Last updated: August 17, 2022

Summarytoggle arrow icon

Vitiligo is a common skin condition in which a patchy loss of epidermal melanocytes results in depigmentation. This loss is hypothesized to be a result of autoimmune destruction, oxidative stress, and/or intrinsic melanocyte defects in genetically predisposed individuals, and is commonly associated with other autoimmune diseases. The clinical course is highly variable, with unilateral or bilateral distribution of well-demarcated, depigmented macules, which may progress during the course of the disease. These lesions have a predilection for facial, acral, extensor, and sun-exposed areas of the body. Vitiligo is often a clinical diagnosis, but Wood lamp examination, dermoscopy, and/or skin biopsy are useful in ambiguous cases. Limited disease may be controlled with topical corticosteroids or topical immunomodulators, while extensive or progressive disease may require systemic therapy, phototherapy, or surgery. Regardless of the treatment modality, patients continue to have episodes of skin depigmentation throughout their lives.

Epidemiologytoggle arrow icon

  • Prevalence: 0.4–2% of the general population worldwide [1]
  • Peak incidence: 10–30 years; can occur in any age group [2]
  • Sex: =

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

  • Vitiligo is characterized by an absence of melanocytes in the depigmented lesions. [2]
  • The etiology is unknown but is thought to be multifactorial. [3]
  • May be triggered by stress or skin injury (e.g., sunburn)

Classificationtoggle arrow icon

According to location [2]

  • Generalized (most common): widespread distribution of lesions, frequently with mucosal involvement
    • Acrofacial: lesions mainly on the hands and face
    • Vulgaris: patches that are widely distributed
    • Mixed: a combination of segmental and non-segmental vitiligo
    • Universal: almost the entire body affected
  • Localized: isolated area affected (e.g., dermatomal)
    • Focal: one or more lesion in one area (commonly trigeminal nerve distribution)
    • Segmental: unilateral, asymmetric lesions that follow dermatomal patterns; a common variant in children
    • Mucosal: only the oral and genital mucosa affected

According to clinical course and prognosis [2]

  • Segmental: early onset, rapidly spreading; depigmented lesions may remain unchanged for life
  • Nonsegmental : A family history and progression of disease are common.

Clinical featurestoggle arrow icon

Diagnosticstoggle arrow icon

Differential diagnosestoggle arrow icon

  • Pityriasis alba: a common hypopigmented scaly patch seen in sun-exposed areas, esp. in children (resolves spontaneously or with topical steroids) [4]
  • Pityriasis versicolor: a fungal infection characterized by scaly hypopigmented macules on the trunk
  • Idiopathic guttate hypomelanosis: multiple hypopigmented macules on the sun-exposed areas; common in elderly individuals
  • Nevus depigmentosus: a well-defined area of depigmentation, present since birth/early childhood, which doesn't enlarge, and requires no treatment
  • Chemical leukoderma: loss of skin pigment due to contact with chemicals

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

Referencestoggle arrow icon

  1. Silverberg NB. The Epidemiology of Vitiligo. Current Dermatology Reports. 2015; 4 (1): p.36-43.doi: 10.1007/s13671-014-0098-6 . | Open in Read by QxMD
  2. Oh SH, Hann S-K. Classification and Clinical Features of Vitiligo. John Wiley & Sons, Ltd ; 2018: p. 33-47
  3. Henning SW, Jaishankar D, Barse LW, et al. The relationship between stress and vitiligo: Evaluating perceived stress and electronic medical record data.. PLoS ONE. 2020; 15 (1): p.e0227909.doi: 10.1371/journal.pone.0227909 . | Open in Read by QxMD
  4. Falabella R. Vitiligo and the melanocyte reservoir. Indian J Dermatol.. 2009; 54 (4): p.313-318.doi: 10.4103/0019-5154.57604 . | Open in Read by QxMD
  5. Aydin AF, Aydıngöz İE, Doğru-Abbasoğlu S, Vural P, Uysal M. Association of Leukotrichia in Vitiligo and Asp148Glu Polymorphism of Apurinic/Apyrimidinic Endonuclease 1.. International journal of trichology. ; 9 (4): p.171-176.doi: 10.4103/ijt.ijt_4_17 . | Open in Read by QxMD
  6. Vitiligo. Updated: August 18, 2020. Accessed: October 25, 2020.
  7. Demirkan S, Onaran Z, Samav G, et al. Decreased choroidal thickness in vitiligo patients. BMC Ophthalmol. 2018; 18 (1).doi: 10.1186/s12886-018-0796-0 . | Open in Read by QxMD
  8. Vitiligo: Diagnosis and Treatment. . Accessed: October 25, 2020.
  9. Rokni GR, Golpour M, Gorji AH, Khalilian A, Ghasemi H. Effectiveness and safety of topical tacrolimus in treatment of vitiligo.. Journal of advanced pharmaceutical technology & research. ; 8 (1): p.29-33.doi: 10.4103/2231-4040.197388 . | Open in Read by QxMD
  10. Grimes PE, Tsao H, Corona R. Vitiligo: Pathogenesis, Clinical Features, and Diagnosis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: February 3, 2017. Accessed: June 18, 2017.
  11. Lyons F, Ousley LE. Dermatology for the Advanced Practice Nurse. Springer Publishing Company ; 2014

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