Vitiligo

Skin colour comes from melanin, a pigment produced by specialised cells called melanocytes, located in the basal layer of the epidermis. In vitiligo, melanocytes disappear from certain areas of the skin, and where they are missing the skin remains white, completely depigmented. The best documented mechanism is autoimmune: the immune system mistakenly recognises melanocytes as foreign and attacks them. A genetic predisposition and increased oxidative stress within the melanocytes, which makes them more vulnerable, both contribute to this process.

Who is affected. Vitiligo occurs in about one in a hundred people, across all populations and equally in both sexes. It most often begins before the age of thirty, sometimes in childhood. Roughly one patient in five has a relative with the same condition, but the disease is not inherited according to a simple rule.

Types of vitiligo.

• Non-segmental vitiligo — the most common form, with patches usually distributed symmetrically on both sides of the body: around the eyes and mouth, on the hands, elbows, knees, armpits and genital area. It progresses in flares, alternating stable periods with periods of spread.
• Segmental vitiligo — patches appear on one side of the body only, usually within a limited territory; it often starts earlier in life, spreads quickly for a few months and then remains stable for a long time. It may also affect the hairs in the area, which turn white.
• Mixed or undetermined forms — when the distribution does not clearly fit the patterns above, for example vitiligo confined to the mucous membranes or to the fingertips.

Triggering and contributing factors. Patients frequently report an event that preceded the appearance of the patches:

• sunburn or intense sun exposure;
• skin injury, repeated mechanical friction, cuts or surgery — patches may appear exactly over the injured area, a phenomenon known as the Koebner response;
• marked emotional stress, bereavement, periods of overwork;
• occupational contact with certain chemicals, particularly phenolic derivatives;
• infections or acute intercurrent illnesses.

Associations. Being autoimmune in nature, vitiligo may be associated with other conditions in the same category: autoimmune thyroiditis and other thyroid disorders, pernicious anaemia, type 1 diabetes, alopecia areata and Addison disease. For this reason, the initial assessment usually includes a check of thyroid function.

What the patient notices and how it evolves. The first sign is usually a smooth white patch, without scaling and without itching, with sharp borders that are sometimes slightly more pigmented than the neighbouring skin. Patches may stay unchanged for years or may spread in unpredictable waves. Spontaneous repigmentation is possible, especially in children and in areas rich in hair follicles, and typically starts as small pigmented dots around the hairs. Areas without follicles — the fingertips, the lips — repigment with the greatest difficulty.

Sun protection. Depigmented skin no longer has the natural defence provided by melanin and burns easily. Consistent protection — covering clothing, a hat, avoiding the middle hours of the day and creams with a high protection factor — reduces the risk of burning, limits the colour contrast with tanned healthy skin, and helps prevent new lesions arising through the Koebner phenomenon.

What makes it worse. Sunburn, friction from tight clothing, straps or belts, aggressive cosmetic procedures and prolonged periods of stress can encourage the patches to spread.

At our practice, vitiligo is approached through the Kozak Method — internal and external treatment, individualised, based on consultation. Results differ from one patient to another.