Advances in Vitiligo Treatment

Abstract

Depigmented patches on the skin and mucosal surfaces are hallmarks of vitiligo, an autoimmune disease that can last for years, often with leukotrichia. Its pathogenesis involves genetic susceptibility, oxidative stress, autoimmunity, and melanocyte defects, with ROS and CD8? T cells contributing to melanocyte destruction. Koebner phenomenon, trichrome lesions, and confetti-like depigmentation are indicators of active disease that support the clinical diagnosis, which is backed by Wood's lamp, histology, and dermoscopy. Treatment aims to halt progression and induce repigmentation. Topical therapies include corticosteroids, calcineurin inhibitors, vitamin D analogues, antioxidants, JAK inhibitors, and prostaglandin analogues. Systemic options include corticosteroids, methotrexate, minocycline, azathioprine, cyclosporine, JAK inhibitors, and melanocyte-stimulating hormone analogues. Phototherapy (PUVA, PUVAsol, NB-UVB), lasers, platelet-rich plasma, microneedling, and surgical grafting are adjuncts, while depigmentation is reserved for extensive or refractory cases. Multimodal, individualized treatment is essential to optimize repigmentation, disease control, and patient quality of life.