Vitiligo is a relatively common skin condition in which patches of the skin lose all pigmentation (color) and become milky-white. Lack of pigmentation may also occur in the hair and mucous membranes (e.g., inside the mouth). The condition is usually progressive, with existing patches of white skin expanding over time and new patches forming. The progression may be rapid or gradual. Vitiligo can occur anywhere on the body. It is usually widespread and scattered, but may be localized.

The white patches of vitiligo occur when melanocytes (cells that produce melanin, the substance responsible for skin color) in the skin either disappear or stop working. It is not known why this happens. The most prevalent theory is that vitiligo is an autoimmune disorder, where antibodies (cells that normally fight infection) attack and kill melanocytes. There may be a genetic link to vitiligo.

The white patches of vitiligo may occur anywhere on the body, but they are more common in certain areas (e.g., face, hands, upper arms or legs, genitals). Vitiligo usually shows no other signs or symptoms. However, it may be associated with certain autoimmune diseases (e.g., high or low levels of thyroid hormones).

Vitiligo is usually diagnosed by a physician from the patient’s medical history and a physical examination. Other tests are not usually necessary, but a skin biopsy and blood test may be used to rule out certain other conditions.

The goal of treatment is to stop patch expansion and to repigment existing patches. Phototherapy is the most common and effective treatment. Other methods include topical corticosteroids, bleaching the normal skin to match the white patches (only in very excessive vitiligo) and transplantation of the patient’s own tissue into the patches. Vitiligo patches may also be masked by cosmetics, stains and tattoos.

Vitiligo is an acquired skin disorder characterized by macules (patches) of depigmented (colorless) skin surrounded by areas of normal skin. It is not contagious and generally poses no medical problems.

The depigmented macules result from a complete absence of functional melanocytes (cells that produce melanin, the substance responsible for skin color). Melanin is produced in the epidermis, the top layer of skin. In addition to the skin, patches of hair, mucous membranes (e.g., inside the mouth) and sometimes the retina of the eye may also be affected.

The onset of vitiligo is usually gradual, with the appearance of a few spots. Often, light-skinned people do not notice these macules until spring or summer time, when increased sun exposure causes skin to tan. The loss of pigment may be rapid or gradual. Periods of pigment loss may be followed by periods of stability, a cycle that may continue indefinitely. There also appears to be a link between stress and illness and additional pigment loss.

There is no way to know how progressive a given case of vitiligo may be. In some cases, depigmentation may spread over the entire body. Color may return to the skin spontaneously, but this is rare and typically very limited.

Vitiligo is a relatively common disorder. According to the National Institutes of Health (NIH), it affects 2 to 5 million people in the United States and 40 to 50 million people worldwide. Men and women of all races are affected equally, although the condition is more pronounced in dark-skinned people due to the sharp contrast between affected and unaffected skin. Onset may occur at any time shortly after birth, but the average age of onset is about 20 years, with most cases beginning when patients are in their 20s or 30s. Onset after the age of 40 is very rare.

There have been many attempts to classify different types of vitiligo with varying degrees of success. The results are often conflicting and rather confusing. Two major forms are generally recognized:

• Bilateral. This is the more common form in both children and adults and may be referred to as vitiligo vulgaris. Macules (patches) of depigmented skin occur evenly on both sides of the body.
  
  
• Unilateral. Also called segmental, it occurs more often in children than adults. This form of vitiligo usually does not cross the middle part of the body. In fact, macules often stop abruptly at this point.

These two forms are very broad in scope. Three more specific types are usually recognized: generalized, localized and universal.

Generalized is the most common type of vitiligo and includes:

• Vulgaris. Scattered, widely distributed macules on both sides of the body.
  
  
• Acrofacial. Macules affecting the extremities (e.g., hands, feet) and the face.
  
  
• Mixed. Macules occurring in both localized and generalized patterns.

Localized include the following:

• Focal. One or more macules in a single area.
  
  
• Unilateral (segmental). One or more macules on one portion of the body, stopping abruptly at the midline.
  
  
• Mucosal. Macules affecting the mucous membranes (e.g., inside the mouth).

Universal is the complete or nearly complete depigmentation of the skin over the entire body. This type of vitiligo is the rarest.

All of these types may involve no functioning melanocytes (cells that produce melanin, the substance responsible for skin color) in the skin at all. In other cases, melanocytes are still present and identifiable in the macules but either do not function or function in a reduced capacity.

There are many variations of vitiligo, including:

• Vitiligo capitis. Vitiligo macules on the scalp. Hair that grows from the affected area lacks pigmentation. Many cases of spontaneous graying in patches of hair have been attributed to this.
  
  
• Koebner phenomenon. Sometimes, vitiligo develops at sites of specific trauma (e.g., cuts, burns, abrasions). This is known as Koebner phenomenon and is observed in both bilateral and unilateral forms.
  
  
• Trichrome vitiligo. In this variation, depigmented macules are bordered with a zone of a uniform, intermediate hue. Melanocytes in this area are decreased, but not absent.
  
  
• Blue vitiligo. Vitiligo with blue colorations, generally developing in areas of darkened skin following inflammation.
  
  
• Vitiligo ponctué. An unusual form of vitiligo with small confetti-like or tiny, discrete macules that may occur on otherwise normal or unusually darkened skin.
  
  
• Inflammatory vitiligo. An uncommon form of vitiligo with macules surrounded by a border that is inflamed and may be itchy.
  
  
• Alezzandrini syndrome. A very rare disorder characterized by depigmentation of the scalp hair, eyebrows and eyelashes, vitiligo macules on the forehead, nose, cheeks, upper lip and skin and vision impairment. This is usually unilateral, with all characteristics occurring on the same side.

Vitiligo macules (patches) result when functional melanocytes (cells that produce melanin, the substance responsible for skin color) disappear from involved skin. The cause has not yet been identified.

Most patients attribute the onset of vitiligo to specific events, such as physical or emotional injury or stress. However, there is no proof that such factors are actually involved, except in the type of vitiligo called Koebner phenomena.

The reason melanocytes disappear or cease functioning is not known, but there are many theories, including:

• Autoimmune disease. This is the most prevalent theory. In autoimmune disorders, antibodies (cells that normally fight infection) attack healthy tissue. In this case, it is believed that these autoantibodies attack and kill melanocytes, causing the skin to lose pigmentation. Further, vitiligo may be associated with certain autoimmune disorders, particularly low or high levels of thyroid hormones (hypothyroidism or hyperthyroidism) and lupus.
  
  
• Chemical exposure. The skin may lose pigmentation when exposed to particular chemicals (e.g., phenol). In some cases, this loss of pigmentation becomes progressive and spreads beyond the site of contact.
  
  
• Nervous disease. Abnormally functioning nerve cells may injure or kill adjacent melanocytes. It is thought that this may be brought about by severe emotional trauma or stressful events. Clinical research on this theory has not been conducted.
  
  
• Genetics. Family cases of vitiligo are common. However, evidence does not support the concept that this is a purely genetic, hereditary condition. Vitiligo may occur in individuals with no family history of the disorder and children with vitiligo-affected parents may not develop the condition. It is thought that vitiligo may be tied to multiple recessive genes. About one-third of cases are genetic.

Vitiligo is characterized by flat macules (patches) of depigmented (colorless) skin, usually completely lacking in functioning melanocytes (cells that produce melanin, the substance responsible for skin color). Macules are usually uniformly milk or chalk-white in color and may not be apparent in very light-skinned people. In dark-skinned people, however, the sharp contrast makes the macules very obvious. Macules tend to have discrete margins and may be round, oval or linear in shape, though they are usually irregular. In some cases, they may be surrounded by margin of darker-than-normal skin.

Macules may vary in size from very tiny to covering large portions of the body and may occur anywhere. The areas most commonly affected include:

• Exposed areas (e.g., face, hands)
  
  
• Areas around body openings (e.g., mouth, nose, eyes, nipples, naval, genitals)
  
  
• Bodily folds (e.g., underarms, groin)
  
  
• Sites of injuries (e.g., scrapes, cuts, burns)
  
  
• Sites subjected to repeated trauma (e.g., bony prominences)
  
  
• Sites of pressure or repeated contact with clothing (e.g., belts, shoulder straps, collars)

Vitiligo macules typically enlarge over time, though the rate of this may be slow or rapid. Loss of color may also occur on mucous membranes (e.g., inside the mouth). When vitiligo affects the scalp, it may cause a localized patch of depigmented hair. This may result in the total depigmentation of all scalp hair or no more than a scattering of white hairs.

Vitiligo patients are usually in good health. This condition typically occurs with no signs or symptoms other than the characteristic macules. In some rare cases, swelling or inflammation may occur immediately prior to the onset of vitiligo. Occasionally, early vitiligo macules may be itchy (pruritus).

Vitiligo may be associated with certain endocrine system disorders, although researchers have not been able to define this connection. The most common of these are hyperthyroidism and hypothyroidism, autoimmune disorders of the thyroid gland.

Other autoimmune conditions that may be associated with vitiligo include:

• Pernicious anemia (low red blood count due to failure to absorb vitamin B₁₂)
  
  
• Addison’s disease (decreased production of certain hormones)
  
  
• Alopecia areata (patches of baldness)
  
  
• Uveitis (inflammation of certain internal eye structures)
  
  
• Diabetes mellitus (a disorder in the body’s ability to break down blood sugar)
  
  
• Lupus (chronic inflammatory disease that affects the skin, joints, blood, and kidneys)

Individuals who notice unusual loss of coloring in their skin, hair or eyes should consult with a physician. The earlier vitiligo is diagnosed, the sooner treatment to prevent or slow further depigmentation can begin.

The diagnosis of vitiligo involves a physician taking a medical history and performing a physical examination. Blood tests or other tests are not normally required. In the evaluation of a patient’s medical history, a physician will look for certain information, including:

• Whether there is a family history of vitiligo
  
  
• Any rash, sunburn or other trauma of the skin two to three months prior to depigmentation
  
  
• Any recent stress or physical illness
  
  
• Presence of gray hair before the age of 35
  
  
• Patient or family history of autoimmune diseases (e.g., thyroid disorder)
  
  
• Any increased sensitivity to the sun

Physical examination includes examination under visible and ultraviolet light. Examination under visible light generally reveals white skin macules (patches), but it may be difficult to distinguish between vitiligo and other causes for light patches of skin. Wood’s lamp examination uses ultraviolet A light to detect truly depigmented areas. The white skin of vitiligo has a characteristic yellow-green or blue fluorescence under this form of examination.

Because the process and cause of vitiligo is unknown, there is no known way to prevent the condition. Although difficult to treat, it may be treated by a dermatologist (skin specialist). The goal of treatment is to repigment skin and stabilize the depigmentation process. Aggressive treatment is typically not recommended in children. All patients respond differently to therapy and what works for one may not work for another.

There are many ways to mask vitiligo macules (patches), including:

• Cosmetics. Macules may be hidden or de-emphasized with cosmetics. A physician may recommend cosmetics with sun protection factors (SPF) to help prevent sun damage to depigmented skin.
  
  
• Tattooing (micropigmentation). Small macules or those in sites known to have a poor rate of repigmentation (e.g., lips) may be camouflaged by tattooing. However, the color frequently does not match perfectly with the surrounding skin and may fade over the years.
  

• Bronzers and skin stains. Products that stain the skin (e.g., self-tanning lotions) may be used to camouflage vitiligo macules. The color may not perfectly match surrounding skin, however, and typically fades over a period of weeks.

Corticosteroids are often used early in the treatment of vitiligo. Topical corticosteroids (e.g., hydrocortisone cream) are used most commonly. These seem to help stabilize the progression of depigmentation and may encourage repigmentation in small, localized areas. These are the simplest and safest actual treatment, though not the most effective.

Topical corticosteroids may be used with other treatments, but may thin the skin or cause dilation of blood vessels. They are not recommended for use on the face. In rare cases, oral corticosteroids may be used to stabilize depigmentation and induce repigmentation. However, these have significant potentials for serious side effects (e.g., loss of bone density), especially long-term use, and use in vitiligo treatment remains controversial.

Immunomodulators (drugs that suppress the immune system) have also been successfully used in very localized areas of vitiligo.

Phototherapy tends to provide the best results, though treatment may need to be long-term. These include:

• Psoralen and long-wave ultraviolet radiation (PUVA). The most common form used for vitiligo. It involves the medication psoralen followed by timed exposure to controlled ultraviolet A light. Psoralen makes the skin very sensitive to light and helps to stimulate melanocytes to divide and fill in areas where pigment was lost. It is usually taken in an oral form, but may be applied topically. However, special care must be taken to avoid severe sun damage with topical applications. Skin cancer is also a potential side effect of PUVA.
  
  

  According to the American Osteopathic College of Dermatology (AOCD), PUVA is partially successful in over 50 percent of cases, but total repigmentation occurs in only 15 to 20 percent. The treatment is least likely to work on the hands and feet. Older people and individuals with pigment loss for more than five years are also poor candidates.
  

• Narrow-band UVB (NB-UVB). Controlled treatment with intense ultraviolet B light is used to induce repigmentation. Advantages over PUVA include shorter treatment times and no need for medications. NB-UVB can be used in children, pregnant or breastfeeding women and people with kidney or liver dysfunction. However, it is not widely available.
  

• Focused microphototherapy. Ultraviolet B light is shone through a dark pad with tiny holes that is applied to the skin. This can be used to irradiate only the affected skin and results are typically good, but it requires expensive equipment and trained personnel, and is not widely available.

Certain areas have a poorer prognosis in terms of repigmentation. These areas include the lips, fingertips, toes and genitals.

When depigmented macules cover more than half of the body, patients and physicians may chose to depigment the remaining skin. A bleaching agent (e.g., monobenzone) is applied to the normal skin to match it with the depigmented skin. However, the patient’s appearance is significantly altered and the skin is made much more sensitive to sun damage. Many patients are allergic to the bleaching agents, so tests must be performed before widespread application. Side effects include contact dermatitis.

Vitiligo macules may occasionally be treated by transplanting (grafting) the patient’s own tissue when other treatments fail. This is typically only done on patients with small patches of stable vitiligo. Patients must have a positive minigrafting test, no tendency to scar and be over the age of 12 years.

Vitiligo macules are highly susceptible to sun damage and must be protected. Patients are recommended to wear sunscreens with a sun protection factor (SPF) of at least 30 over all exposed macules, wear protective clothing and avoid the sun during peak hours (10 a.m. to 4 p.m.).

Patients with widespread vitiligo may suffer from depression, embarrassment or other emotional distress. These individuals may benefit from including psychological counseling and/or support groups as part of their treatment.  

Preparing questions in advance can help patients to have more meaningful discussions with their physicians regarding their conditions. Patients may wish to ask their doctor the following vitiligo-related questions:

1. Do my symptoms indicate vitiligo?
   
   
2. Do you have any experience in treating vitiligo?
   
   
3. What kind of vitiligo do I have?
   
   
4. Is it possible for me to spread vitiligo to others?
   
   
5. Does vitiligo pose a danger to my overall health?
   
   
6. Should I be tested for thyroid dysfunction or other autoimmune disorders?
   
   
7. What treatment options are available to me?
   
   
8. Is it likely that I will develop white patches over more areas of my body?
   
   
9. What is the likelihood that my children will also develop vitiligo?
   
   
10. What steps can I take to prevent sun damage on the affected areas?