Vitiligo

What is vitiligo? 
Vitiligo is a chronic skin disease characterized by the appearance of white spots on different parts precise contours of the body. These are depigmented patches due to destruction of melanocytes - the cells responsible for skin pigmentation. Depigmentation may be more or less important, and affected areas have variable sizes.
The origin of the disease is unknown, but believed that it is an autoimmune disease in which antibodies produced by the body attacking and destroying its own melanocytes.
Vitiligo appears first as small depigmented spots, which expand and grow in size over time. These skin changes in patients determine the occurrence of stress and anxiety due or aesthetic appearance. Vitiligo affects 1% - 2% of the population and usually occurs before the age of 20 years (50% of people affected).
There is no cure for vitiligo. Instead, the aim of treatment is to stop or slow to return pigmentation and skin coloration within certain limits. In rare cases, the spots disappear on their own. People affected by vitiligo have an increased risk of skin cancer because depigmented areas are not protected against sunlight.
Vitiligo - definition
Vitiligo is a pigmentary disorder of the skin and mucous membranes gained characterized by circumscribed depigmented macules and patches. It is a progressive condition in which some or all of the affected skin melanocytes are selectively destroyed. Vitiligo affects 0. 5-2% of world population, and age of onset is 20 years. Vitiligo is a multifactorial polygenic disease with complex pathogenesis.
Vitiligo is manifested as hypopigmented spots or white patches or acquired. Is related to genetics and nongenetici. Although several theories have been proposed for vitiligo pathogenesis, the precise cause remains unknown. Principles generally accepted in the skin are affected by the absence of functional melanocytes and loss of histochemical recognition of melanocytes leading to their destruction.
No single therapy does not cause good results. response to therapy is quite variable. Treatment should be individualized and patients should know the risks associated with therapy. Phototherapy induces systemic satisfactory cosmetic repigmentation in 70% of patients with early or localized disease. Laser therapy is another innovation for limited spots vitiligo stable. Therapy is expensive, however. Steroid therapy with prednisone was used although preungita administration and its toxicity is undesirable. Benefits should be carefully weighed against toxicity. Tacrolimus topical creams therapies are an alternative option for vitiligo.
If it is widespread vitiligo and repigmentation attempts have failed satisfactory depigmentation may be tried in some patients. There are alternative surgical treatment of vitiligo, however due to time-consuming nature of these therapies are limited for localized vitiligo.
Pathogenesis of vitiligo Theories on the destruction of melanocytes include autoimmune mechanisms, cytotoxic mechanisms, the intrinsic defect of melanocytes, oxido-reducing mechanisms and neural mechanisms.
Autoimmune destruction of melanocytes Autoimmune theory proposes altering humoral and cellular immune destruction of melanocytes in vitiligo. Thyroid disorders, especially Hashimoto thyroiditis and Graves' disease and other endocrinopathies such as Addison's disease and diabetes mellitus, alopecia areata, pernicious anemia, inflammatory bowel disease, psoriasis and autoimmune poliglandular syndrome are associated with vitiligo. The most convincing evidence of an autoimmune pathogenesis is the prevalence of circulating antibodies in patients with vitiligo. The role of humoral immunity is supported by observation of melanocytes destroyed healthy skin grafts in a patient with vitiligo. In addition to the mechanisms involved in the pathogenesis of humoral autoimmune vitiligo and indicate the involvement of cellular immunity. Destruction of melanocytes may be directly mediated by CD 8 lymphocytes.
Intrinsic defects of melanocytes Melanocytes in vitiligo may have an intrinsic defect that leads to their death. These melanocytes show various abnormalities, including abnormal endoplsmic reticulum, rough and incomplete synthesis and processing of melanocytes. In addition, abnormalities were detected and the receptor. Early apoptosis of melanocytes has also been suggested as the cause of their low survival, however, reveals that a second investigation succeptibilitatea relative to apoptosis of melanocytes was comparable to the healthy.
Oxidation-reduction system disorders in vitiligo Oxidative stress also plays an essential role in the pathogenesis of vitiligo. Studies suggest that the accumulation of free radicals toxic to melanocytes leading to their destruction. Because patients with vitiligo shows a characteristic fluorescent yellow / green or blue skin clinically affected acasta lead to the discovery that fluorescence is due to specific accumulation of oxygen radicals-pteridine. Pteridine production of an accumulation of hydrogen peroxide melanocitotoxic.
Neural Theory in vitiligo Describe patients with vitiligo and nerve damage which shows hypopigmentation or depigmentation denervata area. Vitiligo appears frecent a dermatome segment suggested that some chemical mediators are released into the depigmented patches of vitiligo with increased adrenergic activity. Increased urinary excretion of vanilmandelic acid-neurometaboliti homovanilic and was documented in patients with vitiligo.
Vitiligo genetic theory Vitiligo is characterized by incomplete penetrance, multiple succeptibilitate loci and genetic heterogeneity. Heredity vitiligo may involve genes associated with melanin biosynthesis, response to oxidative stress and regulating autoimmunity.