Get Answers to Frequently Asked Questions about Vitiligo
Vitiligo is a genetic, autoimmune skin disease causing loss of color (also known as pigment) from areas of the skin, resulting in irregular white spots or patches. Vitiligo affects about 1% of the population and can start at any age, though about half of those with vitiligo develop it before the age of 20, and about 95% before age 40. It affects both genders, and all races and ethnicities.
Vitiligo is not contagious in any way. The precise cause of vitiligo is not well-understood, though it seems to be the result of a combination of genetic and environmental factors. Some people have reported a single event, such as a severe sunburn or emotional distress, that seems to have triggered the condition. Heredity may be a factor because there is an increased incidence of vitiligo in some families. About 30% of affected individuals may report a positive family history (i.e. a family member with vitiligo).
Though the condition is not usually physically painful, the psychological and social effects are well-documented and can be significant. Vitiligo can be especially devastating to children, those with darker skin tones, and those who live in regions that highly stigmatize it.
Vitiligo is pronounced “vittle-EYE-go.”
Melanocytes are the cells in our body that produce the color in our skin. When the melanocytes are attacked by the immune system, they stop functioning, leaving patches of white (or lighter) skin. The underlying cause of melanocyte death is due to an autoimmune attack on these pigment cells. For some, there may be a hereditary (genetic) tendency toward vitiligo. Stress or severe skin trauma may also trigger vitiligo in those that are genetically predisposed.
The likelihood of developing vitiligo results from different combinations of susceptibility genes, even in the same family. Different family members inherit different genetic combinations, just as they do for height or intelligence. Even among identical twins, both develop vitiligo in only one-fourth of cases, despite sharing all genes in common. This is because they don’t share their environmental exposures and other life events. While it is known that environmental triggers are involved, it is still uncertain as to what they are, with stress (physical and emotional), skin trauma, and exposure to certain chemicals being possible triggers.
A dermatologist (a medical doctor specializing in skin) usually begins by asking the person about his or her medical history. Important factors are a family history of vitiligo or other autoimmune diseases; a rash, sunburn, or other skin trauma at the site of vitiligo 2 to 3 months before depigmentation (i.e. loss of color) started; stress or physical illness.
The doctor may take a small sample (biopsy) of the affected skin, and/or a blood sample to do lab work that checks for thyroid antibodies/disease, vitamin D levels, and other conditions that may affect general health or autoimmune status.
The doctor may also use a Woods light (specialized black light) to confirm vitiligo, as even when undetectable by the eye alone, the depigmented areas will glow under this light.
The most obvious sign or symptom of vitiligo is loss of pigment on the skin, resulting in milky-white, irregularly-shaped patches on the skin. Vitiligo typically occurs first on sun-exposed areas (face, hands, feet, arms, legs) or areas where clothing or shoes consistently rub on the skin.
Less common signs include pigment loss or graying of hair on scalp, eyebrows, eyelashes, or other affected areas. Some may also experience loss of pigment on the tissues that line the inside of the mouth (mucous membranes) and the retina of the eye.
Some of those affected by vitiligo experience intense itching at the site of depigmentation during active stages.
Generalized vitiligo is a progressive disease resulting in somewhat unpredictable cycles of spreading and cycles of stability throughout life. For some, it begins slowly with only a few areas of the body affected; for others, it begins rapidly, with many areas affected by both large and small patches of pigment loss. Many patients report going many years without new patches developing, then experience pigment loss years later. Others report spontaneous repigmentation, with no treatment at all.
Vitiligo may be associated with other autoimmune diseases. The most common is thyroid disease, which occurs in about 15% of patients. Other autoimmune diseases like juvenile diabetes mellitus and pernicious anemia are much less common (less than 1%). There is no increased risk for cancer, including cancer of the skin.
Laboratory studies for detection of autoimmune diseases associated with vitiligo may include:
Thyroid profile: especially TSH (to rule out thyroid disease) and thyroid autoantibodies;
Fasting blood sugar (to rule out diabetes);
Complete blood count (to rule out pernicious anemia).
While some people totally depigment through the natural progression of their vitiligo, others make the choice to depigment. For patients considering this option, doctors may request they begin with a psychological screening to determine that this decision is one they fully understand and are emotionally prepared for. It is generally only used in cases of advanced vitiligo, where there is more than 50% loss of pigment, though some physicians may allow its use with a lower percentage when a great deal of the vitiligo is located in the more visible areas.
If a physician determines that a patient is a candidate for this treatment, they begin the fairly simple process by using a topical prescription called monobenzyl ether of hydroquinone (MBEH). It is important to understand that this is a systemic treatment, meaning that once the cream is applied to the skin, it will cause depigmentation in remote areas away from the site of application.
This prescription is a compounded cream for use only by those with extensive vitiligo and is available in strengths of 10%, 20% (most often), 30% or 40%. This cream has been around for at least 30 years, and was formerly manufactured with the trade name of “Benoquin,” but is now most commonly known by its generic name “monobenzone.”
The patient will apply the cream twice daily, perhaps increasing the strength of the active ingredients and/or the coverage area, over a period of a year or more, until the normally pigmented skin has faded to match the vitiligo spots, creating an overall pale appearance. The skin of those who have depigmented looks quite normal, just fair. The paleness is not a stark white, as many fear, but rather a slightly pink tone. Protection from the sun is important after depigmentation is completed in order to prevent sunburns and return of pigmentation from hair follicles.
Genetics have been determined to play a role in developing vitiligo, due to data that shows an increased prevalence of the condition in family members of those diagnosed with vitiligo. However, the heritability of vitiligo gets complicated due to its involvement of several genes in DNA. Each family member inherits different combinations of these genes.
It is important to note that genetics are not the only factor at play with vitiligo. For example, an identical twin of someone with vitiligo only has a 26% chance of having vitiligo despite the two people having essentially the same DNA. Therefore, other factors are involved. Environmental factors have been identified as playing a significant role with evidence pointing to factors such as skin trauma, chemical exposure, sunburn, and stress are also important., stress, and more.
To read more about vitiligo and inheriting it check out this article from our partners at MyVitiligoTeam.
There are two main types of vitiligo which distinguish the manner of spread: Segmental and Non-segmental vitiligo. Segmental vitiligo usually involves only one part of the body such as the leg, arm, or face, and it typically progresses for about a year or two before stopping. Non-segmental vitiligo, the more common form, has a bilateral distribution typically starting on the hands, feet, or face and progresses as cyclic skin color loss which continues throughout the person’s life. This form has a strong link to an autoimmune basis in which immune cells of the body “see” these melanocytes as foreign and result in their destruction. The sites of these autoimmune attacks determine areas affected. Severity and extent of spread varies and is ultimately unpredictable.
The spread of vitiligo is ultimately caused by the death of melanocytes, the cells that produce our skin and hair color. This melanocyte destruction is believed to be due to multifactorial causes such as autoimmune factors, genetics, and inciting events such as skin trauma, chemical exposures, etc.
Response to treatment requires the presence of viable melanocytes (the cells that give skin and hair their color) either in the hair follicle, affected areas of skin, or on the edges of the lesions. In particular, melanocytes are most numerous in the hair follicle. Repigmentation therapy often results in perifollicular repigmentation which refers to skin color return around the hair follicles.
Therefore, areas of the body without hair follicles such as the lips, mucosal surfaces, fingertips, underside of wrists, soles of feet, and genitals tend to be more difficult to treat. In addition, the loss of pigmentation in hair is also an indicator of loss of the hair follicle melanocyte reservoir and suggests poor response to repigmentation therapy.
Vitiligo is a skin condition that results from the intersection of many causative factors including hereditary factors and environmental triggers and trauma. Stress can certainly play a role in the triggering or progression of vitiligo in those that are already predisposed to it.
For example, when an individual experiences high levels of emotional stress, their melanocytes are more likely to be exposed to harmful chemicals (reactive oxygen species). All in all, stress alone is likely not enough to cause vitiligo, but it can certainly combine with harmful genes and environmental factors to trigger its development.