Lichen Sclerosus

❍ At a glance

• Lichen sclerosus is underdiagnosed and undertreated, frequently dismissed as thrush or generalised itch. Untreated LS causes progressive architectural destruction of the vulva and carries a 4-5% lifetime risk of vulval squamous cell carcinoma.¹ Good adherence to topical steroid treatment substantially reduces, though does not eliminate, this risk.²
• Classic triad: intractable vulval itch (worse at night), white atrophic crinkled skin in a figure-of-eight distribution around the vulva and anus, and architectural changes (loss of labia minora, clitoral phimosis, introital narrowing). Posterior fourchette fissures are common and often misattributed to Candida.
• Treatment: clobetasol propionate 0.05% (Dermovate) ointment - induction (daily for 4 weeks, alternate nights for 4 weeks, twice weekly for 4 weeks) then ongoing maintenance as needed. Many women require indefinite twice-weekly use to control symptoms and prevent progression. Under-application is the most common reason for treatment failure.
• Annual review for all established LS, with examination for suspicious areas (thickening, erosion, non-healing ulceration). Urgent referral for any area suspicious for VIN or SCC.

❍ Presentation, diagnosis, and treatment

Presentation: intractable vulval itch worse at night, soreness, dyspareunia, and sometimes painful defecation (perianal involvement is common - the figure-of-eight distribution is characteristic). Examination shows white, atrophic, crinkled ("cigarette-paper") skin of the labia minora, clitoral hood, interlabial sulci, perineum, and perianal skin. Established disease: loss of labia minora (resorption), clitoral phimosis, and introital narrowing. Posterior fourchette fissures are common. In children, LS can be mistaken for sexual abuse; ecchymosis in the absence of trauma is a feature of LS, not necessarily injury.

Diagnosis: clinical in typical presentations - biopsy before starting treatment is not required. Biopsy is indicated when the diagnosis is uncertain, symptoms fail to respond to appropriate treatment, or any area appears suspicious for VIN or SCC.

Treatment: clobetasol propionate 0.05% ointment (preferred over cream - less irritating, better absorbed, avoids preservative contact sensitivity). Standard induction: once daily for 4 weeks, alternate nights for 4 weeks, twice weekly for 4 weeks, then ongoing maintenance as needed. Ensure the entire affected area is treated, including perianal skin. Many women under-apply - inadequate treatment is the most common reason for failure. Skin atrophy concern: at maintenance doses, the benefit-to-risk ratio strongly favours treatment. LS itself causes far more architectural damage than appropriately used topical steroids. Bland emollients (soft white paraffin, petroleum jelly) provide a protective barrier and reduce itch. Avoid soap, scented products, and fabric conditioner on the affected area.

Second-line: topical tacrolimus or pimecrolimus (calcineurin inhibitors) for women who cannot use or do not respond to topical steroids. Introital narrowing: supervised vaginal dilator use; surgical assessment if severe.

❍ Surveillance and referral

Annual review for all established LS: assess symptom control (itch, soreness, dyspareunia); inspect for disease progression, architectural change, and any suspicious areas (thickening, erosion, warty or nodular lesion, non-healing ulceration or leucoplakia not responding to treatment). Educate women to self-examine and report new lumps, persistent sores, or worsening symptoms between reviews.

Refer to dermatology or a specialist vulval clinic for: diagnostic uncertainty; failure to respond to appropriately used clobetasol after 3 months; suspected VIN or SCC (urgent, two-week referral); significant introital narrowing requiring surgical assessment; or children with suspected LS (require specialist assessment). In NZ, specialist vulval clinics are available in major centres through the public hospital system.