Vitiligo is a chronic disorder that causes depigmentation in patches of skin. 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 less than 1 percent.  Non-segmental vitiligo has a greater prevalence than the disorder’s other form(s).
Signs and symptoms The most notable symptom of vitiligo is depigmentation of patches of skin that occurs on the extremities. Although patches are initially small, they often 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 hyperpigmentation around the edges.  In regards to psychological damage, vitiligo can have a significant effect on the mental health of a patient.  Psychological stress may even result in an individual becoming more susceptible to vitiligo. Patients who are stigmatised for their condition may experience depression and similar mood disorders.
Non-segmental vitiligo In Non-segmental vitiligo (NSV), there is usually some form of symmetry in the location of the patches of depigmentation. 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.
Segmental vitiligo Segmental vitiligo (SV) differs in appearance, aetiology and prevalence of associated illnesses. Its treatment is also different to that of NSV. It tends to affect areas of skin that are associated with dorsal roots from the spine. It spreads much more rapidly than NSV and, without treatment, patches of depigmented skin remain throughout life.
Pathogenesis Vitiligo is associated with autoimmune and inflammatory diseases, commonly thyroid overexpression and underexpression. 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.
Among the inflammatory products of NALP1 are caspase 1 and caspase 5, which activate the inflammatory cytokine interleukin-1β. Interleukin-1β is expressed at high levels in patients with vitiligo. There are compounds which inhibit caspase and interleukin-1β, 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 is 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