Vitiligo

Vitiligo

 Key Points
Condition is an autoimmune disease due to destruction of pigment cells resulting in white, irregularly-shaped patches on the skin and premature greying of hair.
Condition occurs in all races and genders, often following physical injury or emotional stress.
There is no known cause of vitiligo.
The severity and de-pigmentation process vary from patient to patient.

Vitiligo is an autoimmune disease resulting in white, irregularly-shaped patches on the skin due to destruction of pigment cells (melanocytes). Any part of the body can be affected, including exposed areas (face, neck, eyes, nostrils, nipples, navel, genitals), body folds (armpits or groin), sites of injury, and around pigmented Moles (halo naevi). Vitiligo may cause premature greying of the hair on the scalp, eyebrows, eyelashes and body. White hair is called Poliosis. The retina may also be affected.

Vitilgo occurs in all races and genders. Pigment loss begins before age twenty in half of sufferers. Often it follows physical injury or emotional stress. While typically in good health, Vitiligo patients face a greater risk of other autoimmune diseases — diabetes, Thyroid disease, pernicious anaemia, Addison's disease, and alopecia areata.

The cause of vitiligo is unknown. Usually, it is a direct result of defect of the melanin-producing cells called melanocytes. There are three prevailing theories — abnormally functioning nerve cells damage the pigment cells, an autoimmune reaction against the pigment cells, or the pigment cells themselves are autotoxic (self-destructive).

The severity of Vitiligo differs with each individual, typically depending on the natural skin tone. Lighter skinned people may not notice difference until summer because of contrast between tanned skin and affected. Darker skinned people may notice the change immediately. In severe cases, pigment may be lost from the entire body and the eyes do not change color. The vitiligo patches themselves may show variance in different shades of white or brown — often called trichrome. Vitiligo begins with a rapid loss of pigment, followed by a period of no change, which may be then followed by even more pigment loss. The process can stop or continue haphazardly.

Differential Diagnosis (Other conditions with similar appearances)
Addison Disease
Halo nevus
Leprosy
Malignant Melanoma
Onchocerciasis (River Blindness)
Piebaldism
Prior treatment with corticosteroids
Scleroderma
Tuberous sclerosis
Waardenburg Syndrome

Diagnosis
Key Points
Diagnoses is based primarily on inspection under a Wood lamp.
Biopsies are useful to determine other autoimmune diseases.

There is no real diagnosis for vitiligo other than inspection under a Wood lamp or recognition of pigmentation loss or skin discoloration. Biopsies can be performed to determine whether or not the white patches of discoloration are the result of a different autoimmune disease or other condition.

Treatment
Key Points
There currently is not a satisfactory treatment for vitiligo.
Preventative measures such as minimising skin injury and sun protection tend to be most effective.
* Topical cortisone creams, calcineurin inhibitors, narrowband UVB phototherapy, PUVA, surgical dermabrasion, and de-pigmentation therapy are all potential treatments.

Preventative measures are the best bet to prevent the spread of vitiligo. Patients are encouraged to minimise skin injury to prevent further patches and protect the white discolored patches from sun exposure as they will burn and also cause further spread of Vitiligo. Typically, the sun protection consists of wearing protective clothing, staying out of peak period sunlight, and applying sunscreen preferably 30+ SPF. Cosmetics, skin dyes, and water-resistant concealer can be used to disguise the vitiligo.

There are various treatments currently in use, but none of them are considered satisfactory. A potent anti-inflammatory cortisone cream may reverse the process if applied to the affected areas for a few weeks in their early stages. Calcineurin inhibitors — such as topical pimecrolimus and tacrolimus — have shown to be safe and effective, and especially useful on the face and neck where strong steroid creams may cause skin thinning. Narrowband UVB phototherapy, in combination with the calcineurin inhibitors and calcipotriol cream, has been helpful for many patients. PUVA ultraviolet light treatment has shown gradual but partial re-pigmentation, with poor response in hands and feet, but only is recommended in prolonged cases and is deemed unsuitable for fair skinned people and children. Surgical treatment has been effective, sandpapering or dermabrading the affected areas and replacing them with skin from normally pigmented areas. And for certain dark skinned people, de-pigmentation therapy has been successful, but does result in a total loss of pigment in the skin.