Витилиго: причины, симптомы и методы лечения потери пигментации кожи.

Skin condition where patches lose pigment

Vitiligo (,/v//ɪ//t//ɪ/'/l//aɪ//ɡ//oʊ/) is a chronic autoimmune disorder that causes patches of skin to lose pigment or color. The cause of vitiligo is unknown, but it may be related to immune system changes, genetic factors, stress, or sun exposure. Treatment options include topical medications, light therapy, surgery and cosmetics. Some people may experience itching before a new patch appears. The patches are initially small, but often grow and change shape. When skin lesions occur, they are most prominent on the face, hands and wrists. Those affected by vitiligo who are stigmatized for their condition may experience depression and similar mood disorders.

Although multiple hypotheses have been suggested as potential triggers that cause vitiligo, studies strongly imply that changes in the immune system are responsible for the condition. Vitiligo has been proposed to be a multifactorial disease with genetic susceptibility and environmental factors both thought to play a role. The National Institutes of Health states that some believe that sunburns can cause or exacerbate the condition, but this idea is not well supported by good evidence.

Melanin is the pigment that gives skin its color; it is produced by skin cells called melanocytes. Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo. A genome wide association study found approximately 36 independent susceptibility loci for generalized vitiligo. The TYR gene encodes the protein tyrosinase, which is not a component of the immune system, but is an enzyme of the melanocyte that catalyzes melanin biosynthesis, and a major autoantigen in generalized vitiligo. Among the inflammatory products of NLRP1 are caspase 1 and caspase 7, which activate the inflammatory cytokine interleukin 1β. Interleukin 1β and interleukin 18 are expressed at high levels in people with vitiligo. 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 is found in humans, chimpanzee, rhesus monkey, and the bush baby. Addison's disease (typically an autoimmune destruction of the adrenal glands) may also be seen in individuals with vitiligo.

An ultraviolet light can be used in the early phase of this disease for identification and to determine the effectiveness of treatment. Using a Wood's light, skin will change colour (fluoresce) when it is affected by certain bacteria, fungi, and changes to pigmentation of the skin.

Classification attempts to quantify vitiligo have been analyzed as being somewhat inconsistent, while recent consensus have agreed to a system of segmental vitiligo (SV) and non segmental vitiligo (NSV). NSV is the most common type of vitiligo. Universal vitiligo: depigmentation encompasses most of the body SV does not improve with topical therapies or UV light; however, surgical treatments such as cellular grafting can be effective. Due to the higher risks of skin cancer, the United Kingdom's National Health Service suggests phototherapy be used only if primary treatments are ineffective. Lesions located on the hands, feet, and joints are the most difficult to repigment; those on the face are easiest to return to the natural skin color as the skin is thinner in nature.

Phototherapy is considered a second line treatment for vitiligo. but narrowband ultraviolet peaked around 311 nm is the choice. It has been constitutively reported that a combination of UVB phototherapy with other topical treatments improves re pigmentation. However, some people with vitiligo may not see any changes to skin or re pigmentation occurring. A serious potential side effect involves the risk of developing skin cancer, the same risk as an overexposure to natural sunlight. Ultraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and ultraviolet A light (PUVA) treatment involves taking a drug that increases the skin's sensitivity to ultraviolet light, then exposing the skin to high doses of UVA light. Treatment is required twice a week for 6–12 months or longer. Because of the high doses of UVA and psoralen, PUVA may cause side effects such as sunburn type reactions or skin freckling. NBUVB phototherapy appears better than PUVA therapy with the most effective response on the face and neck. hydrocortisone plus laser light is better than laser light alone, ginkgo biloba is better than placebo, and oral mini pulse of prednisolone (OMP) plus NB UVB is better than OMP alone. (or 1312 BC) described a group of skin diseases associated with white spots, and a subsequent translation to Greek led to continued conflation of those with vitiligo with leprosy and spiritual uncleanliness. The term vitiligo is believed to be derived from "vitium", meaning "defect" or "blemish". Notable cases include American pop singer Michael Jackson, Canadian fashion model Winnie Harlow, New Zealand singer songwriter Kimbra, American actor David Dastmalchian and Argentine musician Charly García. Professional wrestler Bryan Danielson and French actor Michaël Youn are also affected, as is former French Prime Minister Édouard Philippe, and TV host, model and former Miss Colombia 2007, Taliana Vargas. The Adult Swim animated sitcom The Boondocks satirizes the idea of vitiligo in Uncle Ruckus, one of the show's characters. Ruckus, who is black, frequently claims to be white, often stating that he has "Re vitiligo, the opposite of what Michael Jackson had." He frequently uses this argument to maintain that he is actually Caucasian, leading him to commit delusional and racist antics in nearly every episode.

as of 2013, afamelanotide is in phase II and III clinical trials for vitiligo and other skin diseases. A medication for rheumatoid arthritis, tofacitinib, has been tested for the treatment of vitiligo. In October 1992, a scientific report was published of successfully transplanting melanocytes to vitiligo affected areas, effectively repigmenting the region. The procedure involved taking a thin layer of pigmented skin from the person's gluteal region. Melanocytes were then separated out to a cellular suspension that was expanded in culture. The area to be treated was then denuded with a dermabrader and the melanocytes graft applied. Between 70 and 85 percent of people with vitiligo experienced nearly complete repigmentation of their skin. The longevity of the repigmentation differed from person to person. Current research suggests that the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT pathway) plays a crucial role in the loss of epidermal melanocytes. This pathway is activated by CXCR3+ CD8+ T cells, creating a positive feedback loop with interferon gamma (IFN γ) chemokines from keratinocytes, potentially contributing to vitiligo. JAK inhibitors like ruxolitinib show promise in targeting the IFN γ chemokine signaling axis implicated in vitiligo pathogenesis, and improving nonsegmental vitiligo.