Updated: Jul 20, 2022
  • Author: Shekhar Neema, MD; Chief Editor: Dirk M Elston, MD  more...
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Practice Essentials

Vitiligo is an acquired pigmentary disorder of the skin that is characterized by circumscribed, depigmented macules and patches. The condition is frequently associated with disorders of autoimmune origin, with thyroid abnormalities being the most common. See the image below.

Trichrome vitiligo. Trichrome vitiligo.

Signs and symptoms

Vitiligo lesions are characterized as follows:

  • White or depigmented macules and patches
  • Usually well demarcated
  • Round, oval, or linear in shape
  • Borders may be convex [1]
  • Range from millimeters to centimeters in size
  • Enlarge centrifugally over time at an unpredictable rate

Initial lesions occur most frequently on the hands, forearms, feet, and face, favoring a perioral and periocular distribution.

Clinical variants

  • Trichrome vitiligo

  • Marginal inflammatory vitiligo

  • Quadrichrome vitiligo

  • Koebner phenomenon: Development of vitiligo in sites of specific trauma, such as a cut, burn, or abrasion.

See Presentation for more detail.


Although the diagnosis of vitiligo generally is made on the basis of clinical findings, biopsy is occasionally needed for differentiating vitiligo from other hypopigmenting or depigmenting disorders.

Microscopic examination of involved skin shows a complete absence of melanocytes in association with a total loss of epidermal pigmentation. Superficial perivascular and perifollicular lymphocytic infiltrates may be observed at the margin of vitiliginous lesions, consistent with a cell-mediated process destroying melanocytes.

Other documented histologic findings include the following:

  • Degenerative changes in keratinocytes and melanocytes in the border lesions and adjacent skin

  • Increased numbers of Langerhans cells

  • Epidermal vacuolization

  • Thickening of the basement membrane

Loss of pigment and melanocytes in the epidermis is highlighted by Fontana-Masson staining and immunohistochemistry testing. [2, 3]

See Workup for more detail.


Nonsurgical treatments

  • Phototherapy: Induces satisfactory repigmentation in the majority of patients with early or localized disease [4, 5]
  • Topical corticosteroids and topical calcineurin inhibitors can be used separately or in combination
  • Laser therapy: Effective on limited, stable patches of vitiligo
  • Depigmentation therapy: If vitiligo is extensive and attempts at repigmentation have not produced satisfactory results, depigmentation may be attempted in very carefully selected patients
  • Micropigmentation: Tattooing can be used to repigment depigmented skin in dark-skinned individuals


The basic types of repigmentation surgery include the following [6, 7] :

  • Noncultured epidermal suspensions

  • Thin dermoepidermal grafts

  • Suction epidermal grafting

  • Punch minigrafting

  • Cultured epidermis with melanocytes or cultured melanocyte suspensions

See Treatment and Medication for more detail.



Vitiligo is a pigmentary disorder of the skin, which is characterized by circumscribed depigmented macules and patches. Vitiligo is a progressive disorder in which some or all of the melanocytes in the affected skin are selectively destroyed. Vitiligo affects 0.5-2% of the world population, and the average age of onset is 20 years. While vitiligo may be more obvious in patients with darker skin, this disorder does not have a racial or ethnic predilection. [8]



Vitiligo is a multifactorial polygenic disorder with a complex pathogenesis. It is related to both genetic and nongenetic factors. Although several theories have been proposed about the pathogenesis of vitiligo, the precise cause remains unknown. Generally agreed upon principles are an absence of functional melanocytes in vitiligo skin and a loss of histochemically recognized melanocytes, owing to their destruction. However, the destruction is most likely a slow process resulting in a progressive decrease of melanocytes. Theories regarding destruction of melanocytes include autoimmune mechanisms, cytotoxic mechanisms, intrinsic melanocyte defects, oxidant-antioxidant mechanisms, and neural mechanisms, as follows:

  • Autoimmune and cytotoxic hypotheses: Aberration of immune surveillance results in melanocyte dysfunction or destruction. The autoimmune theory proposes alteration in humoral and cellular immunity in the destruction of melanocytes of vitiligo. [9, 10, 11] This theory is of particular relevance given the fact that nonsegmental vitiligo is more frequently associated with autoimmune conditions than is segmental vitiligo. [12] Hence, making a diagnosis of nonsegmental vitiligo in a person with a family history of autoimmune disease may warrant a more thorough workup. For these reasons, certain disorders have been linked to vitiligo, such as: Hashimoto thyroiditis, Graves disease, Addison disease and diabetes mellitus, alopecia areata, pernicious anemia, inflammatory bowel disease, psoriasis, and autoimmune polyglandular syndrome. The most convincing evidence of an autoimmune pathogenesis is the presence of circulating antibodies against melanocyte proteins in patients with vitiligo. [13] In addition to humoral immune mechanisms, strong evidence indicates involvement of cellular immunity. Destruction of melanocytes may be directly mediated by autoreactive CD8 + T cells. Activated CD8 + T cells have been demonstrated in perilesional vitiligo skin. [10, 11]
  • Neural hypothesis: A neurochemical mediator destroys melanocytes or inhibits melanin production.
  • Oxidant-antioxidant mechanisms: An intermediate or metabolic product of melanin synthesis causes melanocyte destruction.
  • Intrinsic defect of melanocytes: Melanocytes have an inherent abnormality that impedes their growth and differentiation in conditions that support normal melanocytes.

Because none of these theories alone is entirely satisfactory, some have suggested a composite hypothesis.

Genetics of vitiligo

Vitiligo is characterized by incomplete penetrance, multiple susceptibility loci, and genetic heterogeneity. [14] Family and twin studies have shown that inheritance is complex and likely involves both genetic and environmental factors. [15] Additionally, it is believed that genetic factors may influence the age of onset of vitiligo. [16] The inheritance of vitiligo may include genes associated with the biosynthesis of melanin, a response to oxidative stress, and regulation of autoimmunity. [17]

Current research has not identified any associations with a certain human leukocyte antigen (HLA) type in a consistent manner. There is reason to believe that segmental vitiligo and nonsegmental vitiligo may have distinct genetic mechanisms, which could account for their different responses to treatment.



In the United States, the relative rate of vitiligo is 1%. Vitiligo is relatively common globally, with a rate of 1-2%. Approximately 30% of vitiligo cases occur with a familial clustering of cases.

A female preponderance has been reported for vitiligo, but it is not statistically significant and the discrepancy has been attributed to an increase in reporting of cosmetic concerns by female patients.

Although vitiligo may appear at any time from birth to senescence, onset is most commonly observed in persons aged 10-30 years. The average age of onset for vitiligo is approximately 20 years. The age of onset is unlikely to vary between the sexes.