Vitiligo

Vitiligo (/ˌvɪtɪˈlaɪɡoʊ/ VIT-ih-LY-goh) is a chronic autoimmune disorder that causes patches of skin to lose pigment or color.[1] The cause of vitiligo is unknown, but it may be related to immune system changes, genetic factors, stress, or sun exposure, and susceptibility to it may be affected by regional environmental risk factors, especially early in life.[2][3][4] Treatment options include topical medications, light therapy, surgery and cosmetics.[3] The condition causes patches of a light peachy color of any size, which can appear on any place on the body; in particular, nonsegmental vitiligo, the common form, tends to progress, affecting more of the skin over time.[5][6] Vitiligo spots on the skin can also vary in pigmentation over long periods, although they will stay in relatively the same areas.

## Contents

* 1 Signs and symptoms
* 2 Causes
* 2.1 Immune
* 2.2 Autoimmune associations
* 2.3 Oxidative stress
* 3 Diagnosis
* 3.1 Classification
* 3.1.1 Non-segmental
* 3.1.2 Segmental
* 3.2 Differential diagnosis
* 4 Treatment
* 4.1 Immune mediators
* 4.2 Phototherapy
* 4.3 Skin camouflage
* 4.4 Depigmenting
* 5 History
* 6 Society and culture
* 6.1 Notable people with vitiligo
* 6.2 In popular culture
* 7 Research
* 8 References
* 9 External links

## 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.[7][8] Some people may experience itching before a new patch appears.[9] The patches are initially small, but often grow and change shape.[7][10] When skin lesions occur, they are most prominent on the face, hands, and wrists.[7][8] The loss of skin pigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus.[7][8] Some lesions have increased skin pigment around the edges.[11] Those affected by vitiligo who are stigmatized for their condition may experience depression and similar mood disorders.[12]

* Vitiligo on lighter skin

* Non-segmental vitiligo on dark skin

* Non-segmental vitiligo of the eyelids

## 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.[13][14] Vitiligo has been proposed to be a multifactorial disease with genetic susceptibility and environmental factors both thought to play a role.[13] It is hypothesized that damaging environmental factors can disrupt redox reactions necessary for protein folding, so skin cells may initiate the unfolded protein response which releases cytokines, thus mounting an immune response.[15][16]

The National Institutes of Health states that sometimes an event, like a sunburn, emotional distress, or exposure to a chemical, can trigger or exacerbate the condition.[17] Skin depigmentation in particular areas in vitiligo can also be triggered by mechanical trauma: this is an example of the Koebner phenomenon.[18] Unlike in other skin diseases, this can be caused by daily activities, especially chronic friction on particular areas of the body.[18]

### Immune

Variations in genes that are expressed in the immune cells or in the melanocytes have both been associated with vitiligo.[13] It is thought to be caused by the immune system attacking and destroying the melanocytes of the skin.[19] A genome-wide association study found approximately 36 independent susceptibility loci for generalized vitiligo.[20] 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.[13]

### 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.[13][21]

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.[22] 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.[23][24]

### 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.[25][26]

Thus, diseases presenting with altered mitochondrial function such as MELAS, Vogt-Koyanagi-Harada syndrome and Kabuki syndrome are associated with increased risk of vitiligo.[27][28][29]

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.[30][31] 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.[30]

## Diagnosis

UV photograph of a hand with vitiligo UV photograph of a foot with vitiligo

An ultraviolet light can be used in the early phase of this disease for identification and to determine the effectiveness of treatment.[32] 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.[33]

### Classification

Classification attempts to quantify vitiligo have been analyzed as being somewhat inconsistent,[34] while recent consensus has agreed to a system of segmental vitiligo (SV) and non-segmental vitiligo (NSV). NSV is the most common type of vitiligo.[13]

#### Non-segmental

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 generalized over large portions of the body or localized to a particular area. Extreme cases of vitiligo, to the extent that little pigmented skin remains, are referred to as vitiligo universalis. NSV can occur at any age (unlike segmental vitiligo, which is far more prevalent in teenage years).[11]

Classes of non-segmental vitiligo include the following:

* Generalized vitiligo: the most common pattern, wide and randomly distributed areas of depigmentation[35]
* Universal vitiligo: depigmentation encompasses most of the body[35]
* Focal vitiligo: one or a few scattered macules in one area, most common in children[35]
* Acrofacial vitiligo: fingers and periorificial areas[35]
* Mucosal vitiligo: depigmentation of only the mucous membranes[35]

#### Segmental

Segmental vitiligo (SV) differs in appearance, cause, and frequency of associated illnesses. Its treatment is different from that of NSV. It tends to affect areas of skin that are associated with dorsal roots from the spinal cord and is most often unilateral.[13][36] It is much more stable/static in its course, and its association with autoimmune diseases appears to be weaker than that of generalized vitiligo.[36] SV does not improve with topical therapies or UV light; however, surgical treatments such as cellular grafting can be effective.[11]

### Differential diagnosis

Chemical leukoderma is a similar condition due to multiple exposures to chemicals.[1] Vitiligo, however, is a risk factor.[1] Triggers may include inflammatory skin conditions, burns, intralesional steroid injections, and abrasions.[1]

Other conditions with similar symptoms include the following:

* albinism
* halo nevus
* idiopathic guttate hypomelanosis (white sunspots)[35]
* piebaldism[35]
* pityriasis alba
* postinflammatory hypopigmentation
* primary adrenal insufficiency
* progressive macular hypomelanosis[35]
* tinea versicolor[35]
* tuberculoid leprosy

## Treatment

There is no cure for vitiligo, but several treatment options are available.[13] The best evidence is for applied steroids and ultraviolet light in combination with creams.[37] 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.[38] 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.[13]

### Immune mediators

Topical preparations of immunosuppressing medications, including glucocorticoids (such as 0.05% clobetasol or 0.10% betamethasone) and calcineurin inhibitors (such as tacrolimus or pimecrolimus) are considered to be first-line vitiligo treatments.[13]

In July 2022, ruxolitinib cream (sold under the brand name Opzelura) was approved for medical use in the United States for the treatment of vitiligo.[39]

### Phototherapy

Phototherapy is considered a second-line treatment for vitiligo.[13] Exposing the skin to light from UVB lamps is the most common treatment for vitiligo. The treatments can be done at home with a UVB lamp or in a clinic. The exposure time is managed so that the skin does not suffer overexposure. Treatment can take a few weeks if the spots are on the neck and face, and if they have existed for not more than 3 years. If the spots are on the hands and legs and have been there for more than 3 years, it can take a few months. Phototherapy sessions are done 2–3 times a week. Spots on a large area of the body may require full-body treatment in a clinic or hospital. UVB broadband and narrowband lamps can be used,[40][41] 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 re-pigmentation. However, some people with vitiligo may not see any changes to their skin or re-pigmentation 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.[38]

Narrowband ultraviolet B (NBUVB) phototherapy lacks the side effects caused by psoralens and is as effective as PUVA.[13] As with PUVA, treatment is carried out twice weekly in a clinic or every day at home, and there is no need to use psoralen.[38] Longer treatment is often recommended, and at least 6 months may be required for effects to phototherapy.[42] NBUVB phototherapy appears better than PUVA therapy, with the most effective response on the face and neck.[42]

Concerning improved repigmentation: topical calcineurin inhibitors plus phototherapy are better than phototherapy alone,[43] 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.[9]

### Skin camouflage

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 tanning of unaffected skin.[35]

### Depigmenting

In cases of extensive vitiligo, the option to depigment the unaffected skin with topical drugs like monobenzone, mequinol, or hydroquinone may be considered to render the skin an even color. The removal of all the skin pigment with monobenzone is permanent and vigorous. Sun safety must be adhered to for life to avoid severe sunburn and melanomas. Depigmentation takes about a year to complete.[38]

## History

Descriptions of a disease believed to be vitiligo date back to a passage in the medical text Ebers Papyrus c. 1500 BC in ancient Egypt. Also, the Hebrew word "Tzaraath" from the Old Testament book of Leviticus[44] dating to 1280 BC[45] (or 1312 BC[46]) 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.[44]

Medical sources in the ancient world, such as Hippocrates, often did not differentiate between vitiligo and leprosy, often grouping these diseases together. The name "vitiligo" was first used by the Roman physician Aulus Cornelius Celsus in his classic medical text De Medicina.[44]

The term vitiligo is believed to be derived from "vitium", meaning "defect" or "blemish".[44]

Winnie Harlow

## Society and culture

The change in appearance caused by vitiligo can impact a person's emotional and psychological well-being. It may create difficulty in becoming or remaining employed, particularly if vitiligo develops on visible areas of the body, such as the face, hands, or arms. Participating in a vitiligo support group may improve social coping skills and emotional resilience.[47]

### Notable people with vitiligo

Notable cases include American pop singer Michael Jackson,[48] American rapper Krizz Kaliko, Canadian fashion model Winnie Harlow,[49] New Zealand singer-songwriter Kimbra,[50] American actor David Dastmalchian and Argentine musician Charly García. Professional wrestler Bryan Danielson[51] and French actor Michaël Youn are also affected,[52] as is former French Prime Minister Édouard Philippe,[53] Miss Universe Egypt 2024 Logina Salah,[54] Governor of Pampanga and TV host Eddie Panlilio, and model and former Miss Colombia 2007 Taliana Vargas.[55][56]

### 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 in nearly every episode.[57]

## Research

As of July 2013[update], afamelanotide is in phase II and III clinical trials for vitiligo and other skin diseases.[58]

A medication for rheumatoid arthritis, tofacitinib, has been tested for the treatment of vitiligo.[59]

In October 1992, a scientific report was published of successfully transplanting melanocytes to vitiligo-affected areas, effectively repigmenting the region.[60] 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.[61]

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.[62] JAK inhibitors like ruxolitinib show promise in targeting the IFN-γ-chemokine signaling axis implicated in vitiligo pathogenesis, and improving nonsegmental vitiligo.[62][63][64]

## References

1. ↑ 1.0 1.1 1.2 1.3 "36. Disturbances of pigmentation" (in en). Andrews' Diseases of the Skin: Clinical Dermatology (13th ed.). Edinburgh: Elsevier. 2020. pp. 871–874. ISBN 978-0-323-54753-6. https://books.google.com/books?id=UEaEDwAAQBAJ&pg=PA871.
2. ↑ "Vitiligo – Symptoms and causes". https://www.mayoclinic.org/diseases-conditions/vitiligo/symptoms-causes/syc-20355912.
3. ↑ 3.0 3.1 "Vitiligo Symptoms, Treatment & Causes". 12 April 2017. https://www.niams.nih.gov/health-topics/vitiligo.
4. ↑ Silverberg, Jonathan; Reja, Misha; Silverberg, Nanette (December 2014). "Regional Variation of and Association of US Birthplace With Vitiligo Extent". JAMA Network. https://jamanetwork.com/journals/jamadermatology/fullarticle/1886697.
5. ↑ Gandhi, Kavita; Ezzedine, Khaled; Anastassopoulos, Kathryn P.; Patel, Reema; Sikirica, Vanja; Daniel, Shoshana R.; Napatalung, Lynne; Yamaguchi, Yuji et al. (2022-01-01). "Prevalence of Vitiligo Among Adults in the United States". JAMA Dermatology 158 (1): 43–50. doi:10.1001/jamadermatol.2021.4724. ISSN 2168-6084. PMID 34787670.
6. ↑ "Vitiligo". National Library of Medicine. https://medlineplus.gov/genetics/condition/vitiligo/.
7. ↑ 7.0 7.1 7.2 7.3 National Institute of Arthritis and Musculoskeletal and Skin Diseases (March 2007). "What Is Vitiligo? Fast Facts: An Easy-to-Read Series of Publications for the Public Additional". https://www.niams.nih.gov/health-topics/vitiligo.
8. ↑ 8.0 8.1 8.2 "72. Vitiligo". Fitzpatrick's dermatology in general medicine (7th ed.). New York: McGraw-Hill Professional. 2007. ISBN 978-0-07-146690-5. OCLC 154751587.
9. ↑ 9.0 9.1 "Interventions for vitiligo". The Cochrane Database of Systematic Reviews 2015 (2). February 2015. doi:10.1002/14651858.CD003263.pub5. PMID 25710794.
10. ↑ "Vitiligo update". Seminars in Cutaneous Medicine and Surgery 28 (2): 86–92. June 2009. doi:10.1016/j.sder.2009.04.008. PMID 19608058.
11. ↑ 11.0 11.1 11.2 "Vitiligo". Acta Dermatovenerologica Alpina, Pannonica, et Adriatica 14 (4): 137–42, 144–45. December 2005. PMID 16435042. http://www.mf.uni-lj.si/acta-apa/acta-apa-05-4/2.pdf.
12. ↑ "Stressful life events, social support, attachment security and alexithymia in vitiligo. A case-control study". Psychotherapy and Psychosomatics 72 (3): 150–158. 2003. doi:10.1159/000069731. PMID 12707482.
13. ↑ 13.00 13.01 13.02 13.03 13.04 13.05 13.06 13.07 13.08 13.09 13.10 13.11 "Vitiligo". Lancet 386 (9988): 74–84. July 2015. doi:10.1016/s0140-6736(14)60763-7. PMID 25596811.
14. ↑ "Evidence for an autoimmune pathogenesis of vitiligo". Pigment Cell Research 16 (2): 90–100. April 2003. doi:10.1034/j.1600-0749.2003.00023.x. PMID 12622785.
15. ↑ "Vitiligo and Autoimmune Thyroid Disorders". Frontiers in Endocrinology 8 (290). 27 October 2017. doi:10.3389/fendo.2017.00290. PMID 29163360.
16. ↑ "Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention". Frontiers in Cell and Developmental Biology 9. 14 December 2021. doi:10.3389/fcell.2021.797026. PMID 34970551.
17. ↑ "Questions and Answers about Vitiligo". National Institute of Arthritis and Musculoskeletal and Skin Diseases. 30 October 2022. https://www.niams.nih.gov/health-topics/vitiligo#tab-causes.
18. ↑ 18.0 18.1 "Clinical significance of Koebner's phenomenon in vitiligo: a hospital-based epidemiological investigation from China". Chinese Medical Journal 136 (4): 502–504. February 2023. doi:10.1097/CM9.0000000000002431. PMID 36580639.
19. ↑ Mayo Clinic Staff (15 May 2014). "Vitiligo Causes". Mayoclinic. http://www.mayoclinic.org/diseases-conditions/vitiligo/basics/causes/con-20032007.
20. ↑ "Modern vitiligo genetics sheds new light on an ancient disease". The Journal of Dermatology 40 (5): 310–318. May 2013. doi:10.1111/1346-8138.12147. PMID 23668538.
21. ↑ "Current Management of Pediatric Vitiligo". Paediatric Drugs 17 (4): 303–313. August 2015. doi:10.1007/s40272-015-0135-3. PMID 26022363.
22. ↑ "Deregulated inflammasome signaling in disease". Immunological Reviews 243 (1): 163–173. September 2011. doi:10.1111/j.1600-065X.2011.01042.x. PMID 21884175.
23. ↑ "Modern genetics, ancient defenses, and potential therapies". The New England Journal of Medicine 356 (12): 1263–1266. March 2007. doi:10.1056/NEJMe078017. PMID 17377166.
24. ↑ "NALP1 in vitiligo-associated multiple autoimmune disease". The New England Journal of Medicine 356 (12): 1216–1225. March 2007. doi:10.1056/NEJMoa061592. PMID 17377159. http://openaccess.sgul.ac.uk/111251/1/nejmoa061592.pdf. Retrieved 16 December 2019.
25. ↑ "Vitiligo susceptibility at workplace and in daily life: the contribution of oxidative stress gene polymorphisms". Biomedical Dermatology 3 (1). 2019-10-22. doi:10.1186/s41702-019-0043-1. ISSN 2398-8460.
26. ↑ "Vitiligo". Lancet 386 (9988): 74–84. July 2015. doi:10.1016/S0140-6736(14)60763-7. PMID 25596811.
27. ↑ "Increased prevalence of vitiligo, but no evidence of premature ageing, in the skin of patients with bp 3243 mutation in mitochondrial DNA in the mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes syndrome (MELAS)". The British Journal of Dermatology 140 (4): 634–639. April 1999. doi:10.1046/j.1365-2133.1999.02761.x. PMID 10233312.
28. ↑ "TLR3 and TLR4 But not TLR2 are Involved in Vogt-Koyanagi- Harada Disease by Triggering Proinflammatory Cytokines Production Through Promoting the Production of Mitochondrial Reactive Oxygen Species". Current Molecular Medicine 15 (6): 529–542. 2015-08-19. doi:10.2174/1566524015666150731095611. PMID 26238371.
29. ↑ "Immunopathological manifestations in Kabuki syndrome: a registry study of 177 individuals". Genetics in Medicine 22 (1): 181–188. January 2020. doi:10.1038/s41436-019-0623-x. PMID 31363182.
30. ↑ 30.0 30.1 "Vitiligo auto-immune response upon oxidative stress-related mitochondrial DNA release opens up new therapeutic strategies". Clinical and Translational Medicine 14 (8). August 2024. doi:10.1002/ctm2.1810. PMID 39113238.
31. ↑ "Analysis of Matched Skin and Gut Microbiome of Patients with Vitiligo Reveals Deep Skin Dysbiosis: Link with Mitochondrial and Immune Changes". The Journal of Investigative Dermatology 141 (9): 2280–2290. September 2021. doi:10.1016/j.jid.2021.01.036. PMID 33771527.
32. ↑ "Wood's lamp for vitiligo disease stability and early recognition of initiative pigmentation after epidermal grafting". International Wound Journal 14 (6): 1391–1394. December 2017. doi:10.1111/iwj.12800. PMID 28799192.
33. ↑ "Woods Light (Woods Lamp)". StatPearls (StatPearls Publishing). 2019. PMID 30725878.
34. ↑ "Introduction". Vitiligo. Berlin: Springer. 2009. ISBN 978-3-540-69360-4.
35. ↑ 35.00 35.01 35.02 35.03 35.04 35.05 35.06 35.07 35.08 35.09 "Vitiligo". Fitzpatrick's Dermatology in General Medicine (7th ed.). New York: McGraw-Hill Professional. 2007. ISBN 978-0-07-146690-5.
36. ↑ 36.0 36.1 "New insights in segmental vitiligo: case report and review of theories". The British Journal of Dermatology 166 (2): 240–246. February 2012. doi:10.1111/j.1365-2133.2011.10650.x. PMID 21936857.
37. ↑ "Therapeutic interventions for vitiligo". Journal of the American Academy of Dermatology 59 (4): 713–717. October 2008. doi:10.1016/j.jaad.2008.06.023. PMID 18793940.
38. ↑ 38.0 38.1 38.2 38.3 Anon. "Vitiligo -Treatment". Patient UK. NHS. http://www.nhs.uk/Conditions/Vitiligo/Pages/Treatment.aspx.
39. ↑ "Incyte Announces U.S. FDA Approval of Opzelura (ruxolitinib) Cream for the Treatment of Vitiligo". Incyte. 19 July 2022. https://www.businesswire.com/news/home/20220718005819/en/Incyte-Announces-U.S.-FDA-Approval-of-Opzelura™-ruxolitinib-Cream-for-the-Treatment-of-Vitiligo.
40. ↑ "Narrow-band ultraviolet B is a useful and well-tolerated treatment for vitiligo". Journal of the American Academy of Dermatology 44 (6): 999–1003. June 2001. doi:10.1067/mjd.2001.114752. PMID 11369913.
41. ↑ "Treatment of vitiligo with broadband ultraviolet B and vitamins". International Journal of Dermatology 45 (1): 63–65. January 2006. doi:10.1111/j.1365-4632.2005.02447.x. PMID 16426381.
42. ↑ 42.0 42.1 "Phototherapy for Vitiligo: A Systematic Review and Meta-analysis". JAMA Dermatology 153 (7): 666–674. July 2017. doi:10.1001/jamadermatol.2017.0002. PMID 28355423.
43. ↑ "The efficacy of 308-nm excimer laser/light (EL) and topical agent combination therapy versus EL monotherapy for vitiligo: A systematic review and meta-analysis of randomized controlled trials (RCTs)". Journal of the American Academy of Dermatology 74 (5): 907–915. May 2016. doi:10.1016/j.jaad.2015.11.044. PMID 26785803.
44. ↑ 44.0 44.1 44.2 44.3 "Historical Aspects". Vitiligo (Online-Ausg. ed.). Berlin: Springer. 2009. ISBN 978-3-540-69360-4.
45. ↑ The Torah For Dummies. For Dummies. 2008. p. 11. ISBN 978-0-470-28306-6. http://media.wiley.com/product_data/excerpt/59/04701734/0470173459.pdf. Retrieved 2010-08-19.
46. ↑ "History Crash Course #36: Timeline: From Abraham to Destruction of the Temple". Aish.com. http://www.aish.com/jl/h/48944541.html.
47. ↑ "Stigma experience in skin disorders: an Indian perspective". Dermatologic Clinics 23 (4): 635–642. October 2005. doi:10.1016/j.det.2005.05.007. PMID 16112439.
48. ↑ "Black and White: how Dangerous kicked off Michael Jackson's race paradox". The Guardian. 17 March 2018. https://www.theguardian.com/music/2018/mar/17/black-and-white-how-dangerous-kicked-off-michael-jacksons-race-paradox.
49. ↑ "Winnie Harlow: Canadian Model With Rare Skin Condition Lands 2 Major Campaigns" (in en). 18 February 2015. https://www.complex.com/style/2015/02/canadian-model-winnie-harlow-stars-major-fashion-campaigns.
50. ↑ "Kimbra on the tech she carries everywhere". 2018-05-04. https://www.theverge.com/2018/5/4/17234638/whats-in-your-bag-kimbra-primal-heart.
51. ↑ @WWEDanielBryan. "@tarynlove77 It's vitiligo, not any artificial patch, which is an autoimmune disease you can look up on Wikipedia". https://twitter.com/WWEDanielBryan/status/97214858474422272. Missing or empty `|date=` (help)
52. ↑ "Michaël Youn: l'étonnante maladie génétique dont il est atteint... au niveau du pénis – Voici" (in fr). 11 June 2018. https://www.voici.fr/news-people/actu-people/michael-youn-letonnante-maladie-genetique-dont-il-est-atteint-au-niveau-du-penis-647550.
53. ↑ "Dans les coulisses de la campagne d'Edouard Philippe au Havre" (in fr). 26 June 2020. https://www.parismatch.com/Actu/Politique/Dans-les-coulisses-de-la-campagne-d-Edouard-Philippe-au-Havre-1689917.
54. ↑ Bi, Huong (6 October 2024). "Người phụ nữ một con với làn da bạch biến sẽ đối đầu với Kỳ Duyên tại Miss Universe" (in Vietnamese). https://www.saostar.vn/nguoi-mau-hoa-hau/nguoi-phu-nu-mot-con-voi-lan-da-bach-bien-se-doi-dau-voi-ky-duyen-202410061823347328.html.
55. ↑ "Taliana Vargas muestra nuevas marcas de vitiligo en su piel". June 4, 2021. https://www.eltiempo.com/cultura/gente/taliana-vargas-muestra-marcas-de-vitiligo-en-su-piel-593184.
56. ↑ "Taliana Vargas explicó cómo va el tratamiento para su problema de piel". October 26, 2022. https://www.infobae.com/america/colombia/2021/10/26/taliana-vargas-explico-como-va-el-tratamiento-para-su-problema-de-piel/.
57. ↑ "Why I use 'The Boondocks' TV cartoon show to teach a course about race" (in en-US). 2023-03-15. http://theconversation.com/why-i-use-the-boondocks-tv-cartoon-show-to-teach-a-course-about-race-195060.
58. ↑ "A review and update on melanocyte stimulating hormone therapy: afamelanotide". Journal of Drugs in Dermatology 12 (7): 775–779. July 2013. PMID 23884489.
59. ↑ "For vitiligo patient, arthritis drug restores skin color". 24 June 2015. http://news.yale.edu/2015/06/24/vitiligo-patient-arthritis-drug-restores-skin-color.
60. ↑ "Melanocyte transplantation in vitiligo". Lancet 340 (8825): 981. October 1992. doi:10.1016/0140-6736(92)92875-G. PMID 1357390.
61. ↑ "Long-term follow-up of leucoderma patients treated with transplants of autologous cultured melanocytes, ultrathin epidermal sheets and basal cell layer suspension". The British Journal of Dermatology 147 (5): 893–904. November 2002. doi:10.1046/j.1365-2133.2002.04837.x. PMID 12410698.
62. ↑ 62.0 62.1 "Janus Kinase Inhibitors in the Treatment of Vitiligo: A Review". Frontiers in Immunology 12. 2021. doi:10.3389/fimmu.2021.790125. PMID 34868078.
63. ↑ Clinical trial number NCT04052425 for "Topical Ruxolitinib Evaluation in Vitiligo Study 1 (TRuE-V1)" at ClinicalTrials.gov
64. ↑ Clinical trial number NCT04057573 for "Topical Ruxolitinib Evaluation in Vitiligo Study 2 (TRuE-V2)" at ClinicalTrials.gov

## External links

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

Classification|

* ICD-10: L80
* ICD-9-CM: 709.01
* OMIM: 193200
* MeSH: D014820
* DiseasesDB: 13965
* SNOMED CT: 56727007

|

External resources|

* MedlinePlus: 000831
* eMedicine: derm/453

* v
* t
* e

Diseases of the skin and appendages by morphology

Growths|

| Epidermal|

* wart
* callus
* seborrheic keratosis
* acrochordon
* molluscum contagiosum
* actinic keratosis
* squamous-cell carcinoma
* basal-cell carcinoma
* Merkel-cell carcinoma
* nevus sebaceous
* trichoepithelioma

|

Pigmented|

* Freckles
* lentigo
* melasma
* nevus
* melanoma

Dermal and
subcutaneous|

* epidermal inclusion cyst
* hemangioma
* dermatofibroma (benign fibrous histiocytoma)
* keloid
* lipoma
* neurofibroma
* xanthoma
* Kaposi's sarcoma
* infantile digital fibromatosis
* granular cell tumor
* leiomyoma
* lymphangioma circumscriptum
* myxoid cyst

Rashes|

| With
epidermal
involvement|

| Eczematous|

* contact dermatitis
* atopic dermatitis
* seborrheic dermatitis
* stasis dermatitis
* lichen simplex chronicus
* Darier's disease
* glucagonoma syndrome
* langerhans cell histiocytosis
* lichen sclerosus
* pemphigus foliaceus
* Wiskott–Aldrich syndrome
* Zinc deficiency

|

Scaling|

* psoriasis
* tinea (corporis
* cruris
* pedis
* manuum
* faciei)
* pityriasis rosea
* secondary syphilis
* mycosis fungoides
* systemic lupus erythematosus
* pityriasis rubra pilaris
* parapsoriasis
* ichthyosis

Blistering|

* herpes simplex
* herpes zoster
* varicella
* bullous impetigo
* acute contact dermatitis
* pemphigus vulgaris
* bullous pemphigoid
* dermatitis herpetiformis
* porphyria cutanea tarda
* epidermolysis bullosa simplex

Papular|

* scabies
* insect bite reactions
* lichen planus
* miliaria
* keratosis pilaris
* lichen spinulosus
* transient acantholytic dermatosis
* lichen nitidus
* pityriasis lichenoides et varioliformis acuta

Pustular|

* acne vulgaris
* acne rosacea
* folliculitis
* impetigo
* candidiasis
* gonococcemia
* dermatophyte
* coccidioidomycosis
* subcorneal pustular dermatosis

Hypopigmented|

* tinea versicolor
* vitiligo
* pityriasis alba
* postinflammatory hyperpigmentation
* tuberous sclerosis
* idiopathic guttate hypomelanosis
* leprosy
* hypopigmented mycosis fungoides

Without
epidermal
involvement|

| Red|

| Blanchable
Erythema|

| Generalized|

* drug eruptions
* viral exanthems
* toxic erythema
* systemic lupus erythematosus

|

Localized|

* cellulitis
* abscess
* boil
* erythema nodosum
* carcinoid syndrome
* fixed drug eruption

Specialized|

* urticaria
* erythema (multiforme
* migrans
* gyratum repens
* annulare centrifugum
* ab igne)

Nonblanchable
Purpura|

| Macular|

* thrombocytopenic purpura
* actinic/solar purpura

|

Papular|

* disseminated intravascular coagulation
* vasculitis

Indurated|

* scleroderma/morphea
* granuloma annulare
* lichen sclerosis et atrophicus
* necrobiosis lipoidica

Miscellaneous
disorders|

| Ulcers|

|

Hair|

* telogen effluvium
* androgenic alopecia
* alopecia areata
* systemic lupus erythematosus
* tinea capitis
* loose anagen syndrome
* lichen planopilaris
* folliculitis decalvans
* acne keloidalis nuchae

Nail|

* onychomycosis
* psoriasis
* paronychia
* ingrown nail

Mucous
membrane|

* Aphthous stomatitis
* oral candidiasis
* lichen planus
* leukoplakia
* pemphigus vulgaris
* mucous membrane pemphigoid
* cicatricial pemphigoid
* herpesvirus
* coxsackievirus
* syphilis
* systemic histoplasmosis
* squamous-cell carcinoma

* v
* t
* e

Pigmentation disorders/Dyschromia

Hypo-/
leucism|

| Loss of
melanocytes|

| Vitiligo|

* Quadrichrome vitiligo
* Vitiligo ponctué

|

Syndromic|

* Alezzandrini syndrome
* Vogt–Koyanagi–Harada syndrome

Melanocyte
development|

* Piebaldism
* Waardenburg syndrome
* Tietz syndrome

Loss of melanin/
amelanism|

| Albinism|

* Oculocutaneous albinism
* Ocular albinism

|

Melanosome
transfer|

* Hermansky–Pudlak syndrome
* Chédiak–Higashi syndrome
* Griscelli syndrome
* Elejalde syndrome
* Griscelli syndrome type 2
* Griscelli syndrome type 3

Other|

* Cross syndrome
* ABCD syndrome
* Albinism–deafness syndrome
* Idiopathic guttate hypomelanosis
* Phylloid hypomelanosis
* Progressive macular hypomelanosis

Leukoderma w/o
hypomelanosis|

* Vasospastic macule
* Woronoff's ring
* Nevus anemicus

Ungrouped|

* Nevus depigmentosus
* Postinflammatory hypopigmentation
* Pityriasis alba
* Vagabond's leukomelanoderma
* Yemenite deaf-blind hypopigmentation syndrome
* Wende–Bauckus syndrome

Hyper-|

| Melanin/
Melanosis/
Melanism|

| Reticulated|

* Dermatopathia pigmentosa reticularis
* Pigmentatio reticularis faciei et colli
* Reticulate acropigmentation of Kitamura
* Reticular pigmented anomaly of the flexures
* Naegeli–Franceschetti–Jadassohn syndrome
* Dyskeratosis congenita
* X-linked reticulate pigmentary disorder
* Galli–Galli disease
* Revesz syndrome

|

Diffuse/
circumscribed|

* Lentigo/Lentiginosis: Lentigo simplex
* Liver spot
* Centrofacial lentiginosis
* Generalized lentiginosis
* Inherited patterned lentiginosis in black persons
* Ink spot lentigo
* Lentigo maligna
* Mucosal lentigines
* Partial unilateral lentiginosis
* PUVA lentigines

* Melasma
* Erythema dyschromicum perstans
* Lichen planus pigmentosus
* Café au lait spot
* Poikiloderma (Poikiloderma of Civatte
* Poikiloderma vasculare atrophicans)
* Riehl melanosis

Linear|

* Incontinentia pigmenti
* Scratch dermatitis
* Shiitake mushroom dermatitis

Other/
ungrouped|

* Acanthosis nigricans
* Freckle
* Familial progressive hyperpigmentation
* Pallister–Killian syndrome
* Periorbital hyperpigmentation
* Photoleukomelanodermatitis of Kobori
* Postinflammatory hyperpigmentation
* Transient neonatal pustular melanosis

Other
pigments|

| Iron|

* Hemochromatosis
* Iron metallic discoloration
* Pigmented purpuric dermatosis
* Schamberg disease
* Majocchi's disease
* Gougerot–Blum syndrome
* Doucas and Kapetanakis pigmented purpura/Eczematid-like purpura of Doucas and Kapetanakis
* Lichen aureus
* Angioma serpiginosum
* Hemosiderin hyperpigmentation

|

Other
metals|

* Argyria
* Chrysiasis
* Arsenic poisoning
* Lead poisoning
* Titanium metallic discoloration

Other|

* Carotenosis
* Tar melanosis

Dyschromia|

* Dyschromatosis symmetrica hereditaria
* Dyschromatosis universalis hereditaria

See also|

* Skin color
* Skin whitening
* Tanning
* Sunless
* Tattoo
* removal
* Depigmentation

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