Vitiligo !

Vitiligo is a long-term condition in which the immune system destroys pigment cells, leaving sharp milk-white patches. It is not contagious.

Updated 2026-11-01

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Why it happens

What it is

An acquired, chronic depigmenting disorder in which melanocytes are lost from the epidermis, producing well-defined white (amelanotic) macules and patches. It is mostly autoimmune and often occurs with other autoimmune diseases.

Who gets it

Affects roughly 0.5–2% of people worldwide, with no difference between sexes or skin types, although it is far more visible and stigmatising in darker skin, common in Colombia and Latin America. About half of cases start before age 20.

Causes

Autoimmune destruction of melanocytes by cytotoxic CD8+ T cells
Genetic predisposition; family history in a sizeable minority
Oxidative stress in melanocytes and triggers such as skin trauma (Koebner phenomenon), sunburn or emotional stress

Risk factors

Personal or family history of autoimmune disease, especially autoimmune thyroid disease
Family history of vitiligo
Type 1 diabetes, pernicious anaemia, Addison disease or alopecia areata
Repeated friction or injury to the skin

Pathophysiology

Stressed melanocytes release signals that activate innate immunity and then autoreactive CD8+ T cells. Interferon-gamma and the chemokine CXCL10 recruit more T cells, which kill melanocytes in the basal epidermis. Without melanocytes the skin cannot make melanin, so patches turn white; hair in the patch may also turn white (leukotrichia), which predicts poorer repigmentation.

Classification

Non-segmental (generalised) vitiligo: symmetric patches, the most common form, linked to autoimmunity
Segmental vitiligo: one-sided, follows a band of skin, starts early and usually stabilises quickly
Mixed and unclassified forms (focal, mucosal)

Symptoms and signs

Sharply demarcated milk-white or chalk-white macules and patches without scale
Typical sites: around the eyes and mouth, hands, fingertips, wrists, elbows, knees, genitals and skin folds
White hair, eyelashes or eyebrows within patches (leukotrichia)
New patches at sites of injury (Koebner phenomenon)
Usually no itch or pain; sunburn in depigmented skin
Psychological distress, low self-esteem and stigma

Diagnosis

Clinical: Usually clinical: typical distribution of sharply defined white patches. Wood's lamp shows bright blue-white fluorescence and reveals patches hard to see in light skin. Check for leukotrichia, Koebner lesions and signs of activity.
Tests: TSH and anti-thyroid peroxidase antibodies are commonly checked because thyroid autoimmunity is the most frequent association; other autoimmune screening (glucose, blood count, vitamin B12) guided by symptoms. Biopsy only in doubtful cases, showing absent melanocytes.
Imaging: Not needed. Dermoscopy can help separate vitiligo from other hypopigmented lesions.

Differential diagnosis

Pityriasis versicolor (fine scale, positive KOH)
Pityriasis alba (ill-defined, scaly, in children with atopy)
Post-inflammatory hypopigmentation
Leprosy (hypopigmented patches with loss of sensation)
Piebaldism and other congenital depigmentation; chemical leukoderma

Goal of treatment

Stop the spread of active disease, encourage repigmentation, protect depigmented skin from the sun, and support quality of life; associated autoimmune disease is sought and treated.

Treatment

Medical: Topical corticosteroids and topical calcineurin inhibitors (tacrolimus, pimecrolimus) are first-line for limited disease, the latter preferred on the face and folds. Topical JAK inhibitors (ruxolitinib cream) are a newer option.
Procedure: Narrowband UVB phototherapy is the main treatment for widespread or progressive disease; short courses of oral corticosteroids may be used to halt rapidly spreading disease.
Surgical: Melanocyte or skin grafting in stable disease, mainly segmental vitiligo, that has not responded to other treatments.
Lifestyle: Sun protection of white patches, avoiding skin trauma, and cosmetic camouflage; psychological support and patient groups.

Complications

Sunburn and photodamage in depigmented skin
Psychological impact: anxiety, depression, stigma
Associated autoimmune disease, mainly thyroiditis
Ocular and hearing changes are described but rarely significant

Prognosis

Course is unpredictable, with periods of spread and stability. Repigmentation is best on the face and neck and poorest on hands, feet and lips or where hair has turned white. Segmental vitiligo tends to stabilise early.

Test yourself

Think of the answer, then tap the question to see it.

Which cell is lost in vitiligo, and what immune cell destroys it?

The melanocyte, destroyed mainly by autoreactive cytotoxic CD8+ T cells.

Which autoimmune disease is most often associated with vitiligo?

Autoimmune thyroid disease (Hashimoto thyroiditis or Graves disease); TSH and anti-TPO are commonly checked.

What does a Wood's lamp show in vitiligo?

Bright blue-white fluorescence of the depigmented patches, making them stand out sharply.

What is the main treatment for widespread or progressing vitiligo?

Narrowband UVB phototherapy.

How does segmental vitiligo differ from non-segmental vitiligo?

It is one-sided in a band, starts early, stabilises quickly and is less linked to autoimmunity.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Vitiligo (MedlinePlus, US National Library of Medicine, 2026); Vitiligo (National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), 2026).

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Representative model, for educational purposes only.

Skin highlighted on the Durgical 3D model