Vitiligo is a disease characterized by acquired loss of melanocytes, leading to areas of depigmentation.

It is sometimes associated with uveitis and other autoimmune phenomena.

Many autoantibodies can be
demonstrated in vitiligo patients; those against melanocytes may rarely be demonstrable.

There is also a neural hypothesis.
Vitiliginous patches often follow a dermatome.

A neurochemical mediator responsible
for destroying the melanocytes has therefore been suggested.

There is also an occupational vitiligo:

  • Due to chemically induced
  • Seen among workers who are in contact with para-phenolic compounds or hydroquinones (but this is considered a different disorder).

Symptoms and Clinical features of Vitiligo

  1. All ages are affected
  2. The dermatomal type is more common in the paediatric age
  3. The completely depigmented patches have distinct borders.
  4. A few patients may have inflammatory vitiligo with raised erythematous borders.
  5. Some may have hypopigmented skin between the depigmented and normal skin (trichrome vitiligo)

The distribution may be:

  1. Generalized (autoimmune type)
  2. Segmental (dermatomal type)
  3. The hairs on the patches eventually turn white (acquired poliosis)

The generalized type may be symmetrically distributed in the extremities.

Generalized vitiligo continues to spread
while new lesions develop for years.

Spontaneous repigmentation may occur.

Favoured sites are

  1. Extensor surfaces of the extremities
  2. Face and peri-orificial surfaces (around the mouth, eyes, nipples, umbilicus, penis, vulva, and anus)
  3. Focal vitiligo may affect one non
    dermatomal site e.g. lips, vulva or penis
  4. Universal vitiligo applies to cases where the entire body surface is depigmented

Generalized vitiligo may be associated with:

  1. Hyperthyroidism
  2. Hypothyroidism
  3. Pernicious anaemia
  4. Diabetes mellitus
  5. Addison’s disease

Local loss of pigment may occur around a naevus and melanomas, the so-called halo phenomenon.

Vitiligo-like leucoderma occurs in about 1% of melanoma patients.

This is usually a good prognostic sign since it suggests an effective immune reaction against the tumour cells.

Segmental vitiligo affects only one part of the body

  1.  It spreads rapidly in that area and then stabilizes
  2. It is not associated ith autoimmune diseases
  3. Favoured sites are the trigeminal area or an intercostal nerve distribution. (zosteriform pattern)

Just as with albinism, the interplay between the melanocytes of the eyes, ears, and skin is apparent.

The prototype is Vogt-Koyanagi Harada syndrome:

  • Vitiligo of the face, eyelashes, and scalp hair in association with
    • Uveitis
    • Dysacoussis
    • Alopecia areata

Chemical vitiligo affects sites of contact with the chemicals.

When the chemicals are inhaled or a substantial quantity is absorbed through the skin, the distribution of the white patches may simulate the generalized autoimmune type.

Differential diagnoses

  • Post-burns depigmentation
  • Tertiary stage of pinta Morphoea
  • Lichen sclerosis
  • Pityriasis alba
  • Tinea versicolor
  • Piebaldism Hypomelanosis of Ito

Complications of Vitiligo

  • Emotional problems due to cosmetic disfigurement


  • Exclude other autoimmune diseases if clinically suggestive

Treatment for Vitiligo

Treatment objectives

  1. Re-pigmentation
  2. Improve cosmetic appearance
  3. Emotional support

Drug Treatment

A. Topical

i. Corticosteroids

Hydrocortisone 1% or betamethasone valerate

  • Child: apply 1-2 times daily
  • Adult: 0.1% apply once or every 12 hours (for focal or limited lesions)

ii. Psoralens 8-methoxypsoralen (MOP)

0.05% 0.1% in combination with ultraviolet

A radiation (PUVA) for focal or limited

  • Adult and child: apply twice weekly

Tacrolimus 0.1% ointment twice daily for 24 weeks

B. Systemic

i. Systemic 8-methoxypsoralen

  • Adult: 0.5 mg/kg orally
  • The initial UVA dose is 1 or 2 J/cm2, gradually increased.
  • Two or three treatments are done per week for 3-6 months

ii. Systemic corticosteroids

May occasionally be used to arrest the autoimmune process.

Prednisolone tablets 0.5 1.0 mg/kg orally day


  • Pigmented skin grafted onto vitiliginous patches
  • Often the transferred melanocytes
    repigment the depigmented areas

The various techniques include:

  • Suction blister grafts
  • Mini-punch grafts
  • Transfer of either pure melanocyte
    cultures or mixed epidermal cultures to a prepared site

Adjuvant measures

  • Camouflage (cover-up cosmetics)
  • Patient education and emotional support

Notable adverse drug reactions, caution and contraindications


See Dermatitis and Eczema


  • Inadvertent sunburns with blistering
  • Systemic psoralen is contraindicated in:
    • Known photosensitivity
    • Porphyria
    • Liver disease
    • Systemic lupus erythematosus
    • Acquired ochronosis

If systemic therapy is to be used, the following should be done before therapy

  • Ophthalmological examination
  • Full Blood Count
  • Liver function tests
  • Antinuclear Antibody Test

PUVA therapy should be supervised by an experienced dermatologist.

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