Vitiligo affects the skin, eyes, and mucous membranes by destroying cells that produce the body's pigment. The most obvious results of this condition are white splotches in the areas where the skin isn't producing enough pigment. This is not a serious condition, but research physicians are still investigating methods for correct diagnosis, treatments, co-existent diseases, and psychological side effects.
Our hair, eyes, and skin are given color by a pigment called melanin. This material is constantly being broken down and replaced, so it must be replenished by cells called melanocytes. Melanocytes manufacture and distribute the correct amount of melanin, but for people with vitiligo, this process gets disrupted.
As scientists have found, vitiligo destroys melanocytes for unknown reasons. They have categorized it as an auto-immune disorder because no external cause seems to be responsible for it. In auto-immune disorders, your body mistakes itself for an enemy intruder and declares war on those "enemy" cells. Your malfunctioning immune system continues attacking your own cells; in this case, melanocytes.
The most common symptom of vitiligo is light or white patches of skin anywhere on your body. These are commonly found on areas that receive a lot of sunlight, like your face, back of the neck, forearms, hands, and feet. They can also affect other areas, such as underneath your arms and genitals. For the most part, the symptoms are the most serious aspect of this condition, and doctors direct their treatment toward this aspect.
If you suspect you have vitiligo, make sure to go to your physician for an official diagnosis and consultation. You can expect a physical exam of your skin from a dermatologist. At this stage in research, there are a number of different courses of treatment, ranging from light therapy to oral medication to strong sunscreen.
Since vitiligo seems to affect young people more than older people, physicians cite the psychological effects of the disease as a major issue. A person with a visible difference in skin coloring, called depigmentation, may be influenced to see their body as unhealthy or disabled.
Vitiligo may point your physician to another coexisting condition often seen with depigmentation. Anemia, lupus, and hyperthyroidism are often found in people with vitiligo. Genetics are also probably responsible, since the condition seems to run in families. Unfortunately, vitiligo usually gets worse as time goes on. However, it is certainly not contagious.
Three myths about the treatment of vitiligo prevail in the medical profession.
The first myth is that treatment of vitiligo is "impossible." This is clearly not true and the majority of patients can achieve good results.
The second myth is that oral psoralens, which form the basis for some vitiligo treatments are "toxic to the liver." Oral psoralens are not toxic to the liver.
The third myth is that psoralen + UVA (PUVA) treatments for vitiligo "cause cancer of the skin." When used to treat vitiligo, PUVA therapy requires only a limited number of treatments-approximately 150 in number that has not been shown to cause skin cancer. By comparison, PUVA treatments for psoriasis can be as many as double the number for vitiligo. It has been shown that a small percentage of patients who receive more than 250 PUVA treatments can develop treatable squamous cell cancers of the skin.
Some options are currently available for the treatment of vitiligo: sunscreens; restoration of normal skin color; and bleaching of normal skin with topical creams to remove normal skin pigment to make an even color.
The two goals of sunscreen treatments are: to protect unpigmented involved skin from sunburn reaction and to limit the tanning of normal pigmented skin. The sun protection factor (SPF) of sunscreens should be no less than SPF 30, as this grade blocks not only erythema, but also the affects of sunlight on the DNA of the skin cells. Sunscreen treatment skin phototypes 1, 2, and sometimes 3 (those who burn).
Restoration of normal skin color can take the form of spot treatments or whole body treatment.
Spot Treatment: Topical Corticosteroid Creams
Initial treatment with certain topical corticosteroid creams is practical, simple, and safe. If there is no response in 2 months, it is unlikely to be effective. Physician monitoring every 2 months for signs of early steroid atrophy (thinning of the skin) is required.
Spot Treatment: Topical Oxsoralen
Much more complicated is the use of topical Oxsoralen (8-MOP). Oxsoralen is highly phototoxic (likely to cause a sunburn), and the phototoxicity lasts for 3 days or more. This should be performed only as an office procedure, only for small spots, and only by experienced physicians on well-informed patients. As with oral psoralens, 15 or more treatments may be required to initiate a response, and 100 or more to finish.
Spot Treatment: Mini Grafting
Mini grafting, which involves transplanting the patient's normal skin to vitiligo affected areas, may be a useful technique for refractory segmental vitiligo macules. PUVA may be required following the procedure to unify the color between the graft sites. The demonstrated occurrence of Koebnerization in donor sites in generalized vitiligo restricts this procedure to patients who have limited skin areas at risk for vitiligo. "Pebbling" of grafted site may occur.
Whole Body Treatment: PUVA Photochemotherapy (Oral Psoralens + UVA Irradiation)
For more widespread vitiligo, treatment with oral psoralen + UVA (PUVA) is practical. This may be done with sunlight and trimethylpsoralen (Trisoralen) or with artificial UVA (in the doctor's office or at an approved phototherapy facility) and Trisoralen or Oxsoralen-Ultra.
Ophthalmologic examination and ANA blood tests are required before starting PUVA therapy. Outdoor therapy may be initiated with 0.6 mg/kg Trisoralen followed 2 hours later by 5 minutes of New England sunlight (less in southern regions). Treatments should be twice weekly, not 2 days in a row, and sunlight exposure should increase by 3 to 5 minutes per treatment until there is a sign of response, and in a few this causes koebnerization. Individualization is required: treatment options are either 0.4 mg/kg of Oxsoralen-Ultra (well absorbed, efficient potentially very phototoxic, significant risk of nausea) or 0.6 mg/kg of Trisoralen (variably absorbed, not very phototoxic, little nausea).
Initial UVA exposure should be 1.0 J and increments (twice weekly, not two days in a row) 0.5 (Oxsoralen-Ultra) to 1.0 (Trisoralen) J per treatment until there is evidence of response of phototoxicity. The later is the sustaining UVA dose until reasonable repigmentation has been established.
PUVA is up to 85% effective in over 70% of patients with vitiligo of the head, neck, upper arms, legs, and trunk. Distal hands and feet are poorly responsive and alone are not usually worth treating. Genital areas must be shielded and not treated. Macules that have totally repigmented usually stay in the absence of injury/sunburn (85% likelihood up to 10 years), macules less than fully repigmented will slowly reverse once treatments have been discontinued. Maintenance treatments are required.
Risks of treating vitiligo with PUVA include nausea, GI upset, sunburn, hyperpigmentation, and acute dryness. We advise against oral PUVA treatments for children under age 10. Treatment is most likely to be successful in highly motivated patients who clearly have reasonable objectives and understand the risks and benefits. While PUVA is not a cure, most patients who are responding well to treatment are not at the same time developing new vitiligo macules.
The goal of depigmentation is to unify skin color in patients with vitiligo virtually all over the body and those who have failed PUVA, who cannot use PUVA, or who reject the PUVA option. Bleaching with monobenzylether of hydroquinone 20% cream (Benoquin) is a permanent, irreversible process. Since application of Benoquin may be associated with distant depigmentation, Benoquin cannot be used to selectively to bleach certain areas of normal pigmentation, because there is a real likelihood that new and distant white macules will develop over the months of use. Bleaching with Benoquin normally requires twice-daily possible side effects. Uncommonly, contact dermatitis is observed. The success rate is about 93%. Periodically following sun exposure, an occasional patient will observe focal repigmentation, which will require a month or so of local use of Benoquin to reverse.
The end-stage color of skin bleached with Benoquin is the same chalk-white as the vitiligo macules. Most patients are quite satisfied with uniformity and the finality of the results. An occasional patient may wish to take 30 to 60 mg beta-carotene to impart on off-white color to the skin. The only side effect of beta-carotene is the uncommon risk of diarrhea.
Patients who undergo bleaching are at risk for sunburn. They should avoid midday sun exposure and should use a high-SPF sunscreen. To date no long-term untoward effects have been reported from the use of monobenzylether of hydroquinone for skin bleaching.
Your skin gets its colour from a pigment called melanin, which is produced by skin cells called melanocytes. If you have vitiligo, you do not have enough working melanocytes, so not enough melanin is produced in your skin. This causes white patches to develop on your skin or hair.
The causes of non-segmental and segmental vitiligo may be slightly different.
Non-segmental vitiligo, the most common type of vitiligo, is thought to be an autoimmune condition. This means that your immune system (the body’s natural defence system) does not work properly. Instead of attacking foreign cells, such as bacteria, your immune system produces antibodies (infection-fighting proteins) that attack your body’s own healthy cells and tissue. If you have non-segmental vitiligo, your immune system produces antibodies that destroy the melanocyte skin cells that make melanin. Vitiligo can be associated with other autoimmune conditions, such as hyperthyroidism (an overactive thyroid gland).
Segmental vitiligo, the less common type of vitiligo, is thought to be caused by chemicals released from the nerve endings in your skin ('neuro' means to do with nerves). These chemicals are poisonous to the melanocyte skin cells.
You may be at higher risk of developing non-segmental vitiligo if:
you have a family history of the condition; for example, one of your parents has it
you have a family history of other autoimmune conditions – for example, one of your parents has pernicious anaemia (an autoimmune condition that affects your stomach)
you have another autoimmune condition
you have melanoma (a type of skin cancer) or cutaneous T-cell lymphoma (a type of cancer of the lymphatic system)
you have particular changes in your genes (units of genetic material) that are known to be linked to non-segmental vitiligo
It is possible that the vitiligo may be triggered by particular events, for example:
stressful events, such as childbirth
damage to your skin, such as severe sunburn or cuts (this is known as the Koebner response)
exposure to certain chemicals – for example, in your job
Vitiligo is not caused by an infection and you cannot catch it from someone else who has the condition.
People who develop vitiligo usually first notice white patches (depigmentation) on their skin. These patches are more commonly found on sun-exposed areas of the body, including the hands, feet, arms, face, and lips. Other common areas for white patches to appear are the armpits and groin, and around the mouth, eyes, nostrils, navel, genitals, and rectum.
Vitiligo generally appears in one of three patterns:
focal pattern -- depigmentation limited to one or only a few areas
segmental pattern -- depigmented patches that develop on one side of the body
generalized pattern -- the most common pattern. Depigmentation occurs symmetrically on both sides of the body.
In addition to white patches on the skin, people with vitiligo may have premature graying of the scalp hair, eyelashes, eyebrows, and beard. People with dark skin may notice a loss of color inside their mouths.
Focal pattern vitiligo and segmental vitiligo remain localized to one part of the body and do not spread. There is no way to predict if generalized vitiligo will spread. For some people, the depigmented patches do not spread. The disorder is usually progressive, however, and over time the white patches will spread to other areas of the body. For some people, vitiligo spreads slowly, over many years. For other people, spreading occurs rapidly. Some people have reported additional depigmentation following periods of physical or emotional stress.
The diagnosis of vitiligo is made based on a physical examination, medical history, and laboratory tests. A doctor will likely suspect vitiligo if you report (or the physical examination reveals) white patches of skin on the body - particularly on sun-exposed areas, including the hands, feet, arms, face, and lips. If vitiligo is suspected, the doctor will ask about your medical history. Important factors in the diagnosis include a family history of vitiligo; a rash, sunburn, or other skin trauma that occurred at the site of vitiligo 2 to 3 months before depigmentation started; stress or physical illness; and premature graying of the hair (before age 35). In addition, the doctor will ask whether you or anyone in your family has had any autoimmune diseases and whether you are very sensitive to the sun.
To help confirm the diagnosis, the doctor may take a small sample (biopsy) of the affected skin to examine under a microscope. In vitiligo, the skin sample will usually show a complete absence of pigment-producing melanocytes. On the other hand, the presence of inflamed cells in the sample may suggest that another condition is responsible for the loss of pigmentation.
Because vitiligo may be associated with pernicious anemia (a condition in which an insufficient amount of vitamin B12 is absorbed from the gastrointestinal tract) or hyperthyroidism (an overactive thyroid gland), the doctor may also take a blood sample to check the blood-cell count and thyroid function. For some patients, the doctor may recommend an eye examination to check for uveitis (inflammation of part of the eye), which sometimes occurs with vitiligo. A blood test to look for the presence of antinuclear antibodies (a type of autoantibody) may also be done. This test helps determine if the patient has another autoimmune disease.