vitiligo

Vitiligo results from autoimmune-mediated destruction of melanocytes, leading to loss of melanin production in affected areas. The exact etiology is multifactorial, involving genetic susceptibility, autoimmune mechanisms (including CD8+ T-cell-mediated melanocyte destruction), oxidative stress, and possibly neural or biochemical factors. Histologically, there is an absence of melanocytes in the epidermis, and it can be confirmed via Wood's lamp examination showing enhanced depigmentation under UV light. Clinically, it presents as sharply demarcated, symmetric white macules and patches, commonly on the face, hands, and body folds, and can be associated with Koebner phenomenon (new lesions at sites of trauma). Vitiligo is strongly associated with other autoimmune conditions, including autoimmune thyroid disease (Hashimoto thyroiditis, Graves disease), type 1 diabetes mellitus, pernicious anemia, and Addison disease, reflecting a shared autoimmune predisposition. It should be differentiated from other hypopigmentation disorders such as tinea versicolor (caused by Malassezia, with fine scale, KOH positive) and albinism (a genetic disorder with generalized decreased pigmentation due to defective tyrosinase activity, not patchy loss of existing melanocytes). Management includes topical corticosteroids, calcineurin inhibitors, phototherapy (narrowband UVB), and in refractory cases, depigmentation therapy or surgical options like melanocyte transplantation. It's important for absolute boards knowledge to distinguish vitiligo (autoimmune melanocyte destruction) from other pigmentary disorders and to recognize its association with polyglandular autoimmune syndromes.