Vitiligo - WikiHQ

Vitiligo ( ) is a chronic autoimmune disorder that causes patches of skin to lose pigment or color; these vary in size and can appear anywhere on the body. The disorder is thought to be caused by immune system changes with potential genetic factors. It can be brought on by regional environmental risk factors, especially early in life, as well as sun or chemical exposure, stress, and chronic physical trauma. The most common form, nonsegmental vitiligo, tends to affect more skin over time; potential treatments include topical medications and light therapy.

In antiquity, the disorder was often conflated with leprosy, an infectious disease. Some famous individuals have had vitiligo, such as singer Michael Jackson, who obscured his condition until it affected his entire body.

Signs and symptoms

The only sign of vitiligo is the presence of pale, patchy areas of depigmented skin, which tend to occur on the extremities. 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.

File:Vitiligo03.jpg|Vitiligo on lighter skin

File:Vitiligo1.JPG|Nonsegmental vitiligo on dark skin

File:Eyelid vitiligo 06.jpg|Nonsegmental vitiligo of the eyelids

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Causes

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.

Susceptibility to vitiligo may be affected by regional environmental risk factors, especially early in life. An event like a sunburn, exposure to a chemical, stress or emotional distress can trigger or exacerbate the condition. Skin depigmentation can occur at the site of physical trauma, an example of the Koebner phenomenon; unlike in other skin diseases, this can be caused by daily activities, especially chronic friction on particular areas of the body. The phenomenon occurs in a third of patients with nonsegmental vitiligo (NSV) but is rarely seen in segmental vitiligo (SV).

Immune

Variations in genes that are expressed in the immune cells or in the melanocytes have both been associated with vitiligo. A genome-wide association study found approximately 36 independent susceptibility loci for generalized vitiligo. One of them is the TYR gene that encodes the protein tyrosinase, which is an enzyme of the melanocytes that catalyzes melanin biosynthesis, and a major autoantigen in generalized vitiligo.

The disorder has occurred in recipients of bone marrow and lymphocytes from donors with vitiligo.

Autoimmune associations

Vitiligo is sometimes associated with autoimmune and inflammatory diseases such as Hashimoto's thyroiditis, scleroderma, rheumatoid arthritis, type 1 diabetes mellitus, psoriasis, Addison's disease, pernicious anemia, alopecia areata, systemic lupus erythematosus, and celiac disease.

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 are highly conserved in evolution, and are found in humans, chimpanzees, rhesus monkeys, and bush babies. Addison's disease (typically an autoimmune destruction of the adrenal glands) may also be seen in individuals with vitiligo.

Oxidative stress

Numerous whole-exome sequencing studies have demonstrated that vitiligo is associated with polymorphisms in genes involved in the response to oxidative stress, such as CAT, SOD1, SOD2, SOD3, NFE2L2, HMOX1, GST-M1, or GST-T1, supporting the association of elevated levels of reactive oxygen species in melanocytes with the induction of an autoimmune response.

Thus, diseases presenting with altered mitochondrial function such as MELAS, Vogt-Koyanagi-Harada syndrome and Kabuki syndrome are associated with increased risk of vitiligo.

In line with these observations, genetic alterations in mitochondrial DNA (mtDNA) of melanocytes associated with altered mitochondrial function lead to a release of mtDNA that can be detected in the skin of vitiligo patients. This mtDNA can be sensed by the cGAS-STING pathway, resulting in pro-inflammatory cytokine and chemokine production promoting the recruitment of cytotoxic CD8+ T cells. Mitochondrial antioxidants, NRF2 inhibitors, and TBK1 inhibitors are emerging as potential therapeutic options to block this cascade of events. 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.

Past classifications of vitiligo have been somewhat inconsistent, but two forms are currently recognized. and can occur in patches or over large portions of the body. NSV can occur at any age (unlike segmental vitiligo, which is far more prevalent in teenage years).

Universal vitiligo (vitiligo universalis): depigmentation encompasses most of the body It is much more stable/static in its course and is rarely associated with autoimmune diseases. Due to the higher risks of skin cancer, the United Kingdom's National Health Service suggests that 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.

Phototherapy

Phototherapy is considered a second-line treatment for vitiligo. but narrowband ultraviolet peaked around 311 nm is the choice. It has been consistently reported that a combination of UVB phototherapy with other topical treatments improves repigmentation. However, some people with vitiligo may not see any changes in their skin or repigmentation occurring. A serious potential side effect involves the risk of developing skin cancer, the same risk as 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 and then exposing the skin to high doses of UVA light. Treatment is required twice a week for 6–12 months or longer. Due to 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; 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

American pop singer Michael Jackson had the condition, which he obscured via costumes and makeup until it covered his body. This led to some inaccurate speculation that he bleached his skin. Other notable cases include American rapper Krizz Kaliko, Canadian fashion model Winnie Harlow, New Zealand singer-songwriter Kimbra, American actor David Dastmalchian, Argentine musician Charly García, professional wrestler Bryan Danielson, French actor Michaël Youn, former French Prime Minister Édouard Philippe, Miss Universe Egypt 2024 Logina Salah, governor of Pampanga and television host Eddie Panlilio, and Colombian model Taliana Vargas.

In popular culture

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 white, leading him to commit delusional and racist antics.

Research

, 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 the 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.

References

External links

Questions and Answers about Vitiligo – US National Institute of Arthritis and Musculoskeletal and Skin Diseases