Vulvar lichen sclerosus: an immunologic study.

OBJECTIVE: To investigate the seroimmunologic (CD3, CD4, CD8 lymphocytes, C3c and C4 complement fractions, and several autoantibodies) and immunohistochemical (T lymphocyte subpopulations, B lymphocytes, natural killer cells, macrophages, immunoglobulin [Ig] G, Ig M, and C3c complement fraction) characteristics of vulvar lichen sclerosus. METHODS: Serum samples from 68 women with histologically proven lichen sclerosus were compared with those from 53 healthy controls, and tissue samples from 14 of 68 women chosen at random were compared with those from 14 of 53 healthy controls. A scoring system was constructed to compare the number of cells in the tissue. RESULTS: Patients had significantly lower counts of circulating lymphocytes CD3 and CD4 than controls (P < .05) and a higher number of autoantibodies (P < .01). Analysis of the tissue samples confirmed a lower number of CD2 cells (two-tailed P = .002 in epidermis, .005 in dermis), CD3 cells (two-tailed P = .001 in epidermis and in dermis), CD4 cells (two-tailed P = .002 in epidermis, .011 in dermis), and CD8 cells (two-tailed P = .002 in epidermis, .051 in dermis) in subjects than in controls. Numbers of monocyte-macrophage cells were similar in the epidermis but different in the dermis (two-tailed P = .003). No natural killer CD56 cells or B lymphocytes (CD19-CD21) were detected in the affected areas. Deposits of IgG, IgM, and C3 were no greater in biopsy specimens of patients than in those of controls. CONCLUSION: Vulvar lichen sclerosus is not caused by a T cell-mediated response, and a viral origin is unlikely. The absence of CD19 and CD21 cells excludes local production of autoantibodies. Our data do not confirm an autoimmune pathogenesis for vulvar lichen sclerosus but help explain why systemic cortisone is of no benefit and justify the use of petroleum jelly to relieve pruritus.

Immunological study of vulvar lichen sclerosus: preliminary considerations.

Sclero-atrophic lichen (LSA) is a dermatosis that is well defined from the clinical and histological viewpoints, but the etiology remains unknown. The main symptom is a permanent pruritus which results in a gynecological consultation. We have studied the immunological status of 48 patients with LSA and 33 controls. The LSA patients showed a significant diminution of peripheral CD3 and CD1 and tissue CD2, CD3, CD1 and CD8. There was no difference of IgG, IgM or tissue C3c, or serum C3c and C4. These patients also had a higher incidence of autoantibodies.