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The Special Pathogenesis Of Vitiligo

The Special Pathogenesis Of VitiligoAs we al known that the incidence of the vitiligodisease is still unknown , about pathogenesis opinions, there is generally believed that the disease is genetic quality of individuals in a variety of internal and external factors stimulate performance for the disorder of immune function, neurological and endocrine and metabolic functions, leading to inhibition of the enzyme system, black prime cell destruction, melanosomes generated or blackening process barriers, and ultimately cause depigmentation.

1. The genetic theory ,it is said that 25% ~ 30% of the patients had a family history, genetic pattern is unknown. An autosomal dominant disorder with an autosomal dominant pattern.

2. Many clinical studies of the spirit and nerve theory ,it show that the mental factors are closely related to the incidence of vitiligo. About 2/3 patients with skin lesions in the generation or expansion of mental tension, the paralysis of the spinal cord is generally not involved in the paralysis of limbs, diabetic neuropathy of the skin to restore pigmentation. Vitiligo lesions often segment distribution, Merkel cells disappeared in early lesions. An increase in the number of neuropeptide in the skin lesions and normal skin adjacent to the normal skin, and the abnormal ultrastructure of the nerve fibers.

3. The autoimmune theory, this type disease patients or family members often accompanied by autoimmune diseases, such as hyperthyroidism, diabetes, alopecia areata, lupus, scleroderma, and so on. Anti thyroglobulin protein in serum and anti smooth muscle, anti gastric parietal cell or anti adrenal tissue specificity antibody positive rate increased significantly; about 82% of the serum of patients in the presence of anti melanocyte antibodies, and normal no this antibody. The incidence of vitiligo in patients with autoimmune diseases is 10 to 15 times higher than that of the normal population.

Although for patients with vitiligo in peripheral blood lymphocyte count and classification of many research results are not uniform, but most of the research results show that duration in patients less than 1 year, in the peripheral blood of auxiliary T cells (CD4 + T cells) were significantly reduced and soluble interleukin-2 receptor (sIL-2R) and white blood cell migration inhibitory factor was significantly increased. The infiltrating lymphocytes in the skin lesions were mainly T lymphocytes, which speculated that the destruction of melanocytes may be mainly mediated by T lymphocytes or directly.

4 melanocytes in their own destruction theory, vitiligo is more likely to occurs at the site of exposure and pigmentation, and its basic lesions are epidermal melanocytes partial or complete loss of function. Lerner in 1971 put forward this theory, believe that vitiligo is due to the epidermal melanocytes hyperfunction, prompting the loss and early recession, and may be due to cell toxicity of synthetic black pigment precursor accumulation caused by.

5. Tyrosine, copper ions relative lack theory, the production of black pigment is a complex biochemical process, and DOPA is black element is the predecessor of adrenaline, originate from tyrosine, tyrosinase and oxidation. When excessive mental stress, the body consumes large amounts of adrenaline. At this time DOPA guided epinephrine synthesis, and the synthesis of melanin affected. Some scholars have found that vitiligo patients in the blood and skin of copper or ceruloplasmin (serum copper oxidase) value is lower than that of normal control group, which leads to reduction in tyrosinase activity, thus affecting the metabolism of melanin. However, some studies have found that there is no significant difference between the normal group and the serum levels of the serum and hair of patients with vitiligo.


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