FAQ | Pigmentation Disorders

Pigmentation of the skin normally varies according to racial origin and the amount of sun exposure. Pigmentation disorders are often more troublesome in skin of colour. The melanocytes of dark skinned people produce more melanin than those of people with light skin. This is not modifiable. Dark skin always tans fast on exposure to sun light. The pigment cells or melanocytes are located at the base of the epidermis and produce the protein melanin. Melanin is carried by keratinocytes to the skin surface. The melanisation process in dark skin is protective against sun damage, but melanisation in white skin (for example after sunburn) is much less protective. So melanoma skin cancer is very rare in dark skin.

Generalised hyperpigmentation

If pigmentation affects an exposed site, daily application of broad-spectrum SPF 50+ sunscreen is important to minimise darkening caused by UVR. Cosmetic camouflage can be used. The following agents can be used to lighten epidermal melanosis, alone or, more effectively, in combination: hydroquinone, topical retinoid, topical corticosteroid, glycolic acid and other fruit acids, azelaic acid, L-Ascorbic acid (vitamin C). Do not any of the medication without prescription from the doctor. Resurfacing using chemical peels, laser, intense pulsed light (IPL) or dermabrasion may be effective but unfortunately risks further damage to the epidermis and formation of more pigment. Cosmetic camouflage using make-up is sometimes the best advice.


Vitiligo is an acquired depigmenting disorder of the skin, in which pigment cells (melanocytes) are lost. It presents with -white patches of skin. Vitiligo can be cosmetically very disabling, particularly in people with dark skin. Vitiligo affects 0.5–1% of the population, and occurs in all races. It may be more common in India than elsewhere. In 20%, other family members also have vitiligo. Males and females are equally affected. The exact cause of vitiligo is unknown. It is thought to be a systemic autoimmune disorder, associated with deregulated innate immune response. Common sites are exposed areas (face, neck, eyelids, nostrils, finger tips and toes), body folds (armpits, groin), nipples, navel, lips and genitalia. Vitiligo also favours sites of injury (cuts, scrapes, thermal burns and sunburn). Blood tests to assess other potential autoimmune diseases or polyglandular syndromes may be arranged, such as thyroid function, B12 levels and autoantibody screen. Treatment of vitiligo is currently unsatisfactory. Repigmentation treatment is most successful on face and trunk; hands, feet and areas with white hair respond poorly. Compared to longstanding patches, new ones are more likely to respond to medical therapy. Minimise skin injury: wear protective clothing. Treatments for vitiligo include: Corticosteroid creams, calcineurin inhibitors, Phototherapy ( narrowband (311 nm) UVB, Excimer laser UVB (308 nm) or targeted UVB for small areas of vitiligo or photochemotherapy (PUVA). If repigmentation is observed, treatment is continued until repigmentation is complete or for a maximum of 1–2 years.

Surgical treatment of stable vitiligo: Surgical treatment for stable and segmental vitiligo requires removal of the top layer of vitiligo skin (by shaving, dermabrasion, sandpapering or laser) and replacement with pigmented skin removed from another site.