It occurs when the melanocytes, the cells responsible for skin pigmentation which are derived from the neural crest, die or are unable to function. The precise pathogenesis, or cause, of vitiligo is complex and not yet fully understood. There is some evidence suggesting it is caused by a combination of autoimmune, genetic, and environmental factors. It is also common in people with thyroid disorders. The population incidence worldwide is considered to be between 1% and 2%. Non-segmental vitiligo has a greater prevalence than the disorder's other form(s).
Although patches are initially small in size, they can often start to enlarge and change shape. When skin lesions occur, they are most prominent on the face, hands and wrists. Depigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus. Some lesions have a tendency to hyperpigment around the edges. In a more general sense, vitiligo is similar in appearance to leprosy, and as such (in countries where leprosy is prevalent), individuals with vitiligo can be stigmatized for the similarities in appearance.
New patches also appear over time, and can be generalised over large portions of the body, or localised to a particular area. Vitiligo where little pigmented skin remains is referred to as vitiligo universalis . NSV can come about at any age, unlike segmental vitiligo which is far more prevalent in teenage years.
A study comparing 656 people with and without vitiligo in 114 families found several mutations (single-nucleotide polymorphisms) in the NALP1 gene.The NALP1 gene, which is on chromosome 17 located at 17p13, is on a cascade that regulates inflammation and cell death, including myeloid and lymphoid cells, which are white cells that are part of the immune response. NALP1 is expressed at high levels in T cells and Langerhan cells, white blood cells that are involved in skin autoimmunity.
Interleukin-1 is expressed at high levels in patients with vitiligo. There are compounds which inhibit caspase and interleukin-1, and so might be useful drugs for vitiligo and associated autoimmune diseases. In one of the mutations, the amino acid leucine in the NALP1 protein was replaced by histidine (Leu155-> His). The original protein and sequence is highly conserved in evolution, and found in humans, chimpanzee, rhesus monkey, and bush baby, which means that it's an important protein and an alteration is likely to be harmful. Addison's disease (typically an autoimmune destruction of the adrenal glands) may cause vitiligo.
In mild cases, vitiligo patches can be hidden with makeup or other cosmetic camouflage solutions. If the affected person is pale-skinned, the patches can be made less visible by avoiding sunlight and the sun tanning of unaffected skin. However, exposure to sunlight may also cause the melanocytes to regenerate to allow the pigmentation to come back to its original color.
It is the only organisation which offers support and understanding to people with vitiligo and their families in the UK and the Republic of Ireland. The Vitiligo Society strives to support people anywhere in the world who asks for help and provides reliable information to the general public and health professionals about vitiligo and available treatment for the condition.
Source: Wikipedia > Vitiligo
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