Human Papillomavirus–Induced Squamous Intraepithelial Lesions in Vulvar Lichen Planus

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Approximately 50% of vulvar cancers arise after transforming infections with human papilloma virus (HPV) via the precursor squamous intraepithelial lesion (SIL). Lichen planus (LP)–associated vulvar cancers are typically HPV negative and arise via the precursor differentiated vulvar intraepithelial neoplasia (d-VIN).


An index case of vulvar high-grade squamous intraepithelial lesion (H-SIL) in an LP patient prompted this 12-year retrospective analysis about frequency of HPV-induced SIL in 785 biopsies of 584 patients with vulvar LP. All SIL were analyzed for p53 and p16ink4a overexpression and for presence of DNA of 32 HPV subtypes.


Nine (1.6%) of 584 women with papular (3) and mucosal “erosive” LP (6) presented with H-SIL (7) and low-grade SIL (2). All SILs harbored HPV16-DNA and showed p16ink4a-overexpression. Concomitant immune suppression included T-suppressor lymphocyte deficit (1), systemic (1), and topical (2) cortisone therapy. H-SILs regressed spontaneously (1) or after imiquimod therapy (3). Three women with erosive LP discontinued imiquimod because of side effects and had laser destruction (1), skinning vulvectomy (1), and surgery (1) for definitive treatment. Two women have recurrent vulvar SILs, and 1 woman progressed to invasive SCC. In the same patient population, 16 of 584 women had a d-VIN, and 9 of 16 with progression to SCC.


H-SILs in vulvar LP are rare and may occur in the setting of risk factors. If clinical suspicion arises, biopsy and histological examination assist in correct etiologic classification of a precancerous lesion and subsequent therapy decisions. The minimal risk for H-SIL development in vulvar LP patients should not preclude therapy of LP.

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