About one in every 200 persons in the US and Europe have this puzzling condition. Although it’s mostly considered a cosmetic problem with no serious ill-effects, it can be psychologically very distressing to sufferers.

For a third of patients, the condition is temporary and resolves spontaneously. But for the rest, the condition is permanent, and may be a sign of a general autoimmune disorder heralding the later development of other conditions such as Addison’s disease (where the adrenals are exhausted), diabetes, pernicious anaemia, an overactive or other thyroid disorders and even patchy hair loss (alopecia areata).

What causes it? Although all experts agree that the condition results from the destruction of melanocytes in the epidermis, no one has a clue as to why it happens. It is generally agreed that oxidative stress plays some role in the process. The latest research from the National Vitiligo Foundation in Tyler, Texas, advances the hypothesis that melanocytes of patients with vitiligo have a molecular alteration that makes them more susceptible to cell death when challenged by, say, too much sunlight (ultraviolet B radiation) or exposure to phenol (disinfectants) or catechol (used in dyeing and tanning). Some believe there is a link with emotional and physical stress.

Studies at Loyola University Medical Center in Chicago have shown that immune cells are present in the skin when it is actively losing pigment. What’s more, the immune cells appear to be in direct contact with the cells that normally produce skin pigment.

This suggests that an immune response is in some way involved in the process that results in the destruction of pigmentation cells (Lab Invest, 2000; 80: 1299-309). Although scientists still do not know what the immune cells are responding to, it is believed that it is the proteins that are found exclusively in melanocytes. Again, the findings suggest that the trigger mechanism may be too much sun exposure, which vitiligo sufferers are especially sensitive to.

What doctors tell you The usual treatment is to cosmetically disguise, attempt to repigment the skin, or take the if-you-can’t-beat-’em approach and strip the rest of the skin of its pigment.

In mild cases, the usual treatment is topical corticosteroids such as triamcinolone acetonide, which appears to be effective, but at a cost, particularly in younger patients who have to use them long term. Topical steroids have the same effects as their oral cousins, including thinned skin, a humpback, osteoporosis, growth problems and immune disorders. Doctors also suggest that patients expose patches the affected skin to the sun in the hope that the ultraviolet radiation will promote repigmentation.

For more extreme cases, the most accepted treatment is to attempt to attract more pigmented cells to the skin surface using psoralen plus ultraviolet A (PUVA) radiation. This can cause nausea, skin blistering, and liver and eye damage, such as cataracts. Doctors may also attempt to destroy pigment, usually with benoquin, a mix of monobenzone and hydroquinone. This leaves the skin a ghostly white, and may also cause skin inflammation, contact dermatitis, greying hair, photosensitivity and corneal pigment deposits.

Lynne McTaggart