Abstract

The pathophysiology of vitiligo is very complex. It is an autoimmunity disease that causes white patches on the skin. Basically, when we decrease the melanin production in our body, they cause the skin depigmentation. Highly sensitive C-reactive protein is a susceptible marker for the systemic inflammation in the body. Interlukins-6 and TNF-alpha are the inflammation mediators they cause systemic inflammation. Homocysteine is increased they play a vital role in the pathophysiology of vitiligo. When the nutrient deficiency then increases the level of homocysteine because they inhibit the tyrosine enzyme by binding with copper it is reversible hypopigmentation. The S100B protein is increased in the patient with vitiligo. This protein is reacted with less than 6 months in all vitiligo patients. When the rapidity increases the concentration of S100B protein in the patients they cause neuronal dysfunction and cell death. It produces pro-inflammatory cytokines that are harmful for the tissue. The neutrophil growth factor is also the factor causing the depigmentation of skin because when the person is suffering from schizophrenia, depression and other mental disorders they are also causing the depigmentation. When we decrease the vitamin D level in our body then they cause different diseases such as diabetes mellitus, rheumatoid arthritis, depigmentation, multiple sclerosis, and other diseases. It is affecting the variable immune response through receptor T or B lymphocytes and dendritic cells. The treatment of depigmentation to form a combination of vitamin D with UV light or corticosteroids is to increase the repigmentation.