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   home >Skin Treatment> Vitiligo
  Vitiligo ( leucoderma )  
 

Vitiligo is an acquired pigmentary disorder of the skin and mucous membranes that is characterized by circumscribed, de-pigmented (white) patches. The condition is frequently associated with disorders of autoimmune origin, with thyroid abnormalities being the most common.
Signs and symptoms
Vitiligo lesions are characterized as follows:

  1. White or hypopigmented
  2. Usually well demarcated
  3. Round, oval, or linear in shape
  4. Enlarge centrifugally over time at an unpredictable rate
  5. Initial lesions occur most frequently on the hands, forearms, feet, and face, favoring a perioral and periocular distribution.

What are the common sites for Vitiligo?
Vitiligo lesions may be localized or generalized, with the latter being more common than the former. The most common sites of vitiligo involvement are the face, neck, and scalp.
Many of the most common sites of occurrence are areas subjected to repeated trauma, including the following:

  1. Bony prominences
  2. Extensor forearm
  3. Ventral wrists
  4. Dorsal hands
  5. Digital phalanges

Involvement of the mucous membranes is frequently observed in the setting of generalized vitiligo. Vitiligo often occurs around body orifices such as the lips, genitals, gingiva, areolas, and nipples.
Body hair (leukotrichia) in vitiligo patches may be depigmented (turn white). Vitiligo of the scalp usually appears as a localized patch of white or gray hair, but total depigmentation of all scalp hair may occur. Scalp involvement is the most frequent, followed by involvement of the eyebrows, pubic hair, and axillary hair, respectively.
Leukotrichia(White hair) may indicate a poor prognosis in regard to re-pigmentation. Spontaneous repigmentation of white hair in vitiligo does not occur.

Diagnosis
Although the diagnosis of vitiligo generally is made on the basis of clinical findings, biopsy is occasionally helpful for differentiating vitiligo from other hypopigmentary disorders.
What causes Vitiligo?
It is related to both genetic and nongenetic factors. Although several theories have been proposed about the pathogenesis of vitiligo, the precise cause remains unknown. Generally agreed upon principles are an absence of functional melanocytes in vitiligo skin and a loss of melanisn, owing to their destruction.
Theories regarding destruction of melanocytes include autoimmune mechanisms, cytotoxic mechanisms, intrinsic melanocyte defects, oxidant-antioxidant mechanisms, and neural mechanisms.

  1. Autoimmune and cytotoxic hypotheses: Aberration of immune surveillance results in melanocyte dysfunction or destruction.
  2. Neural hypothesis: A neurochemical mediator destroys melanocytes or inhibits melanin production.
  3. Oxidant-antioxidant mechanisms: An intermediate or metabolic product of melanin synthesis causes melanocyte destruction.
  4. Intrinsic defect of melanocytes: Melanocytes have an inherent abnormality that impedes their growth and differentiation in conditions that support normal melanocytes.

Because none of these theories alone is entirely satisfactory, some have suggested a composite hypothesis.
Is it hereditary?
There is certainly a higher probability of developing Vitiligo if a close family member is affected than otherwise.
Vitiligo is relatively common, with a rate of 1-2% of general population. However, approximately 30% of vitiligo cases occur with a familial clustering of cases.
Investigations and Tests in Vitiligo patient
Although the diagnosis of vitiligo generally is made on the basis of clinical findings, biopsy is occasionally helpful for differentiating vitiligo from other hypopigmentary disorders.
Vitiligo may be associated with other autoimmune diseases, especially thyroid disease and diabetes mellitus. Other associated autoimmune diseases include pernicious anemia, Addison disease, and alopecia areata. Patients should be made aware of signs and symptoms that suggest the onset of hypothyroidism, diabetes, or other autoimmune disease. If signs or symptoms occur, appropriate tests should be performed.
Vitiligo is diagnosed by means of inspection with a Wood lamp.
Dermascopic Examination gives a better idea to surgeon about differential diagnosis and further line of managament.
Overview of Treatment Options
Nonsurgical treatments

  1. Systemic phototherapy: Induces cosmetically satisfactory repigmentation in up to 70% of patients with early or localized disease.
  2. Laser therapy: Effective on limited, stable patches of vitiligo.
  3. Steroid therapy: Systemic steroids (prednisone) have been used, although prolonged use and their toxicity are undesirable.
  4. Topical therapies.
  5. Depigmentation therapy: If vitiligo is widespread and attempts at repigmentation have not produced satisfactory results, depigmentation may be attempted in selected patients.
  6. Micropigmentation: Tattooing can be used to repigmentdepigmented skin in dark-skinned individuals.

Surgery
The basic types of repigmentation surgery are as follow :

  1. Noncultured epidermal suspensions
  2. Thin dermoepidermal grafts
  3. Suction epidermal grafting
  4. Punch minigrafting
  5. Cultured epidermis with melanocytes or cultured melanocyte suspensions

No single therapy for vitiligo produces predictably good results in all patients; treatment must be individualized, and patients should be made aware of the limitations and care associated with each therapy.
During medical therapy, pigment cells arise and proliferate from the following 3 sources:

  1. The pilosebaceous unit, which provides the highest number of cells, migrating from the external root sheath toward the epidermis
  2. Spared epidermal melanocytes not affected during depigmentation.
  3. The border of lesions, migrating up to 2-4 mm from the edge.

Systemic phototherapy
Systemic phototherapy induces cosmetically satisfactory repigmentation in up to 70% of patients with early or localized disease.
Narrow-band UV-B phototherapy is widely used and produces good clinical results. Narrow-band fluorescent tubes with an emission spectrum of 310-315 nm and a maximum wavelength of 311 nm are used. Treatment frequency is 2-3 times weekly, but never on consecutive days. This treatment can be safely used in children, pregnant women, and lactating women. Short-term adverse effects include pruritus and dryness of skin. A 2009 study concluded that oral vitamin E may represent a valuable adjuvant therapy, increasing the effectiveness of narrow-band UV-B therapy.
Narrow-band UV-B has become the first choice of therapy for adults and children with generalized vitiligo.
Psoralenphotochemotherapy involves the use of psoralens combined with UV-A light (PUVA) and has often been the most practical choice for treatment, especially in patients with darker skin types who have widespread vitiligo. Psoralens can be applied either topically or orally, followed by exposure to artificial UV light or natural sunlight. Vitiligo on the back of the hands and feet is highly resistant to therapy.
The best results from PUVA can be obtained on the face, trunk, and proximal parts of the extremities. However, 2-3 treatments per week for many months are required before repigmentation from perifollicular openings merges to produce confluent repigmentation. The total number of PUVA treatments required is 50-300. Repigmentation occurs in a perifollicular pattern.
The advantages of narrow-band UV-B over PUVA include shorter treatment times, no drug costs, no adverse GI effects (eg, nausea), and no need for subsequent photoprotection.
Laser therapy
Another innovation is therapy with an excimer laser, which produces monochromatic rays at 308 nm to treat limited, stable patches of vitiligo. This new treatment is an efficacious, safe, and well-tolerated treatment for vitiligo when limited to less than 30% of the body surface. However, therapy is expensive. Localized lesions of vitiligo are treated twice weekly for an average of 24-48 sessions.
According to studies from 2004 and 2007, combination treatment with 0.1% tacrolimus ointment plus the 308-nm excimer laser is superior to 308-nm excimer laser monotherapy for the treatment of UV-resistant vitiliginous lesions.
A retrospective chart and photographic review of 80 patients concluded that segmental vitiligo has a better repigmentation response with excimer laser treatment used at earlier stages of the disease.The study also concluded that long-term use and high cumulative UV energy of the excimer laser had better response.
Steroid therapy
Systemic steroids (prednisone) have been used, although prolonged use and their toxicity are undesirable. The benefits versus the toxicity of this therapy must be weighed carefully.
A topical steroid preparation is often chosen first to treat localized vitiligo because it is easy and convenient for both doctors and patients to maintain the treatment. The results of therapy have been reported as moderately successful, particularly in patients with localized vitiligo and/or an inflammatory component to their vitiligo, even if the inflammation is subclinical.
Topical therapies
Topical tacrolimus ointment (0.03% or 0.1%) is an effective alternative therapy for vitiligo, particularly when the disease involves the head and neck. Combination treatment with topical tacrolimus 0.1% plus the 308-nm excimer laser is superior to monotherapy with the 308-nm excimer laser monotherapy for UV-resistant vitiliginous lesions
Topical PUVA is of benefit in some patients with localized lesions. Cream and solution of 8-methoxypsoralen (0.1-0.3% concentration) are available for this treatment. It is applied 30 minutes prior to UV-A radiation. It should be applied once or twice a week. Physicians who prescribe PUVA therapy should be thoroughly familiar with the risks associated with the treatment. Additional UV-A exposure should be avoided while skin is sensitized because severe burns may occur if patients receive additional UV-A exposure.
Of general concern, tanning of surrounding normal skin exaggerates the appearance of vitiligo, and this is prevented by sun protection. Sunscreens with a sun protection factor of 15 or higher are best.
Surgical Treatments
Surgical alternatives exist for the treatment of vitiligo; however, because of the time-consuming nature of surgical therapies, these treatment regimens are limited to segmental or localized vitiligo. Patients who have small areas of vitiligo with stable activity are candidates for surgical transplants.
The most important factors indicating stability are as follows:

  1. No progression of lesions for at least 2 years
  2. Spontaneous repigmentation indicates vitiligo inactivity
  3. A positive minigrafting test disclosing repigmentation at 4-5 minigrafts, which, to date, is the most accurate evidence of vitiligo stability
  4. Absence of new white patches, including at the donor site for the minigrafting test
  5. Unilateral vitiligo is the most stable form of vitiligo

Five basic methods for repigmentation surgery are as follows

  1. Noncultured epidermal suspensions: After the achromic epidermis is removed, an epidermal suspension with melanocytes and keratinocytes previously prepared by trypsinization of normally pigmented donor skin is spread onto the denuded area and immediately covered with nonadherent dressings. Using noncultured epidermal cellular grafts, 71% of patients in one study achieved more than 75% repigmentation. Color mismatches were common, and generalized vitiligo did not repigment quite as well.
  2. Thin dermoepidermal grafts: The depigmented epidermis is removed by superficial dermabrasion, including the papillary dermis, and very thin dermoepidermal sheets harvested with dermatome are grafted onto the denuded skin.
  3. Suction epidermal grafting: Epidermal grafts can be obtained by vacuum suction, usually with 150 mm Hg. The recipient site can be prepared by suction, freezing, or dermabrasion of the sites 24 hours before grafting. The depigmented blister roof is discarded, and the epidermal donor graft is placed on the vitiliginous areas.
  4. Punch minigrafting: Small donor grafts are inserted into the incision of recipient sites and held in place by a pressure dressing. The graft heals readily and begins to show repigmentation within 4-6 weeks. Some pebbling and cobble stone appearance is inevitable.
  5. Cultured epidermis with melanocytes or cultured melanocyte suspensions: Depigmented skin is removed using liquid nitrogen, superficial dermabrasion, thermosurgery, or carbon dioxide lasers; very thin sheets of cultured epidermis are grafted or suspensions are spread onto the denuded surface.
  6. Micropigmentationis another option. Tattooing can be used to repigmentdepigmented skin in dark-skinned individuals. Color matching is difficult, and the color tends to fade. Skin can be dyed with dihydroxyacetone preparations, although the color match is often poor.

 

 

 
 
 
 

 

 
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