É uma doença não-contagiosa em que ocorre a perda da pigmentação natural da pele. Sua etiologia ainda não é bem compreendida, embora o fator autoimune pareça ser importante. Contudo, estresse físico, emocional, e ansiedade são fatores comuns no desencadeamento ou agravamento da doença.
Patologicamente, o vitiligo se caracteriza pela redução no número ou função dos melanócitos, células localizadas na epiderme responsáveis pela produção do pigmento cutâneo - a melanina. A doença pode surgir em qualquer idade, sendo mais comum em duas faixas etárias: 10-15 anos e 20-40 anos.
Esta despigmentação ocorre geralmente em forma de manchas brancas (hipocrômia) de diversos tamanhos e com distruição focal ou difusa. Pode ocorrer em qualquer segmento da pele, inclusive na retina (olhos). Os locais mais comuns são a face, mãos e genitais. Os pêlos localizados nas manchas de vitiligo se tornam esbranquiçados. O local atingido fica bastante sensível ao sol, podendo ocorrer sérias queimaduras caso exposto ao sol sem protetor, conferindo um risco para o desenvolvimento de câncer de pele.
Via de regra, o vitiligo é um distúrbio crônico. Existem vários tipos clínicos de vitiligo, cada qual com prognóstico próprio. Porém, dependendo do seu tipo clínico pode haver regressão espontânea ou com tratamento médico. O vitiligo pode permanecer focal indefinidamente ou se generalizar.
Se necessita de ajuda, por favor consulte um profissional de saúde.
Existem inúmeras opções terapêuticas para o vitiligo, a saber: corticosteróides, imunomoduladores, helioterapia, PUVA e enxertos cirúrgicos.
Esteróides têm sido usados para remover as manchas brancas, porém não são muito eficientes. Outro tratamento mais radical é tratar quimicamente para remover todo o pigmento da pessoa para que a pele fique mais uniforme.
VITILIGO SKIN DISEASE
Vitiligo Skin Disease - Vitiligo is a pigmentation disorder in which the cells are destroyed. The cells that make pigment in the skin, the tissues that line the interior of the mouth, nose, genital and rectal areas, the inner layer of the eyeball are all areas that can be affected by Vitiligo Skin Disease. The hair in these areas some often turn white.
No One knows for sure what causes Vitiligo Skin Disease, but there are a few theories floating around which include that some people develop antibodies that destroy the melanocytes in their bodies, that melancytes destroys themselves, and some people have stated that a sunburn or even emotional stress brought on the symptoms of Vitiligo Skin Disease. None of these theories have been proven scientifically.
Symptoms of Vitiligo usually begin with white patches on your skin. These white patches usually appear in the sun exposed areas such as hands, feet, arms, face, and lips. Other areas where these patches are common include are the armpits and groin and around the mouth, eyes, nostrils, navel, and genitals.
There are three patterns associated with Vitiligo Skin Disease. The first one is the focal pattern; this depigmentation is limited to one area of the body. The segmental pattern is seen only one side of the body. The last pattern is the most common and occurs on different parts of the body and is called the generalized pattern. Many people with Vitiligo Skin Disease not only have white patches on the skin but may also have premature graying of the scalp hair, eyelashes, eyebrows, and beards. With people with dark skin you may also notice a loss of color inside your mouth.
Vitiligo Skin Disease can spread; many times it does spread to other areas of the body. The spreading is usually slow but in some people it can be very fast. Vitiligo Skin Disease affects each person with different spreading and some may experience no spreading all.
There are several treatment options available for Vitiligo Skin Disease. The goal of these treatments is to restore the function of the skin and to improve your appearance. The current treatments at this time include medical, surgical and therapies that can be used along with both of these treatments.
Medial Therapies include topical steroid therapy which can help with returning the color of the white patches back to their normal color. This therapy is best when used in the early stages of Vitiligo Skin Disease.
Psoralen Photochemotherapy has been noted as being the most beneficial treatment available in the United States. This is a very time consuming treatment and there can be side effects that may be severe.
Topical Psoralen Photochemotherapy is best for people with only a small amount of depigmented patches usually only affecting about 20 percent of the body. This treatment can be used for children of the age of two and above. Side effects do occur with this type of treatment.
Oral Psoralen Photochemotherapy is used for those with severe Vitiligo Skin Disease meaning that over 20 percent of their body has been affected. This treatment will be given two to three times per week. Some side effects do occur.
Depigmentation is a treatment that involves fading the rest of the skin to match the white areas. This may be the best treatment for people who have Vitiligo Skin Disease over 50 percent of their body.
Surgical Therapies are pretty new and should be viewed as experimental. These surgical treatments include:
Autologous Skin Grafts is when a person’s own skin tissue is used to attach to the affected areas. This type of treatment is mainly used with people that have just a few white patches.
With Skin Grafts Using Blisters, the doctor will create blisters on the pigmented skin and then cut off the top of the blisters and transplant the skin graft onto the white patches.
Micropigmentation or tattooing is best for the lip area and those with dark skin. This treatment can fade over time.
Other home remedies that are popular include sunscreens, cosmetics, and support groups or counseling. Sunscreen is used to provide protection from ultraviolet light that may increase the white patches. Cosmetics such as stains, makeup or self-tanning lotions will help to cover up the white spots and is great for those that only have small patches. Since, Vitiligo Skin Disease also affects your appearance it can cause emotional problems. There are several support groups that can help you with all of the emotional aspects of this vitiligo skin disease.
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Human Immune Leukoderma: Vitiligo
There are several diseases marked by a lack of pigment in the skin that are grossly referred to as leukoderma; some are caused by an inability of melancocytes to produce melanin, while others are caused by melanocytes either not being present or being destroyed. The latter are the pathology of the phenotypically similar traits piebaldism and the disease vitiligo. Piebaldism, which is present from birth, is a lack of melanocytes in the skin, while vitiligo is a progressive disease in which the melanocytes are gradually destroyed causing unpigmented areas on the skin. The exact etiology of vitiligo is unknown, but four main theories exist to explain it: the autoimmune hypothesis, the neural hypothesis, the self-destruct hypothesis, and the growth factor defect hypothesis. It is believed that vitiligo is a polygenic trait and that a convergence theory, combining elements of different theories across a spectrum of expression is the most accurate etiology (Njoo & Westerhof 2001). Vitiligo is not a physically damaging disease; other than an increased sensitivity to UV radiation most of the disease’s effects are social and psychological, especially for dark-skinned races. There are both surgical and non-surgical treatments for vitiligo (Taneja 2002).
Overview of Melanogenesis and Melanocytes:
The color in human hair, skin and irises is produced by the pigment melanin, which is produced by the dermal melanoycte cells. The melanocyte cells transform the peptide tyrosinase into two different forms of melanin, which then is spread throughout the dermal cells and the keratinocytes via melanosomes to darken tissue. Figure 1 shows the chemical metabolism that occurs intra-cellulary to produce melanin from the precursors phenylalanine and tyrosine; this figure is somewhat inaccurate as the end product of melanogenesis should be two different types of melanin, eumelanin and pheomelanin. Eumelanin is metabollized from DHICA and produces a brown color in hair in its intact form; pheomelanin is metabolized from 5,6-indolequione, which produces a red color in hair in its intact form. From these two slightly different forms of pigment in various degrees of structural integrity come all the differing shades of Caucasian hair (Prota 2000). In addition to coloration, melanin pigmentation in the skin also provides photoprotection from UV radiation to the skin. However, the melanocytes themselves are not immune from radiation damage: melanomas are tumors of the melanocytes, which often present themselves as discolorations owing to the pigment-producing nature of the cells (Janeway 2001).
Theories for the etiology of Vitiligo
There is great anecdotal evidence that an autoimmune disorder causes the destruction of melanocytes, and this theory is now generally accepted as the common cause of vitiligo. It is known vitiligo appears in conjunction with several other autoimmune disorders, such as juvenile diabetes mellitus, Addison's disease, and pernicious anemia, and additionally organ-specific antibodies can often be seen in patients with vitiligo. If the immune system raises antibodies or cytotoxic T cells to damage melanocytes, the mode of action the cells take against the melanocytes could be apoptosis induction directly against melanocytes or Ig induced complement-both are demonstrated in figure 3. Proving this theory, there is histological evidence in vitiligo patients that apoptosis is occurring in the unpigmented skin lesions: there is damage to the melanocytes and keratinocytes in these areas, and the melanocytes exhibit nuclear shrinking, vacuolization, loss of dendrites, and detachment. If antibodies do cause vitiligo, some research suggests the Ig’s may bind to tyrosinase related proteins 1 and 2, which are important for melanogenesis, instead of Ig's targeting the melanocytes directly (Huang et al. 2002).
There is also evidence that peripheral nerve endings may secrete a substance that is cytotoxic to melanocytes and causes their destruction. This is supported by the segmental variety of vitiligo, which occurs in specific dermatomes, indicating the skin is possibly only being affected by the nerves of that specific dermatome. Additionally, vitiligo appears with certain neurological disorders such as encephalitis, and trauma that causes peripheral nerve damage. Nerve endings in depigmented areas were seen to produce abnormal neuropeptides and nerve growth factors, and displayed axonal degeneration-these abnormal chemicals may be toxic to melanocytes. Additionally, depigmented areas showed some abnormal autonomic function, such as increased adrenergic tone, increased norepinephrine, and an increased concentration of catecholamines. These data then suggest that neurotransmitter release could, directly or indirectly, have an affect on melanocyte destruction and depigmentation.
It is known that some of the intracellular pre-melanogenesis metabolites are toxic to melanocytes, such as dopa and dopachrome. Normally melanocytes possess cellular measures to counteract these toxic substances, but it is believed that cells may lose the ability to counteract these toxic metabolites and are destroyed by leakage of metabolites into the cytoplasm and eventually cell lysis. There is evidence that points to this in that certain hydroquinone derivatives that are similar to these intra-cellular metabolites cause leukoderma experimentally.
Growth Factor Defect Hypothesis:
A study in the 1980's found that melanocytes in lesions from vitiligo patients contained melanocytes, but that these cells exhibited "defective growth and passage capacities." The researchers then noted that the growth defects of the melanocytes were partially corrected by adding a growth factor to their culture, additionally suggesting that growth defects may be part of the pathology of vitiligo. In depigmented areas, cellular analysis showed that there were melanocytes but that they grew poorly. These data suggest that, whether a primary or secondary cause, growth defects appear to play a role in leukoderma and vitiligo (Njoo & Westerhof 2001).
There does appear to be a strong genetic influence in vitiligo: a positive family history has been reported in about 20% of patients and it has been found in monozygotic twins. Studies have shown that vitiligo does not progress via a simple Mendelian pattern, but more likely is coded polygenically and can be expressed across a spectrum. There has been some evidence both proving and disproving the involvement of the HLA system in the occurrence of vitiligo. So, it is believed that genetic factors probably play a key role in the pathogenesis of vitiligo, but the exact cause is unknown.
A team of researchers used the family histories kept by the American Vitiligo Foundation to examine the Mendelian inheritance of vitiligo, and found that most instances of the disease were clustered in families. They found that for patients of vitiligo, offspring have the highest chance of developing the disease, followed by siblings, parents and grandparents (Majumder et al. 1988). Before this work Majumder's team published a report in 1988 suggesting a multiple recessive homozygous model for the disease. In 1994 a seperate team of researchers validated Majumder's proposition of multiple homozygous recessive alleles, causing non-Mendelian inheritance of the disease; this team found that 3 "epistatically interacting autosomal diallelic loci" are involved in the pathogenesis of the disease and affected individuals exhibit homozygous recessive genotypes for all 3 loci (Nath et al. 1994).
Following genetic studies, researchers have begun to lean towards a multi-faceted etiology for vitiligo, that combines components of the aforementioned theories and genetics. This theory states that genetic influences have a role in causing vitiligo in addition to other elements, such as stress, accumulation of toxic compounds, infection, autoimmunity, mutations, and impaired melanocyte proliferation (Njoo & Westerhof 2001).
No person has brought more attention to vitiligo and its treatment possibilities than the erratic performer Michael Jackson; Jackson was born black but claims to suffer from vitiligo, causing his skin to become extremely pale. Despite many repigmenting therapies, Jackson assumedly chose a bleaching treatment to rid his skin of remaining pigment. Both re-pigmenting and bleaching treatments will be discussed.
Immuno Suppressive Treatments:
As vitiligo is believed to be an autoimmune disorder, supressing the immune system would then be an effective treatment at halting the spread of vitiligo and even inducing repigmentation. Corticosteroids are the main choice for this treatment and they effectively halt the progressive spread of vitiligo and also lead to repigmentation of lesioned areas. For small, localized lesions, topical and intralesional corticosteroids are used once a day. For rapidly spreading vitiligo or vitiligo universalis, systemic corticosteroids are employed; however, the role of systemic corticosteroids is controversial due to the serious adverse side effects.
Non-surgical Treatment: phototherapy and photochemotherapy
Currently, the most popular treatments for vitiligo are forms of phototherapy; it is known that various sources of UV light can be successfully used to stimulate repigmentation. Phototherapy can either be used by itself or in conjunction with light-sensitizing drugs.
PUVA treatment is the most popular treatment for vitiligo currently; the concept for the treatment dates back thousands of years, when the plants Psoralea coryifolia Linnaues and Ammi majus Linnaeus where eaten or used topically in Egypt and India to treat vitiligo. Today, isolates of the plants are used topically or orally in conjunction with a synthetic compound to chemically increase sensitivity to light. The patient is then exposed to a measured amount of natural sunlight (PUVASOL) or artificial UV radiation (PUVA) to induce re-pigmentation.
The amino phenylalanine is also used to treat vitiligo, although it is not a photo-sensitizing chemical. It is known that phenylalanine is a precursor for melanin via L-tyrosine, and it appears that there is a problem with L-phenylalanine metabolism in vitiligo. A combination of topical application and oral ingestion of phenylalanine with natural sunlight exposure resulted in repigmentation for 83% of patients.
In addition to photochemotherapy, there are several forms of phototherapy, without the light-sensitizing chemicals.
UV light in the wavelengths from 290-320 nm are often used to treat vitiligo. There are few studies reporting the efficacy of this treatment, but anecdotally the treatment appears effective, though not as good as other forms of phototherapy. In addition to broad band UV (BUVB), there is also narrow band UV treatment (NBUVB). This is a more recent form of UV phototherapy and was initially used to treat psoriasis. This UV treatment operates between 305 and 311 nm, and is highly effective for treating psoriasis and moderately effective at treating vitiligo. When used as monotherapy, NBUVB is slightly but not significantly more effective at stimulating repigmentation than PUVA treatment.
In addition to UV treatment, the excimer laser has now been implemented as phototherapy for vitiligo. The 308 nm laser produces light similar to the narrow band UVB treatment, and has shown good results in stimulating repigmentation of about 90% of patients. The excimer laser also allows more focused treatment on specific lesions, or hard to reach areas of the body.
There is little scientific evidence examining why phototherapies are effective at stimulating repigmentation; however, it is very strongly believed that if there are stores of unaffected but immature melanyocytes in the lesioned area, these melanocytes can be induced to produce melanin in the lesioned areas. Likewise, there are often functional, but not melanin producing melanocytes at lesion boundaries that can produce melanin that spreads into the lesions causing repigmentation.
In addition to phototherapy, there is also surgical treament for vitiligo that mainly consists of grafting patches of skin with healthy melanocytes to lesioned sites. In both minigrafting and suction blister grafting, superficial layers of skin are removed from normally-pigmented skin and these patches then grafted onto the lesioned areas. These techniques are believed to work by healthy melanocytes from the grafts proliferating into the lesioned areas and repopulating them. Success rates for these techniques are between 80% and 90%. Full thickness grafts of skin are implanted in minigrafting, using 1-2 mm healthy skin punches from areas such as the buttocks and followed by exposure to sunlight or PUVA treatment. Success of minigrafting is around 67% in patients.
The future of surgical treatment for vitiligo is actually extracting melanocytes from a donor area of the patient's healthy skin, culturing these melanocytes into a large population, then grafting them as sheets onto the lesioned areas. Preleminary trials with this technique have been highly successful; however there is some concern about controlling malignancy in the cultured melanocytes.
In addition to treatments to repigment skin, in extremely progressive, full-body vitiligo called vitiligo universalis, the patient can opt to bleach the remaining pigment off healthy skin. This treatment does have profound psychosocial implications, especially for naturally dark-skinned individuals who become light or white-skinned. This is the proposed medical scenario with performer Michael Jackson, who claims to have been afflicted with vitiligo universalis. As opposed to seeking repigmentation, Jackson opted instead for depigmentation of remaining, naturally dark areas. This is a feasible scenario, although there is great debate as to the authenticity of Jackson's claim (Taneja 2002).
Janeway, C. A. Jr., Travers, P., Walport, M., and Shlomchik, M. J. Immunobiology 5. New York: Garland Publishing, 2001.
Huang, C.L., Nordlund, J.J., & Boissy, R. 2002. "Vitiligo: A manifestation of apoptosis?" American Journal of Clinical Dermatology 3(5): 301-308.
Majumder, P.P., Das, S.K., Li, C.C. 1988. "A genetical model for vitiligo." American Journal Human Genetics 43: 119-125.
Majumder, P.P., Nordlund, J.J., Nath, S.K. 1993. "Pattern of familial aggregation of vitiligo." Archives of Dermatology 129: 994-998.
Nath, S.K., Majumder, P.P., Nordlund, J.J. 1994. "Genetic epidemiology of vitiligo: multilocus recessivity cross-validated." American Journal of Human Genetics 55: 981-990.
Njoo, M.D., & Westerhof, W. 2001. "Vitiligo: Pathogenesis and Treatment." American Journal of Clnical Dermatology 2(3): 167-181.
Prota, G. 2000. "Melanins, Melanogenesis and Melanocytes: Looking at Their functional significance from the chemist's viewpoint." Pigment Cell Research 13: 283-293.
Taneja, A. 2002. "Treatment of Vitiligo." Journal of Dermatological Treatment 13: 19-258.
Vitiligo is a condition in which your skin loses melanin, the pigment that determines the color of your skin, hair and eyes. Vitiligo occurs when the cells that produce melanin die or no longer form melanin causing slowly enlarging white patches of irregular shapes to appear on your skin.
An estimated 1 to 2 million Americans have vitiligo. It affects both sexes and all races, but is often more noticeable and more disfiguring in people with darker skin. Vitiligo usually starts as small areas of pigment loss that spread and become larger with time. These changes in your skin can result in stress and worries about your appearance.
There is no cure for vitiligo. The goal of treatment is to stop or slow the progression of pigment loss and, if you desire, attempt to return some color to your skin.
Back to TopSymptomsClick to Enlarge Vitiligo
The main sign of vitiligo is pigment loss that produces milky-white patches (depigmentation) on your skin.
Other less common signs may include:
Premature whitening or graying of the hair on your scalp, eyelashes, eyebrows or beard
Loss of color in the tissues that line the inside of your mouth (mucous membranes)
Loss or change in color of the inner layer of your eye (retina)
Although any part of your body may be affected by vitiligo, depigmentation usually develops first on sun-exposed areas of your skin, such as your hands, feet, arms, face and lips. Although it can start at any age, vitiligo often first appears between the ages of 20 and 30. Vitiligo generally appears in one of three patterns:
Focal. Depigmentation is limited to one or a few areas of your body.
Segmental. Loss of skin color occurs on only one side of your body.
Generalized. Pigment loss is widespread across many parts your body.
The natural course of vitiligo is difficult to predict. Sometimes the patches stop forming without treatment. In other cases, pigment loss can involve most of the surface of your skin.
Back to TopCausesClick to Enlarge Illustration of the layers of your skin
Vitiligo occurs when melanin — the dark pigment in the epidermis that gives your skin its normal color — is destroyed or not produced. The involved patch of skin then becomes white. Why this occurs isn't known.
Doctors and scientists have theories as to what causes vitiligo. It may be due to an immune system disorder. Heredity may be a factor because there's an increased incidence of vitiligo in some families. Some people have reported a single event, such as sunburn or emotional distress, that triggered the condition. However, none of these theories has been proved as a definite cause of vitiligo.
Back to TopWhen to seek medical adviceSee your doctor if areas of your skin, hair or eyes lose coloring. Although there's no cure for vitiligo, treatments exist that may help to stop or slow the process of depigmentation and attempt to return some color to your skin.
Back to TopTests and diagnosisIf your doctor suspects you have vitiligo, he or she will ask about your medical history. Important factors in your medical history include:
A family history of vitiligo
A rash, sunburn or other skin trauma at the site of vitiligo within two to three months of the start of pigment loss
Premature graying of the hair
Stress or physical illness
In addition, your doctor needs to know whether you or anyone in your family has had an autoimmune disease and will ask if your skin is sensitive to the sun. He or she will examine you to rule out other medical problems or skin conditions, such as dermatitis or psoriasis.
Your doctor may take a small sample (biopsy) of your affected skin. He or she may take a blood sample to check your blood cell count and thyroid function. In some cases, your doctor may recommend an eye examination to check for inflammation in your eye (uveitis). A blood test to look for the presence of anti-nuclear antibodies (a type of autoantibody) also may be done to determine if you have an autoimmune disease.
Back to TopTreatments and drugsIn some cases, medical treatment for vitiligo may not be necessary. Self-care steps, such as using sunscreen and applying cosmetic camouflage cream, may improve the appearance of your skin. For fair-skinned individuals, avoiding tanning can make the areas almost unnoticeable.
Depending on the number, size and location of the white patches, you may decide to seek medical treatment. Medical treatments for vitiligo aim to even out skin tone, either by restoring color (pigment) or destroying the remaining color.
Depending on the type of therapy, treatment for vitiligo may take from six to 18 months. Medical treatment choices are based on the number of white patches you have and how widespread they are. Each person responds differently to treatment, and a particular therapy may not work for you.
Topical corticosteroid therapy. Corticosteroids may help return color to your skin (repigmenting), particularly if the medication is started early in the disease. These drugs, which include cortisone, are similar to the hormones produced by your adrenal glands. Your doctor may prescribe a mild topical corticosteroid cream or ointment for children younger than 10 years old or a stronger form for adults. You may need to apply the cream or ointment to the white patches on your skin for at least three months before you see any results. This treatment is simple and safe, but your doctor will monitor you closely for side effects, such as thinning of the skin (atrophy) and streaks or lines on your skin (skin striae). Calcipotriene (Dovonex), a vitamin D derivative, also may be used topically and is sometimes used with corticosteroids or ultraviolet light.
Topical psoralen plus ultraviolet A (PUVA). Topical PUVA may be a treatment option if you have a small number of depigmented patches (affecting less than 20 percent of your body). PUVA, also called photochemotherapy, is performed under artificial UVA light once or twice a week in your doctor's office. Your doctor or a nurse will apply a thin coating of psoralen to the depigmented patches of your skin about 30 minutes before UVA light exposure. You're then exposed to an amount of UVA light that turns the affected area of your skin pink. Your doctor may slowly increase the dose of UVA light over many weeks. Eventually, the pink areas of your skin fade and a more normal skin color appears.
Potential short-term side effects of topical PUVA therapy include severe sunburn and blistering and too much repigmentation or darkening of the treated patches or the normal surrounding skin (hyperpigmentation). You can minimize your chances of sunburn by avoiding exposure to direct sunlight after each treatment. Hyperpigmentation is usually a temporary problem and eventually disappears when treatment stops.
Oral psoralen photochemotherapy, or oral PUVA. Oral PUVA therapy may be used if you have extensive vitiligo (affecting more than 20 percent of your body) or if you haven't responded to topical PUVA therapy. Oral PUVA isn't recommended for children younger than 10 years of age because of an increased risk of damage to the eyes, such as cataracts. For oral PUVA therapy, you take a prescribed dose of psoralen by mouth about two hours before exposure to artificial UVA light or sunlight. Your doctor adjusts the dose of light until the skin areas being treated become pink. Treatments are usually given two or three times a week, with at least one day in between.
If you don't have access to a PUVA facility, your doctor may prescribe psoralen to be used with natural sunlight exposure. Your doctor will give you careful instructions on carrying out treatment at home and monitor your progress with frequent office visits.
Short-term side effects of oral PUVA may include sunburn, nausea and vomiting, itching, abnormal hair growth, and too much repigmentation or darkening of the treated patches or the normal surrounding skin (hyperpigmentation). If received for longer periods of time, this type of treatment may increase your risk of skin cancer. To avoid sunburn and reduce your risk of skin cancer, apply sunscreen and avoid direct sunlight for 24 to 48 hours after each treatment. Wear protective UVA sunglasses for 18 to 24 hours after each treatment to avoid eye damage, particularly cataracts.
Narrow-band ultraviolet B (UVB) therapy. In recent years, narrow-band UVB, a special form of UVB light, has been used as an alternative to PUVA. This type of therapy can be administered like PUVA and given up to three times a week. However, no pre-application of psoralen is required, thus simplifying the treatment process. Narrow-band UVB may be a safer long-term alternative to PUVA. Because it is simpler to administer, this type of phototherapy is gaining wide acceptance. However, more research is needed to determine if it is superior to PUVA.
Depigmentation. Depigmentation involves fading the rest of the skin on your body to match the already-white areas. If you have vitiligo on more than 50 percent of your body, depigmentation may be the best treatment option. In this procedure, the drug monobenzone (Benoquin) is applied twice a day to the pigmented areas of your skin until they match the already-depigmented areas. Avoid direct skin-to-skin contact with others for at least two hours after applying the drug.
The major side effect of depigmentation therapy is redness and swelling (inflammation) of the skin. You may experience itching, dry skin or abnormal darkening of the membrane that covers the white of your eyes. Depigmentation is permanent and cannot be reversed. In addition, if you undergo depigmentation you will always be extremely sensitive to sunlight.
Autologous skin grafts or "minipunch" skin transfer. This type of skin grafting uses your own tissues (autologous). Your doctor removes tiny pieces of skin from one area of your body and attaches them to another. This procedure is sometimes used if you have small patches of vitiligo. Your doctor removes very small sections of your normal, pigmented skin (donor sites), often containing a small hair and places them on the depigmented areas (recipient sites). Possible complications of this procedure include infection at the donor or recipient site, but this is rare. The recipient and donor sites may develop scarring, a cobblestone appearance, spotty pigmentation, or may fail to repigment at all.
Blister grafting. In this procedure, your doctor creates blisters on your pigmented skin primarily by using suction. The tops of the blisters are then cut out and transplanted to a depigmented skin area where a blister of equal size has been created and removed. The risks of blister grafting include the development of a cobblestone appearance, scarring and lack of repigmentation. However, there's less risk of scarring with this procedure than with other types of skin grafting.
Tattooing (micropigmentation). Tattooing implants pigment into your skin with a special surgical instrument. For treatment of vitiligo, tattooing works best for the lip area, particularly if you have dark skin. However, it may be difficult for your doctor to match your natural skin color. Tattooing tends to fade over time, and when used on the lips it may lead to episodes of blisters caused by the herpes simplex virus.
In a procedure called an autologous melanocyte transplant, your doctor takes a sample of your normal pigmented skin and places it in a laboratory dish containing a special cell culture solution to grow melanocytes. When the melanocytes in the culture solution have multiplied, they're transplanted to your depigmented skin patches. This procedure is experimental and performed only in a few institutions where vitiligo research is conducted.
Back to TopLifestyle and home remediesCertain self-care tactics may help you care for your skin and improve its appearance:
Protect your skin. If you have vitiligo, particularly if you have fair skin, use sunscreen to protect your skin from the sun's harmful rays. Sunscreen helps protect your skin from sunburn and long-term damage. Sunscreen also minimizes tanning, which makes the contrast between normal and depigmented skin less noticeable.
Conceal imperfections. Cosmetics may lessen the appearance of the white patches and help you feel better about yourself. These cosmetic products may be particularly effective if you have vitiligo in limited areas of your body. You may need to experiment with several brands of concealing cosmetics before finding a product that blends best with your normal skin tone. Sunless tanning products (self-tanners) also may help conceal imperfections by adding color to depigmented areas. The coloring doesn't wash off, but it gradually fades as the dead skin cells slough off. In most cases, the color is completely gone after several days.
Back to TopCoping and supportThe change in appearance caused by vitiligo can affect your emotional and psychological well-being. You may experience emotional stress, particularly if vitiligo develops on visible areas of your body, such as your face, hands, arms or feet. You may feel embarrassed, ashamed, depressed or worried about how others will react. Young people, who are often particularly concerned about their appearance, can be devastated by widespread vitiligo.
Certain strategies may help you cope with vitiligo.
Consider these tips:
Make a good connection. Find a doctor who's knowledgeable about vitiligo. A dermatologist is a doctor who specializes in the care of skin.
Learn all about it. Find out as much as you can about vitiligo and its treatment options so that you can participate in making important decisions about your health care.
Communicate your feelings. Let your doctor know if you're feeling depressed. He or she can refer you to mental health professionals who specialize in helping people deal with depression.
Talk with others. Ask your doctor about support groups in your area for people who have vitiligo. Take your loved ones along with you.
Confide in loved ones. Seek understanding and support from your family and friends.
Faculdade paulista aplica tratamento inovador em pacientes com vitiligo
Raspar a pele esbranquiçada levando a mesma à repigmentação é o novo método que a Faculdade da Medicina da Fundação do ABC (FMABC) está realizando em pacientes com vitiligo. O tratamento foi adotado e vem sendo acompanhado em 16 pacientes do laboratório de vitiligo da instituição e serviu de base à dissertação de mestrado do dermatologista Jefferson Alfredo de Barros – o trabalho conquistou o primeiro lugar como melhor artigo de investigação da revista Anais Brasileiros de Dermatologia da Sociedade Brasileira de Dermatologia (SBD).
O vitiligo caracteriza-se pela destruição das células que determinam a cor da pele e apresenta como conseqüência manchas brancas em qualquer parte do corpo – é mais comum que elas apareçam em áreas que sofreram algum trauma, escoriações ou ferimentos. Entre 2002 e 2005, Barros estudou maneiras de estimular a pele a se recompor caso fosse submetida a uma seqüência de raspagens (curetagem). Após três sessões, com intervalo de trinta dias entre delas, notou que havia o aumento dos melanócitos, células que produzem a melanina, proteína responsável pela pigmentação.
O dermatologista explicou que já havia experiência de seu colega Carlos Machado Filho, professor FMABC, em torno de um trabalho de curetagem, porém acrescido de implante de pele no local afetado. “Com base nisso, passei a avaliar através de biópsia como é o comportamento da pele só com a sucessão de raspagens estimulando a produção de melanina”, observou Barros. Além dele e Machado, participaram do estudo a bioquímica Maria Aparecida da Silva Pinhal, a bioestatista Lourdes da Conceição Martins e a patologista Juliana Pettinati.
Os pacientes avaliados continuam sob acompanhamento, alguns com uso de medicamentos, outros na condição de curados. Estimativas avaliam que o vitiligo (que não tem causas conhecidas) atinge aproximadamente entre 1% e 2% da população mundial – a doença não é transmissível nem ocasiona outros problemas. Os tratamentos mais convencionais envolvem repigmentação ou despigmentação (quando mais de 75% do corpo foi atingido e se promove o branqueamento total).
(Fonte: Faculdade de Medicina do ABC – FMABC-
Vitiligo is an acquired de-pigmenting skin condition that results from loss of functioning melanocytes. It is a major cosmetic and psychosocial disorder among the Indian population. The prevalence of this disease is approximately 0.5-3% of dermatological consultations in India. Vitiligo, known as 'leucoderma', is a social stigma. Vitiligo is appearance of single or multiple de-pigmented patches on any part of the body. These patches gradually increase in size & cause lot of psychological stress in the patient. It is an autoimmune condition and may have a genetic predisposition in up to 20% of the cases. Treatment of Vitiligo usually takes a long time, several years at least. Medical treatment may not help to arrest the spread of de-pigmentation in all patients. In majority of the cases, bio-medical therapy fails to cause re-pigmentation completely. However, re-pigmentation in cases of 'stable Vitiligo' can be achieved by various dermato-surgical techniques although in such lesions might recur. PUVA therapy is the “gold standard” in the management of Vitiligo in Western medicine. However it is not been successful in producing complete relief to all patients of Vitiligo and continues to be unavailable & expensive in rural India. No single therapeutic regimen prevents relapse or halt progression. Therefore, search for new treatments is continuous by both doctors and patients.
Will integration of therapies help?
The Institute of Applied Dermatology carried out a clinical research project on integrating ayurveda and modern medicine for Vitiligo patients during 2003-04. This study was supported by Mahatma Gandhi institute for rural industrialization, a unit of Indian Institute of Technology, New Delhi & KVIC, Mumbai. Results revealed that ayurveda might have significant role in halting the progression and regimenting in non hairy areas. Another study was conducted during 2004-05, supported by Kerala State Council for Science, Technology and Environment gave additional evidence that integration works and that addition of homeopathy in select cases reduces the disease induced stress, thus accelerating repigmentation in non-hairy areas.
The assumption here is that integration of therapies would help in several probable ways
To reduce the pitta dusti/prakopa and help to reduce the disease activity
Complete shodhana karma done as 14-30 days hospitalized treatment helps the body to react to the medicines in a better way than giving the medicines with out this procedure. This is done only in selected cases
Monthly pulses of controlled induced purgation help in maintaining the repigmentation
Internal medications of ayurveda & homeopathy have their own basis of repigmentation as explained in their classical texts.
However all the systems of therapy agrees that recurrence does occur in most patients on long term follow up and therefore one has to take prolonged treatment or repeat the treatment if necessaryWhat are the methods practiced in Institute of Applied Dermatology of treating Vitiligo patients using integrated therapy?
Counseling is the first step: patients decide if they want to take the treatment or not
Patients give written consent for the treatment
Complete evaluation of clinical presentation by allopathic dermatologist, ladies by lady dermatologist and gentlemen by a male dermatologist; ayurveda doctor and homeopathy doctor
Woods lamp examination of patients to know if any areas not seen for visible light is involved
There are several patient care protocols developed by Institute of Applied Dermatology
All of them in common have hospitalized shodhana karma unless the procedure is not contraindicated to the patient. Ayurvedic shodhana karma is regarded as the fundamental procedure before any therapy to obtain the best results. However patients can opt for their preferred treatments protocols with or with out shodhana karma
Follow up at the interval of 4 months, 6 months, 9 months and one year is proposed
Patients’ preference is taken into consideration
Treatment aims to slow the disease progression
Combination of different systems of medicine are used for the defined role of each, unique to them
Repigmentation of white patches is the major thrust of treatment