Current Debates on Etiopathogenesis and Treatment Strategies for Vitiligo

Curr Drug Targets. 2022;23(13):1219-1238. doi: 10.2174/1389450123666220406125645.

Abstract

Vitiligo is an acquired, chronic, and progressive depigmentation or hypopigmentation characterized by the destruction of melanocytes and the occurrence of white patches or macules in the skin, mucosal surface of eyes, and ears. Melanocytes are the melanin pigment-producing cells of the skin which are destroyed in pathological conditions called vitiligo. Approximately 0.5 - 2.0% of the population is suffering from vitiligo, and a higher prevalence rate of up to 8.8% has been reported in India. It is caused by various pathogenic factors like genetic predisposition, hyperimmune activation, increased oxidative stress, and alteration in neuropeptides level. Genetic research has revealed a multi- genetic inheritance that exhibits an overlap with other autoimmune disorders. However, melanocytes specific genes are also affected (such as DDR1, XBP1, NLRP1, PTPN22, COMT, FOXP3, ACE, APE, GSTP1, TLR, SOD, and CTLA-4). A number of therapeutic options are employed for the treatment of vitiligo. The topical corticosteroids and immunomodulators are currently in practice for the management of vitiligo. Phototherapies alone and in combinations with other approaches are used in those patients who do not respond to the topical treatment. The main focus of this review is on the etiopathological factors, pharmacological management (phototherapy, topical, systemic, and surgical therapy), and herbal drugs used to treat vitiligo.

Keywords: Depigmentation; autoimmune; melanin; melanocytes; neuropeptides; oxidative stress; vitiligo.

Publication types

  • Review

MeSH terms

  • Administration, Topical
  • Humans
  • Hypopigmentation* / pathology
  • Melanocytes / pathology
  • Phototherapy
  • Vitiligo* / genetics
  • Vitiligo* / therapy