|Classification and external resources|
Non-segmental vitiligo of the hand.
Vitiligo // is a condition that causes depigmentation of parts of the skin. It occurs when skin pigment cells die or are unable to function. The cause of vitiligo, aside from cases of contact with certain chemicals, is unknown, but research suggests it may arise from autoimmune, genetic, oxidative stress, neural, or viral causes. The incidence worldwide is less than 1%, with some populations averaging between 2-3% and as high as 16%.
- 1 Signs and symptoms
- 2 Causes
- 3 Classification
- 4 Diagnosis
- 5 Treatment
- 6 History
- 7 Notable cases
- 8 See also
- 9 References
- 10 External links
Signs and symptoms
The only symptom of vitiligo is the presence of pale patchy areas of depigmented skin which tend to occur on the extremities. 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. The loss of skin pigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus. Some lesions have increased skin pigment around the edges. Patients who are stigmatized for their condition may experience depression and similar mood disorders.
Although multiple theories have been suggested as potential triggers that cause vitiligo, studies have most strongly implicated changes in the immune system as being responsible for the condition. While genetic predisposition to vitiligo undoubtedly exists, it is believed that vitiligo onset is strongly affected by environmental factors.
Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo.[medical citation needed]
In one case, the gene TYR, which makes the skin pigment cell (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. Therefore, people with vitiligo caused by the TYR gene are less likely to have malignant melanoma.[medical citation needed]
A genomewide association studies found approximately 36 independent susceptibility loci for generalized vitiligo[Ref]. 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 major histocompatibility complex (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.
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.
Inflammatory and thyroid associations
Vitiligo is sometimes associated with autoimmune and inflammatory diseases, 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 blood 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. Polymorphisms of CD4 were shown to be associated with the vitiligo and other autoimmune diseases like type I Diabetes Mellitus.
Among the inflammatory products of NALP1 are caspase 1 and caspase 7, which activate the inflammatory cytokine interleukin-1β. Interleukin-1β is expressed at high levels in patients 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.
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).
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. 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).
Classes of non-segmental vitiligo include the following:
- Generalized Vitiligo: the most common pattern, wide and randomly distributed areas of depigmentation
- Universal Vitiligo: depigmentation encompasses most of the body
- Focal Vitiligo: one or a few scattered macules in one area, most common in children
- Acrofacial Vitiligo: fingers and periorificial areas
- Mucosal Vitiligo: depigmentation of only the mucous membranes
Segmental vitiligo (SV) differs in appearance, cause 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 spinal cord and is most often unilateral. It spreads much more rapidly than NSV and, without treatment, it is much more stable/static in course and is not associated with auto-immune diseases. SV is a very treatable condition that responds to topical treatment.
A black light (also referred to as a UVA light, Wood's lamp, or simply ultraviolet light) can be used in the early phase of this disease for identification and to determine effectiveness of treatment. Skin with vitiligo, when exposed to a black light, will glow blue. In contrast, healthy skin will have no reaction.
Conditions with similar symptoms include the following:
- Pityriasis alba
- Tuberculoid leprosy
- Postinflammatory hypopigmentation
- Tinea versicolor
- Idiopathic guttate hypomelanosis
- Progressive macular hypomelanosis
- Primary adrenal insufficiency
There are many treatments for vitiligo with the best evidence for applied steroids and the combination of ultraviolet light in combination with creams. Due to the higher risks of skin cancer, the United Kingdom's National Health Service suggests phototherapy only be used if primary treatments are ineffective. In general, non-segmental vitiligo is responding to treatment better than segmental form. Better efficiency consistently observed when disease duration is shorter and at younger age. The most hard-to-repigment lesions located on hands, feet and joints, with lesions on head and neck being easiest to return natural skin color.
Exposing the skin to UVB light from UVB lamps is the most common treatment for vitiligo. The treatments can be done at home with a domestic UVB lamp or in a clinic. It is important to control the exposure time so that the skin does not burn from overexposure. Treatment can take a few weeks if the spots are on the neck and face and if they existed not more than 3 years. If the spots are on the hands and legs and have been there 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. Both UVB broadband and UVB narrowband lamps can be used. but narrowband ultraviolet picked around 311 nm is the choice. It has been constitutively reported that combination of UVB phototherapy with other topical treatments improves repigmentation.
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.
Narrowband ultraviolet B (UVB) phototherapy is now used more commonly than PUVA as it is less damaging to the skin and lack side-effects caused by psoralens. 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.
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 affected skin.
Most vitiligo is idiopathic; however, in cases where it is triggered by skin bleaching or other substances, it is said to be chemical after being treated with bleaching agents. 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 with monobenzone is permanent and vigorous. Sun-safety must be adhered to for life to avoid severe sun burn and melanomas. Depigmentation takes about a year to complete.
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 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. By now, a number of transplantation techniques has been developed, including transplantation of melanocyte precursors derived from hair follicles. Transplantation procedures are frequently used to treat segmental vitiligo which is poorly responsive to other types of treatment. In non-segmental vitiligo, success is achieved when treating patches that are not expanding (so called stable vitiligo).
Descriptions of a disease believed to describe vitiligo date back to around 2200 BC to an ancient Iranian text "Tarkh-e-Tibble" and to a passage in the medical text Ebers Papyrus circa 1500 BC in ancient Egypt. Mentions of whitening of the skin was also present circa 1400 BC in sacred Inidian texts such as Atharvaveda as well as Shinto prayers in the Far East circa 1200 BC. The Hebrew word "Zora'at" from the Old Testament book of Leviticus dating to 1280 BCE (or 1312 BCE) described a group of skin disease associated with white spots, and a subsequent translation to Greek led to continued conflation of those with vitiligo with leprosy and spiritual uncleanliness. Medical sources in the ancient world such as Hippocrates often did not differentiate between vitiligo and leprosy, often grouping these diseases together. In Arabic literature, the word "alabras" has been associated with vitiligo, with this word found in the Koran. The name "vitiligo" was first used by the Roman physician Aulus Cornelius Celsus in his classic medical text De Medicina.
The etymology of the term "vitiligo" is believed to be derived from "vitium", meaning "defect" or "blemish".
- Michael Jackson revealed in an interview with Oprah Winfrey in February 1993 that he had vitiligo. This was confirmed by the autopsy report following his death in 2009.
- Jon Hamm reported developing stress-induced vitiligo while working on the series Mad Men.
- UFC fighter Scott Jorgensen suffers from a particularly aggressive form of the disease and has received the unofficial nickname 'Spotty' as a result of the appearance it causes his skin to have. In 2012 Jorgensen claimed to have allowed the disease to "pretty much take over" and as a result give his skin a uniform colour.
- The Canadian model Chantelle Brown-Young has a prominent form of vitiligo. Her participation in the America's Next Top Model contest led to her being called a "vitiligo spokesmodel".
- American rapper Krizz Kaliko is diagnosed with the condition, and titled his debut album Vitiligo.
- Lee Thomas, broadcast reporter, speaker, and best-selling author of Turning White: A Memoir of Change, which covered his experience of living with vitiligo
- Albinism, uniform absence of melanin
- Alphos, a non-contagious leprosy formerly referred to as "vitiligo"
- Amelanism, lack of pigmentation
- Erythrism, excessive red pigmentation
- Heterochromia iridum, another condition characterized by pigment variations
- Leucism, reduced pigmentation
- Melanising agents
- Melanism, uniform saturation of melanin
- Nevus depigmentosus
- Pityriasis alba
- Quadrichrome vitiligo, characterized by patches of reduced but not absent pigment
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- Duke, Alan (7 May 2013). "Autopsy reveals Michael Jackson's secrets". CNN Entertainment (CNN). Retrieved 7 May 2013. "The autopsy confirmed what Jackson told people who questioned why his skin tone became lighter in the 1980s. Jackson had 'vitiligo, a skin pigmentation disease,' [LA coroner Dr. Christopher] Rogers said. 'So, some areas of the skin appear light and others appear dark.'"
- "Mad Men star Jon Hamm blames skin disease on stress | Don Draper". Theage.com.au. Retrieved 2014-02-11.
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