ANA-negative systemic lupus erythematosus

CMYK243 Kanwar et al reported 20-nail dystrophy in a patient of AA due to LP. Brenner et al reported a case of coincidence of five dermatological disorders: vitiligo, AA, onychodystrophy, morphea and LP. Similarly, ulcerative colitis, myasthenia gravis, LP, AA and vitiligo were present in a single patient reported. Patients with AA were found to be at a higher risk for developing LP (RR=2.7; 95% confidence interval, 1.1 to 6.5). However, co-localization is very rare. Dhar et al had reported one child with co-localization of lesions both conditions. The incidence of AA in the Indian population is 0.7%7 whereas it is 0.8% for LP.8 The coexistence of these disorders may be purely coincidental. Gilhar et al found that induction of AA was possible with injection of CD8+ cells cultured with follicular homogenate but not with cultured CD4+ cells. The T lymphocyte is also pivotal in regulating epidermal cell recognition and epithelial destruction in lichen planus. T cells become activated via antigen-presenting cells such as Langerhans cells in conjunction with epidermal keratinocytes and co-stimulatory molecules. Though both CD4+ and CD8+ T cells are found in the lesional skin of LP, progression of disease leads to the preferential accumulation of CD8+ cells. The majority of the lymphocytes in the infiltrate of LP are CD8+ and CD45RO (memory)-positive cells and express the g/d T-cell-receptor. The ensuing immune reaction by CD8+ T lymphocytes against activated keratinocytes results in epidermal cell damage and development of the lichenoid reaction that is the hallmark of lichen planus.