Vitiligo: Wikis

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Vitiligo
Classification and external resources
ICD-10 L80.
ICD-9 709.01
OMIM 193200
DiseasesDB 13965
MedlinePlus 000831
eMedicine derm/453
MeSH D014820

Vitiligo (US: /ˌvɪtəl.ˈaɪɡoʊ/, UK: /ˌvɪtɨˈlaɪɡoʊ/) 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.[1] Non-segmental vitiligo has a greater prevalence than the disorder's other form(s).

Contents

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.[2] In regards to psychological damage, vitiligo can have a significant effect on the mental health of a patient.[3] 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.[4].

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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.[2]

Segmental vitiligo

Segmental vitiligo (SV) differs in appearance, aetiology and prevalence from associated illnesses. Its treatment is also 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, patches of depigmented skin remain throughout life.[2]

Pathogenesis

Vitiligo is a complex, polygenic disorder characterized by patchy loss of skin pigmentation due to abnormal melanocyte function. Both genetic and environmental etiological factors have been proposed for vitiligo and lack of molecular markers renders difficulties to predict development and progression of the disease. Identification of dysregulated genes has the potential to unravel biological pathways involved in vitiligo pathogenesis, facilitating discovery of potential biomarkers and novel therapeutic approaches. 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.[5]

Vitiligo is sometime associated with autoimmune and inflammatory diseases,[6] 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.[7][8]

Treatment

There is no cure for vitiligo but there are a number of treatments available which can slow down or 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:[9]

Sunblock and other means to protect the pale skin

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.[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 sunlight and the sun tanning of unaffected skin. However, exposure to sunlight may also cause the melanocytes to regenerate to allow the pigmentation to come back to its original color.[citation needed]

Treatments that aim to reverse the changes in the skin

The traditional treatment used by dermatologists is the application of corticosteroid cream.[10]

Studies have also shown that immunomodulator creams such as Protopic and Elidel also cause repigmentation in some cases, when used with UVB narrowband treatments.[11][12]

In October 1993, a scientific report was published of successfully transplanting melanocytes to vitiligo affected areas, effectively repigmenting the region.[13] 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.[14]

In early 2008 scientists at King's College London discovered that piperine, a chemical derived from black pepper, can shorten the repigmentation process in skin and reduce the UVB exposures, produces a longer lasting and more even pigmentation.[15]

A limited 2003 study in India of 25 patients with limited and slow-spreading vitiligo given orally-taken Ginkgo biloba found it to be "fairly effective therapy for arresting the progression of the disease".[16] A 2008 review of natural health products found studies to generally be of poor quality but concluded that L-phenylalanine used with phototherapy, and oral Ginkgo biloba as monotherapy showed promise.[17]

Ulltraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and Ultra Violet A light (PUVA) treatment involves taking a drug which makes the skin very sensitive to light. The skin is then exposed to ultra violet 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.[9] Narrowband ultaviolet 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.[9]

Treatment to completely de-pigment the skin

In cases of extensive vitiligo the option to de-pigment the unaffected skin 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.[9]

Public figures with vitiligo

Michael Jackson two years after he was diagnosed with vitiligo universalis, pictured in the early stages of the disease.[18]

See also

Notes

  1. ^ Nath SK, Majumder PP, Nordlund JJ (November 1994). "Genetic epidemiology of vitiligo: multilocus recessivity cross-validated". American Journal of Human Genetics 55 (5): 981–90. PMID 7977362. 
  2. ^ a b c Huggins RH, Schwartz RA, Janniger CK (December 2005). "Vitiligo". Acta Dermatovenerologica Alpina, Panonica, et Adriatica 14 (4): 137–42, 144–5. PMID 16435042. http://www.mf.uni-lj.si/acta-apa/acta-apa-05-4/2.pdf. 
  3. ^ Mechri A, Amri M, Douarika AA, Ali Hichem BH, Zouari B, Zili J (October 2006). "Psychiatric morbidity and quality of life in Vitiligo: a case controlled study [Psychiatric morbidity and quality of life in Vitiligo: a case controlled study]" (in French). La Tunisie Médicale 84 (10): 632–5. PMID 17193855. 
  4. ^ Picardi A, Pasquini P, Cattaruzza MS, et al. (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. 
  5. ^ Strömberg S, Björklund MG, Asplund A, et al. (April 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. 
  6. ^ Hedstrand H, Ekwall O, Olsson MJ, et al. (September 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. 
  7. ^ Gregersen PK (March 2007). "Modern genetics, ancient defenses, and potential therapies". The New England Journal of Medicine 356 (12): 1263–6. doi:10.1056/NEJMe078017. PMID 17377166. 
  8. ^ Jin Y, Mailloux CM, Gowan K, et al. (March 2007). "NALP1 in vitiligo-associated multiple autoimmune disease". The New England Journal of Medicine 356 (12): 1216–25. doi:10.1056/NEJMoa061592. PMID 17377159. 
  9. ^ a b c d e Anon. "What are the treatment options for vitiligo?". Patient UK. EMIS & PiP. http://www.patient.co.uk/health/Vitiligo.htm. Retrieved 1 February 2010. 
  10. ^ Kwinter J, Pelletier J, Khambalia A, Pope E (February 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. 
  11. ^ Tanghetti EA (February 2003). "Tacrolimus ointment 0.1% produces repigmentation in patients with vitiligo: results of a prospective patient series". Cutis 71 (2): 158–62. PMID 12635898. 
  12. ^ Silverberg NB, Lin P, Travis L, et al. (November 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. 
  13. ^ Olsson MJ, Juhlin L (October 1992). "Melanocyte transplantation in vitiligo". Lancet 340 (8825): 981. doi:10.1016/0140-6736(92)92875-G. PMID 1357390. 
  14. ^ Olsson MJ, Juhlin L (November 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. 
  15. ^ http://news.bbc.co.uk/1/hi/health/7244474.stm
  16. ^ Parsad D, Pandhi R, Juneja A (May 2003). "Effectiveness of oral Ginkgo biloba in treating limited, slowly spreading vitiligo". Clinical and Experimental Dermatology 28 (3): 285–7. doi:10.1046/j.1365-2230.2003.01207.x. PMID 12780716. 
  17. ^ Bernard A, Knowles RW, Naito K, et al. (December 1986). "A unique epitope on the CD2 molecule defined by the monoclonal antibody 9-1: epitope-specific modulation of the E-rosette receptor and effects on T-cell functions". Human Immunology 17 (4): 388–405. doi:10.1016/0198-8859(86)90299-5. PMID 2432048. 
  18. ^ Original by Alan Light
  19. ^ Campbell (1995), p. 14–16
  20. ^ Lewis p. 165–168
  21. ^ George, p. 45–46
  22. ^ a b 'I'm a black man turning white on television'", BrisbaneTimes, December 18, 2007
  23. ^ Pathania, Amit (7 november 2009). "Michael Jackson's Glove Hid Skin Problem". Top News. http://topnews.us/content/26135-michael-jacksons-glove-hid-skin-problem. Retrieved 1 February 2010. 
  24. ^ http://www.imdb.com/name/nm0000821/bio
  25. ^ Lynn Barber interviews Graham Norton | Food monthly | The Observer
  26. ^ Turning White
  27. ^ Associated Press (2007-12-17). "FOX TV Reporter Refuses to Give In to Skin Disorder Turning Him White". Fox News Channel. http://www.foxnews.com/story/0,2933,317065,00.html. 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.'" 
  28. ^ (FLV) Big Krizz Kaliko. 2007-10-25. http://vids.myspace.com/index.cfm?fuseaction=vids.individual&videoid=20806073. Retrieved 2008-02-04. "Be looking for my album coming out Spring of 08, it's called Vitaligo, I am the Funkra, you know what I'm saying? Vitaligo that's the pigmentation disease I have in case you don't know." 
  29. ^ Thomas Lennon entry from the Vitiligo Guide
  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. ^ [1]
  33. ^ http://www.texasmonthly.com/preview/1996-03-01/health
  34. ^ http://www.vitiligos.com/people-with-vitiligo/famous-people/

References

External links

Support organizations


Simple English

[[File:|right|thumb|200px|A young woman with vitiligo]] Vitiligo is a long lasting skin disease that causes the losing of color from the skin. It occurs when the melanocytes, cells that give skin their color, die or do not work.

How is it caught?

The exact cause of vitiligo is complex and not fully understood. It may be caused by the immune system, genetic, and environmental factors. Vitiligo may also be caused by stress that affects the immune system, leading the body to react and start eliminating skin pigment.

People over 20 years old rarely develop this disease. These patches often occur to both sides symmetrically and may change shape.

Effects of vitiligo

  • color of the skin is lighter because there are no pigments
  • purple or golden brown patches on and around the eyes, nose, and mouth
  • puffiness of the middle layer of the eye
  • quicker graying of hair
  • more sensitive to sun

This disease can also affect the mental state of the patient.

Curing it

Today, doctors do not understand what causes the disease, so right now, it can not be cured. Some things can be done to fight its effects, though. Makeup or cosmetics can cover up the parts of the skin with vitiligo. Also, staying out of the sun to prevent tanning is good. But the treatment given by most skin doctors is cortico steroid cream. Breakthrough discovery in 2004 allowed for the transplant of melanocytes to vitiligo affected areas, repigmenting the region.



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