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Lichen sclerosus is an atrophic, shrinking disease that usually occurs in postmenopausal women. The main symptom, if any, is pruritus. It can appear in children but remits after the menarche. The skin thins to a dry, shiny, fragile, finely wrinkled, parchment-like appearance and the external genitalia contract and lose their shape and definition. White patches fuse into a symmetric, "keyhole" pattern, often encompassing the perianus. Telangiectasia and mid-line skin "splits" are common. Histologically the epidermis is thin with flattened rete pegs. The dermis is edematous and hyalinized, with a loss of elastic fibers. There is a chronic inflammatory infiltrate in the lichen sclerosus, liken sclerosis, lichen sclorosis, lichen sclerosis
Autoimmunity may play a role in the development. Patients with lichen sclerosus have an increased incidence of autoimmune antibodies and diseases; the main mechanism, however, may be testosterone deficiency or dysfunction. The principle trophic hormone for the ectoderm-derived skin is
In older women there is an association of lichen sclerosus with invasive cancer. Lynch estimates that 4% of patients with lichen sclerosus will develop invasion--a ten fold increased risk. Whether lichen sclerosus plays an etiologic role in carcinogenesis is
Diagnosis can be made by inspection, but biopsy is confirmatory and will also determine if there is a hyperplastic or neoplastic component that would
Treatment is replacement of the deficient hormone. Testosterone propionate (2%) in
Maintenance therapy (about twice weekly) is needed indefinitely. Android side effects such as clitoral hypertrophy, increased libido, and hirsutism merit surveillance and adjustment of dose. Estrogen is
If pruritus is severe, it is best controlled with corticoid cream. This should be used only briefly since it will compound the