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Vitiligo

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Vitiligo
SpecialtyDermatology Edit this on Wikidata

Vitiligo (Template:Pron-en) is a chronic disorder that causes depigmentation of patches of skin. It occurs when melanocytes, the cells responsible for skin pigmentation, die or are unable to function. The cause of vitiligo is unknown, but research suggests that is may arise from autoimmune, genetic, oxidative stress, neural, or viral causes.[1] The incidence worldwide is less than 1%.[2] The most common form is non-segmental vitiligo.

Signs and symptoms

Symptoms usually begin between ages 10 years and age 30 years,[3] including:

  • whitening or graying of hair[4]
  • loss of skin color inside the mouth[3]
  • loss of eye color[4]

The most notable symptom of vitiligo is depigmentation of patches of skin that occurs on the extremities.[5][3] Although patches are initially small, they often enlarge and change shape.[1][3] When skin lesions occur, they are most prominent on the face, hands and wrists.[5][3] Depigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus.[5][3] Some lesions have hyperpigmentation around the edges.[6] Patients who are stigmatised for their condition may experience depression and similar mood disorders.[7]

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 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.[6]

Classes of non-segmental Vitiligo include:

  • Generalized Vitiligo: the most common pattern, wide and randomly distributed areas of depigmentation[4]
  • Universal Vitiligo: depigmentation encompasses most of the body[4]
  • Focal Vitiligo: one or a few scattered macules in one area, most common in children[4]
  • Acrofacial Vitiligo: fingers and periorificial areas[4]
  • Muscosal Vitiligo: depigmentation of only the mucous membranes[4]

Segmental

Segmental vitiligo (SV) differs in appearance, aetiology and prevalence from 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 spine. It spreads much more rapidly than NSV and, without treatment, it is much more stable/ static in course and not associated with auto-immune diseases and a very treatable condition that responds to topical treatment.[6]

Differential diagnosis

Conditions with similar symptoms include:

Pathogenesis

Vitiligo is a disorder characterized by patchy loss of skin pigmentation due to immune attacks on melanocytes, which can be caused by defects in many genes. Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo. The immune system genes are associated with other autoimmune disorders.

In one case, the gene TYR, which makes the melanocyte more susceptible to the immune system in vitiligo, also makes the melanocyte more susceptible to the immune system in the skin cancer malignant melanoma. So people with vitiligo caused by the TYR gene are less likely to have malignant melanoma.

A genomewide association study found 10 independent susceptibility loci for generalized vitiligo, responsible for 7.4% of the genetic risk. Some patients had vitiligo alone; others had generalized vitiligo with other autoimmune diseases. Most loci were associated with both forms. (The exception was PTPN22, which was only associated with generalized vitiligo.) In the MHC region, which controls the immune system, major association signals were identified in the class I gene region (between HLA-A and HLA-HGC9) and class II gene region (between HLA-DRB1 and HLA-DQA1). Outside the MHC region, association signals were identified near RERE, PTPN22, LPP, IL2RA, GZMB, UBASH3A and C1QTNF6 genes, which are associated with other autoimmune diseases. TYR encodes 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. The major alleles of TYR are associated with vitiligo, and the minor alleles are associated with malignant melanoma. Vitiligo-associated 402R tyrosinase may be more efficiently presented to the immune system. Melanoma-associated 402Q may fail to be identified by the immune system.[8]

The transcriptional profile of melanocytes from vitiligo patients have been studied. Oligonucleotide microarrays containing approximately 16,000 unique genes were used to analyse mRNA expression in melanocytes from vitiligo patients and age-matched healthy controls. In total, 859 genes were identified as differentially expressed.[9]

Vitiligo is sometime associated with autoimmune and inflammatory diseases,[10] 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.[11][12]

Treatment

There is no cure for vitiligo, but there are a number of treatments that improve the condition. In fair-skinned people, avoiding tanning of normal skin can make patches of vitiligo much less noticeable. Treatment options generally fall into four groups:[13]

Sunblock

A high protection sun-block (factor 20 or above) is applied to areas of vitiligo to prevent sunburn. Affected areas of skin are protected when the sun is strong, especially in the middle of the day by wearing, for example, a wide brimmed hat and long sleeved clothing.[13]

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 sunlight and the sun tanning of unaffected skin.[4]

Reversal

The traditional treatment used by dermatologists is the application of corticosteroid cream.[14]

Studies have shown that immunomodulator creams such as Protopic and Elidel also cause repigmentation in some cases, when used with UVB narrowband treatments.[15][16]

In October 1993, a scientific report was published of successfully transplanting melanocytes to vitiligo affected areas, effectively repigmenting the region.[17] The procedure involved taking a thin layer of pigmented skin from the patient'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 patients experienced nearly complete repigmentation of their skin. The longevity of the repigmentation differed from person to person.[18]

Ulltraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and Ultraviolet A light (PUVA) treatment involves taking a drug which makes the skin very sensitive to light. The skin is then exposed to ultraviolet A light (UVA). Treatment is required twice a week for 6–12 months or longer. PUVA may cause side effects such as 'sunburn' type reactions or skin freckling.[13] Narrowband ultraviolet B (UVB) phototherapy is now used more commonly than PUVA as it is less damaging to the skin than PUVA. As with PUVA, treatment is carried out twice weekly but there is no requirement to pre-sensitise the skin and the treatment sessions are much shorter.[13]

De-pigmenting

In cases of extensive vitiligo the option to de-pigment the unaffected skin with topical drugs like monobenzone, mequinol or hydroquinone may be considered to render the skin an even colour. The removal of all the skin pigment is permanent and it takes about a year to complete.[13]

Notable cases

Michael Jackson two years after he was diagnosed with vitiligo universalis, pictured in the early stages of the disease.[19]
  • Michael Jackson was diagnosed with vitiligo in 1986. In a 90-minute interview with Oprah Winfrey in February 1993, Jackson claimed that he didn't bleach his skin, stating for the first time that he had vitiligo. A friend claimed he started wearing his signature sequin glove to cover the vitiligo that had begun to appear in the early 80s.[20] It is also confirmed on his autopsy report.[21][22] It was also confirmed by Jackson during a leaked deposition tape in 1996, that he did not "bleach" his skin[23]. The tape was leaked months after his death in June of 2009. According to police reports, 19 tubes of hydroquinone and 18 tubes of benoquin(monobenzone) were found in Michael Jackson's home after his death.[24] In July 2010, Michael Jackson's eldest son Prince Michael Jr is seen in a picture with a patch of de-pigmented skin on his right underarm leading to speculations that he may be suffering from vitiligo like his father Michael Jackson.[25]
  • Graham Norton the UK television personality.[26]
  • Lee Thomas, a news anchor and entertainment reporter for WJBK (Fox) Detroit.[27][28][29]
  • Yvette Fielding, British TV presenter, has had vitiligo from age 11; her mother developed it at age 24.[30][31]
  • John Wiley Price, the Dallas County Commissioner, also has vitiligo.[32]
  • Amitabh Bachchan, the famous bollywood actor , also has vitiligo.[33]

See also

Notes

  1. ^ a b Halder RM, Chappell JL. Vitiligo update. Semin Cutan Med Surg. (2009);28(2):86-92. PMID: 19608058
  2. ^ Nath SK, Majumder PP, Nordlund JJ (1994). "Genetic epidemiology of vitiligo: multilocus recessivity cross-validated". American Journal of Human Genetics. 55 (5): 981–90. PMC 1918341. PMID 7977362. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  3. ^ a b c d e f What Is Vitiligo? Fast Facts: An Easy-to-Read Series of Publications for the Public, National Institute of Arthritis and Musculoskeletal and Skin Diseases, March 2007, http://www.niams.nih.gov/Health_Info/Vitiligo/vitiligo_ff.asp#c, Accessed 7-18-10 Cite error: The named reference "niams" was defined multiple times with different content (see the help page).
  4. ^ a b c d e f g h i j k l Halder RM, et al. Vitiligo. In: Wolff K, et al. Fitzpatrick's Dermatology in General Medicine. 7th ed. New York, N.Y.: McGraw-Hill Professional; 2007
  5. ^ a b c Halder RM; et al. (2007). "72. Vitiligo". In Wolff K, Freedberg IM, Fitzpatrick TB (eds) (ed.). Fitzpatrick's dermatology in general medicine (7th ed. ed.). New York: McGraw-Hill Professional. ISBN 9780071466905. OCLC 154751587. {{cite book}}: |edition= has extra text (help); |editor= has generic name (help); Explicit use of et al. in: |author= (help)CS1 maint: multiple names: editors list (link)
  6. ^ a b c Huggins RH, Schwartz RA, Janniger CK (2005). "Vitiligo" (PDF). Acta Dermatovenerologica Alpina, Panonica, et Adriatica. 14 (4): 137–42, 144–5. PMID 16435042. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  7. ^ Picardi A, Pasquini P, Cattaruzza MS, Gaetano P, Melchi CF, Baliva G, Camaioni D, Tiago A, Abeni D, Biondi M (2003). "Stressful life events, social support, attachment security and alexithymia in vitiligo. A case-control study". Psychotherapy and Psychosomatics. 72 (3): 150–8. doi:10.1159/000069731. PMID 12707482.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Jin Y, Birlea SA, Fain PR; et al. (2010). "Variant of TYR and autoimmunity susceptibility loci in generalized vitiligo". N. Engl. J. Med. 362 (18): 1686–97. doi:10.1056/NEJMoa0908547. PMC 2891985. PMID 20410501. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ Strömberg S, Björklund MG, Asplund A; et al. (2008). "Transcriptional profiling of melanocytes from patients with vitiligo vulgaris". Pigment Cell & Melanoma Research. 21 (2): 162–71. doi:10.1111/j.1755-148X.2007.00429.x. PMID 18426409. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ Hedstrand H, Ekwall O, Olsson MJ; et al. (2001). "The transcription factors SOX9 and SOX10 are vitiligo autoantigens in autoimmune polyendocrine syndrome type I". The Journal of Biological Chemistry. 276 (38): 35390–5. doi:10.1074/jbc.M102391200. PMID 11423552. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  11. ^ Gregersen PK (2007). "Modern genetics, ancient defenses, and potential therapies". The New England Journal of Medicine. 356 (12): 1263–6. doi:10.1056/NEJMe078017. PMID 17377166. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ Jin Y, Mailloux CM, Gowan K; et al. (2007). "NALP1 in vitiligo-associated multiple autoimmune disease". The New England Journal of Medicine. 356 (12): 1216–25. doi:10.1056/NEJMoa061592. PMID 17377159. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  13. ^ a b c d e Anon. "What are the treatment options for vitiligo?". Patient UK. EMIS & PiP. Retrieved 1 February 2010.
  14. ^ Kwinter J, Pelletier J, Khambalia A, Pope E (2007). "High-potency steroid use in children with vitiligo: a retrospective study". Journal of the American Academy of Dermatology. 56 (2): 236–41. doi:10.1016/j.jaad.2006.08.017. PMID 17224367. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  15. ^ Tanghetti EA (2003). "Tacrolimus ointment 0.1% produces repigmentation in patients with vitiligo: results of a prospective patient series". Cutis. 71 (2): 158–62. PMID 12635898. {{cite journal}}: Unknown parameter |month= ignored (help)
  16. ^ Silverberg NB, Lin P, Travis L; et al. (2004). "Tacrolimus ointment promotes repigmentation of vitiligo in children: a review of 57 cases". Journal of the American Academy of Dermatology. 51 (5): 760–6. doi:10.1016/j.jaad.2004.05.036. PMID 15523355. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  17. ^ Olsson MJ, Juhlin L (1992). "Melanocyte transplantation in vitiligo". Lancet. 340 (8825): 981. doi:10.1016/0140-6736(92)92875-G. PMID 1357390. {{cite journal}}: Unknown parameter |month= ignored (help)
  18. ^ Olsson MJ, Juhlin L (2002). "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. doi:10.1046/j.1365-2133.2002.04837.x. PMID 12410698. {{cite journal}}: Unknown parameter |month= ignored (help)
  19. ^ Original by Alan Light
  20. ^ Pathania, Amit (7 november 2009). "Michael Jackson's Glove Hid Skin Problem". Top News. Retrieved 1 February 2010. {{cite web}}: Check date values in: |date= (help)
  21. ^ http://www.nydailynews.com/gossip/2010/02/10/2010-02-10_michael_jackson_autopsy_report_confirms_singer_suffered_from_vitiligo_wore_wig_h.html
  22. ^ http://www.nowpublic.com/culture/vitiligo-michael-jackson-autopsy-confirms-skin-disorder-2572670.html
  23. ^ http://www.youtube.com/watch?v=g3u_HyCis4Y
  24. ^ Skin-whitening creams found at Michael Jackson's home
  25. ^ Like Father, Like Son? Prince Michael Appears to Have Vitiligo
  26. ^ Barber, Lynn (2001-10-28). "Glad to be Graham". The Guardian. London. Retrieved 2010-04-09.
  27. ^ 'I'm a black man turning white on television'", BrisbaneTimes, December 18, 2007
  28. ^ Turning White
  29. ^ Associated Press (2007-12-17). "FOX TV Reporter Refuses to Give In to Skin Disorder Turning Him White". Fox News Channel. Retrieved 2009-02-09. 'I'm a black man turning white on television and people can see it,' says Thomas, an anchor and entertainment reporter for the local Fox Broadcasting Company affiliate. 'If you've watched me over the years, you've seen my hands completely change from brown to white.'
  30. ^ Baxter, Biddy; Barnes, Edward (1989). "Chapter Nine: Crest of a Wave". Blue Peter: The Inside Story. Letchworth: Ringpress. pp. 214–216. ISBN 0-948955-50-3.
  31. ^ Epstein, Angela; Fielding, Yvette (6 May 2003). "My skin colour changed from dark olive to a bleach white". Daily Mail. London: Associated Newspapers. p. 39. ISSN 0307-7578.
  32. ^ http://www.texasmonthly.com/preview/1996-03-01/health
  33. ^ http://www.vitiligos.com/people-with-vitiligo/famous-people/

References

Wikimedia Commons has media related to Vitiligo.

Support organizations

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