What causes vitiligo

If you want to effectively treat vitiligo, you need to pay attention to the causes of these diseases. Vitiligo is hereditary, and family members with vitiligo are also more likely to suffer from some autoimmune diseases, such as thyroiditis and hyperthyroidism.

1. Genetic theory

Some studies suggest that vitiligo may be an autosomal dominant skin disease. Foreign authors have calculated that 30% of patients have a positive family history and found that both monozygotic twins developed the disease. The domestic reported rate of positive family history is 3% to 12%, which is lower than that reported abroad.

2. Autoimmunity theory

The relationship between autoimmunity theory and the pathogenesis of vitiligo is gaining increasing attention. Many scholars have noticed that the incidence of comorbid autoimmune diseases in patients and their family members is relatively high, including thyroiditis, hyperthyroidism or hypothyroidism, diabetes, chronic adrenal insufficiency, pernicious anemia, rheumatoid arthritis, malignant melanoma, etc. In the serum of vitiligo patients, specific antibodies to multiple organs have been detected, such as anti-thyroid antibodies, anti-gastric parietal cell antibodies, anti-adrenal gland antibodies, anti-parathyroid gland antibodies, anti-smooth muscle antibodies, etc., and the detection rate is significantly high. In addition, the incidence of vitiligo in people with autoimmune diseases is 10 to 15 times higher than that in the general population. Recently, it has been discovered that vitiligo patients have antibodies against melanocyte surface antigens, called vitiligo antibodies. The titer of these antibodies is related to the degree of skin depigmentation in the patient, and the titer increases with the expansion of the skin lesion area. It has also been found that animals with vitiligo also have similar phenomena, suggesting that the disease is an autoimmune disease of melanocytes. Behl (1977) found that in the progressive stage of white spots, monocytes aggregated at the edge and invaded the dermal-epidermal junction, entering the epidermis through the damaged basement membrane, causing the absence of melanocytes and melanin in that area. He believed that this disease might be an autoimmune disease of delayed hypersensitivity reaction. In addition, oral or topical corticosteroids, especially for skin lesions that are not distributed according to dermatomes, have a good therapeutic effect, which also indirectly proves the immune mechanism of this disease.

3. Psychological and neurochemical theory

Many clinicians have found that mental factors are closely related to the onset of vitiligo. It is estimated that about 2/3 of patients suffer from mental trauma, excessive tension, depression or frustration at the onset or development of skin lesions. Tension can lead to an increase in catecholamines, such as adrenaline, which can directly affect depigmentation; stress can also increase ACTH secretion, leading to increased corticosteroid secretion, mobilizing sugar and free fatty acids, and stimulating insulin secretion. Insulin indirectly stimulates the increase of L-tryptophan in the brain, thereby increasing the synthesis of serotonin in the brain. The metabolite of serotonin is melatonin. Excessive activity of pheomelanin receptors plays an important role in the onset of vitiligo. Excessive activity of melatonin receptors can increase the activity of theazolamins, which inhibit melanin biochemistry, but later activate its biochemistry, resulting in the accumulation of toxic intermediates of melanin metabolism in melanocytes, causing melanocyte death and ultimately leading to vitiligo. Some scholars have observed that the nerve endings in the white spots undergo degeneration, and the degree of change seems to be related to the course of the disease. This phenomenon also supports the neurochemical theory.