient) or an asymptomatic lesion found on routine examination. Diagnosis is with vulvar biopsy, which evaluates for depth of invasion and determines management options.
Patients with chronic lichen sclerosus have continued inflammation and hyperplasia of the vulvar epithelium that can result in malignant transformation and development of a neoplastic lesion. This lesion typically develops over the labia majora and can become pruritic, friable, and ulcerated.
In patients with lesions concerning for malignancy, the best next step in management is vulvar biopsy, which distinguishes between benign (eg, lichen sclerosus) and neoplastic disease
In those with neoplastic changes, biopsy further determines the depth of invasion and differentiates between noninvasive (ie, vulvar intraepithelial neoplasia) or invasive (ie, vulvar cancer) disease.