Abstract :
Vitiligo is also known as Safed Daagh, Safed Kodh, Phuleri and Savitra in vernacular. Vitiligo causes social and psychological distress, affecting 0.1 to 2 Percent global population. The pathology demonstrates depigmentation of the skin, with loss of melanocytes by autoreactive cytotoxic T cells. The vitiligo-infiltrating lymphocytes were T lymphocytes, and most were CD8 The elevated levels of H2O2 in the skin mediate the production of proinflammatory cytokines like IL-1β, IL6, and IL-8 indirectly by activating the calreticulin pathway. Autoimmunity in vitiligo is driven by the IFN-?-CXCL10 cytokine (motif chemokine ligand) signaling pathway. No drug can stop the process of vitiligo. Most of the drugs are used in combination. Light therapy can help to restore some color. Topical steroids, calcineurin inhibitors, and narrow-band ultraviolet (UV)–B phototherapy are widely used. New depigmenting therapies are emerging such as helium-neon (He–Ne) lasers and prostaglandin E2 analogs. In cases of stable disease, surgical procedures such as skin grafting, blister grafting, orCellular suspension transplant are often tried. Ruxolitinib is the first medication that can restore pigment in patients with nonsegmental vitiligo. Tildrakizumab is also being evaluated in form of Topical Cream. Unfortunately, vitiligo is life long condition which is difficult to treat with satisfaction.
Keyword :
Vitiligo, Disease, Pathogenesis, Melanocytes, Steroids, Biologicals