Randy Jacobs, M.D. Patient Education

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Vitiligo is an auto immune condition which results in depigmentation: various sized, white, sharply demarcated macules and patches of the skin. In vitiligo, the patient's own immune system is responsible for "attacking" the skin's own pigment cells. Because the pigment cells are "attacked," the skin loses its color. Vitiligo is an auto immune condition similar in mechanism to rheumatoid arthritis. In rheumatoid arthritis, the patient's own immune system is responsible for attacking the joints, resulting in inflammation and arthritis. In vitiligo, the patient's own immune system attacks the pigment cells of the skin. Your immune system normally functions to attack and remove foreign invaders such as viruses, bacteria, and tumor cells. Auto immune conditions occur when the patient's own immune system malfunctions and mistakenly attacks the wrong thing. In the case of vitiligo, the immune system mistakenly attacks pigment cells, because the immune system mistakenly thinks that the pigment cells are foreign to the body. Vitiligo is sometimes familial, but not always. Vitiligo has been associated with Addison's disease, diabetes, pernicious anemia, and thyroid disease.


What causes vitiligo?

One clue is that vitiligo is sometimes passed from one generation to another, suggesting there are genetic factors that determine whether or not an individual is susceptible to having vitiligo. This may depend on the genes they inherit from their parents. Unlike other "well known" genetic diseases involving single genes, such as cystic fibrosis, vitiligo and other autoimmune diseases appear to involve many susceptibility genes. Some of these genes might be important for the immune system, which normally patrols the body and eliminates infectious agents and tumor cells. But in some vitiligo patients the immune system appears to attack and destroy melanocytes, the pigment-producing cells of the skin. Other vitiligo susceptibility genes might be involved in melanocyte function, as researchers have shown that there are biochemical differences in the skin cells of vitiligo patients. Finally, there are also probably environmental factors, such as viral infections or damage to the skin caused by sunburn or trauma, which may contribute to the onset and/or progression of vitiligo.


Clinical presentation:

Vitiligo consists of various sized, white, sharply demarcated macules and patches of the skin. In vitiligo, centrifugal growth with coalescence of adjacent lesions often results in the formation of large irregularly shaped areas of depigmentation. This gyrate configuration in such patients is quite distinctive. No scales are present visually, or by scraping. The lesions of vitiligo are asymptomatic. Vitiligo can result in patches of white hair. Vitiligo can occur at any age but the peak incidence occurs from late childhood to mid adult life. The lesions of vitiligo are most commonly found on the dorsal surfaces of the hands, periorificial areas of the face, and in the axillae (underarms). Patients with extensive vitiligo may have depigmented areas anywhere on the body. In most instances of vitiligo, the distribution pattern is bilateral and fairly symmetrical. However, unilateral, segmental patterns are occasionally seen. In those with very fair skin, lack of contrast between normal and depigmented skin makes recognition of the lesions difficult. In such a situation, examination with a Wood's lamp (UV) may be helpful. The diagnosis of vitiligo is made on a clinical basis in which the skin appears to be depigmented with a complete loss of pigment.


Course and prognosis:

The onset of vitiligo is usually before the age of 20. Vitiligo usually develops in a few small patches and slowly extends to new areas of the skin over succeeding months and years. At some unpredictable point, which cannot be foretold in advance, extension of the depigmentation may develop within the lesions, but complete repigmentation is almost never seen. Vitiligo patients whose initial depigmentation occurs in segmental cutaneous distribution, have a slightly better chance for early stabilization and re-establishment of an even pigment return. Lesions of vitiligo occurring on sun exposed areas will tend to sunburn very easily and sometimes present as reddened patches. At least 10% of patients with vitiligo will have serologic blood tests or clinical evidence of one or more associated auto immune diseases. These include conditions such as auto immune thyroid disease, Addison's disease, type I diabetes mellitus, pernicious anemia, alopecia areata, and uveitis. These conditions may either precede or follow pigment loss.



The treatment for vitiligo is not very satisfactory. Think about it. If money could buy a cure, wouldn't millionaire Michael Jackson be able to buy a cure? Of course he would, but there is no sure way of curing vitiligo. The skin in most patients can be induced to regain some color, but complete and permanent repigmentation is rarely achieved. Lasers work, but are expensive and not widely available. The 308-nm excimer laser is an effective modality for the treatment of vitiligo. However, similar to other non-surgical treatment modalities, the therapeutic effect is mainly dependent on the location of vitiligo lesions. Narrow band UVB is also helpful. Dr. Jacobs may suggest topical steroid therapy for mild vitiligo. The creams are applied to help reduce the inflammation that causes pigment loss. Other treatment may depend on the ingestion or application or various psoralen compounds, which, because of their photosensitizing properties, can stimulate resting melanocytes in the deeper portion of the skin to come to the surface. This actual treatment program is much Like the (PUVA) ultra violet light, treatment for psoriasis. The problem with this type of therapy is skin cancer. Because UV light is used, this type of therapy can result in skin cancers later in life. Rarely, in cases of very extensive vitiligo, it is more practical to lighten the surrounding skin with repeated applications of quinone type bleaches. If patients choose not to undergo therapy of any type, or if therapy is unsuccessful, water proof opaque make-up such as Lydia O'Leary's covermark or Derma blend can be used to mask the lesions. Sun screen should be applied to prevent the occurrence of sun damage in any case. The National Vitiligo foundation may also have additional information and support for you:


National Vitiligo Foundation

611 South Fleishel Ave.  Tyler, TX  75701

Phone: (903) 531-0074  Fax: (903) 525-1234