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Vitiligo is an acquired pigmentary disorder of the skin. It is characterized by circumscribed depigmented sections of skin. The cause of vitiligo is unknown and it is related to both genetic and nongenetic factors.


Vitiligo is signified by acquired white or hypopigmented macules or patches. Affected areas are generally well differentiated, and are spherical, oblong, or linear in shape. Borders can be convex [9]. Generally, the lesions grow centrifugally as the time passes at an erratic rate. Size of the lesions can differ from millimeters to centimeters. In the beginning, lesions appear very often on the hands, forearms, feet, and face. Perioral and periocular areas are most favorable sites.

Vitiligo lesions may be seen only in an area or many areas all over the body, but commonly it widely affects the entire body. In such cases, the macules are generally seen on both sides of the trunk, either evenly or unevenly aligned.

Vitiligo commonly affects the face, neck, and scalp. Mostly, it affects the areas that are subjected to recurrent trauma. Common involvements are bony prominences, extensor surface of forearm, ventral aspects of wrists, dorsal side of hands, and digital phalanges.

Mucous membranes are involved in cases of generalized vitiligo. It generally develops surrounding the body orifices like the lips, genitals, gingiva, areolas, and nipples.

Depigmented body hair (leukotrichia) can be seen in vitiliginous macules. Vitiligo affecting the scalp develops as a limited area of white or gray hair, but complete depigmentation of entire scalp hair may take place. Scalp is involved very frequently, followed by the eyebrows, axillary hair, and pubic hair.

  • […] polygenic inheritance.[ 6, 7 ] The effects of vitiligo can be cosmetically and psychologically devastating, resulting in low self-esteem, poor body image, and difficulties in sexual relationships.[ 8 ] Because the disease is still not understood, there is a plethora[ncbi.nlm.nih.gov]
  • Herein we present a case of vitiligo in an area of chronic cheilitis after isotretinoin treatment.[ncbi.nlm.nih.gov]
  • We report the case of a 17-year-old boy who presented to our clinic with trauma-induced skin blistering, alopecia, deafness, dental caries, nail dystrophy and vitiliginous areas.[ncbi.nlm.nih.gov]
  • In this article, we describe a case with simultaneous presence of segmental vitiligo, alopecia areata, psoriasis and a halo naevus. To our knowledge, this is the first case with this exceptional combination.[ncbi.nlm.nih.gov]
  • Topical immunotherapy made by diphenylcyclopropenone (DPCP) is an alternative treatment that can be used safely and efficaciously in recalcitrant alopecia areata patients. DPCP-induced vitiligo is a rare, but documented, unwanted side effect.[ncbi.nlm.nih.gov]
  • Compared with the general US population, we found a higher prevalence of thyroid disease (12.9%, P .001), alopecia areata (3.8%, P .001), inflammatory bowel disease (0.9%, P .046), pernicious anemia (0.5%, P .007), systemic lupus erythematosus (0.3%,[ncbi.nlm.nih.gov]
  • Brett King, assistant professor of dermatology and principal investigator of the research, broke new ground when he published a paper demonstrating the effectiveness of the JAK inhibitor tofacitinib citrate in treating hair loss caused by alopecia areata[web.archive.org]
Koebner Phenomenon
  • Evaluation was also made by dermatologists to define vitiligo subtype, body surface area, Koebner phenomenon (KP), and so on. Data were assessed by computer software. Results were considered statistically significant if p 0.05.[ncbi.nlm.nih.gov]
  • Multivariate analysis demonstrated that the Koebner phenomenon (KP; OR 10.632, P 0.0001), multiple HN (OR 3.918, P 0.0001), and a familial history of vitiligo (OR 3.222, P 0.014) were independent factors associated with HNV.[ncbi.nlm.nih.gov]
  • CONCLUSIONS: Detachment and transepidermal elimination of melanocytes following minor mechanical trauma in non lesional vitiligo skin is probably the cause of depigmentation occurring in the isomorphic response (Koebner phenomenon).[ncbi.nlm.nih.gov]
  • According to Falabella, [3] a lesion with lack of progression or no new lesions for 2 years, absence of recent Koebner phenomenon, positive minigrafting test, absence of Koebner phenomenon at donor site, and evidence of repigmentation of existing patches[jcasonline.com]
  • The importance of Koebner’s phenomenon in the induction of vitiligo vulgaris lesions. Eur J Dermatol. 1995; 5 :704–708. [ Google Scholar ] Gauthier Y, Benzekri L. Vitiligo. In: Picardo M, Taieb A, editors. The Koebner’s phenomenon.[ncbi.nlm.nih.gov]
  • In vitiligo and piebaldism the lack of melanin in the epidermis is due to the fact that melanocytes are missing.[ncbi.nlm.nih.gov]
  • Schwartz, Piebaldism: an update, International Journal of Dermatology, 43, 10, (716-719), (2004).[doi.org]
  • […] surrounded by a ring of depigmentation Cancer associated: Extramanmmary Paget's disease, Melanoma-associated leucoderma Others: Idiopathic guttate hypomelanosis, Leucoderma punctata, Progressive macular hypomelanosis of the trunk, nevus depigmentosus, piebaldism[americanskin.org]
  • Vitiligo, also called piebald skin or acquired leukoderma, is a condition in which pigment, produced by cells called melanocytes, is lost from areas of the skin, causing whitish, smooth patches.[verywell.com]
  • Post-inflammatory hypopigmentation, following inflammatory skin conditions such as eczema. Pityriasis alba. This may be a type of eczema or an inflammatory reaction following mild eczema. Leprosy, especially the tuberculoid variety. Halo naevus.[patient.info]
  • Post-inflammatory hypopigmentation , following inflammatory skin conditions such as eczema. Pityriasis alba. This may be a type of eczema or an inflammatory reaction following mild eczema. Leprosy , especially the tuberculoid variety. Halo naevus .[patient.info]
  • Topical pimecrolimus or tacrolimus Pimecrolimus and tacrolimus are a type of medicine called calcineurin inhibitors that are normally used to treat eczema.[web.archive.org]
  • Topical pimecrolimus or tacrolimus Pimecrolimus and tacrolimus are a type of medicine called calcineurin inhibitors, which are normally used to treat eczema .[nhs.uk]
  • Other options include pimecrolimus and tacrolimus, creams that are usually used for eczema, which can help repigment the skin, says Dr Stevens.[dailymail.co.uk]
Premature Graying of the Hair
  • In addition to white patches, vitiligo can cause premature graying of the hair. Credit: Wikimedia Commons Vitiligo is believed to affect 0.5 percent to 1 percent of the world's population, or up to 65 million people.[cbsnews.com]
  • In some families, premature graying of the hair results from an autoimmune loss of melanocytes in the hair follicles.[nytimes.com]
  • Be sure to report any events that could be contributing factors, like recent sunburns, premature graying of your hair, or any autoimmune diseases you may have.[healthline.com]
  • Important factors in the diagnosis include a family history of vitiligo; a rash, sunburn, or other skin trauma that occurred at the site of vitiligo before depigmentation started; stress or physical illness; and premature graying of the hair (usually[web.archive.org]
Facial Scar
  • All three patients gave a history of small pox in childhood and had pitted facial scars typical of previous small pox infection. Vitiligo iridis may be associated with the secondary glaucoma as a long-term sequelae of small pox.[ncbi.nlm.nih.gov]
  • Destruction of pigment cells in vitiligo may not remain limited to the skin; the eyelashes, iris, ciliary body, choroid, retinal pigment epithelium and meninges may also be affected.[ncbi.nlm.nih.gov]


Diagnosis of vitiligo usually is made with the help of clinical findings, but sometimes biopsy is beneficial in individualization of vitiligo from various hypopigmentary disorders.

Vitiligo is sometimes seen along with various autoimmune diseases like thyroid disease, diabetes mellitus, pernicious anemia, Addison disease, and alopecia areata. Individuals should have knowledge about manifestations of these diseases. In case the disease is manifested than necessary tests should be done [10]. Vitiligo lesions are analyzed with the help of a Wood lamp.

Pericardial Effusion
  • We describe a 75-year-old man with lung adenocarcinoma, stage 4 with pleural and pericardial effusion, that progressed after first-line chemotherapy. Subsequently, he was treated with nivolumab as second-line therapy.[ncbi.nlm.nih.gov]


No drug can stop the process of vitiligo, but some drugs when used individually, or along with light therapy, may be helpful in improving the skin's appearance.

  • Local application: A topical corticosteroid may help repigment the skin, especially when used in the beginning of the disease. For several months there might be no change in skin color. Topical calcipotriene which is a form of vitamin D may be used along with corticosteroids or ultraviolet light. Ointments comprising of tacrolimus or pimecrolimus (calcineurin inhibitors) can be beneficial for people with tiny areas of depigmentation, particularly on the face and neck.
  • Combined medication and light therapy: In this treatment a drug called psoralen is combined with light therapy (photochemotherapy) to regain color on the light patches. Once psoralen is taken by mouth or applied on the affected skin, than the person is exposed to ultraviolet A (UVA) or UVB light. The drug affects your skin in such a way that the skin becomes more sensitive to the light, and it turns pink. As the skin starts healing, normal skin color starts appearing.
  • Light therapy: In this therapy narrow band UVB light is used. Maximum results are seen on the face, trunk and limbs
  • Laser therapy: In this treatment an excimer laser is used to bring back the color in areas of light skin. It makes use of a particular wavelength of UVB light. This laser can be used on small areas only, and is generally used along with a drug applied on the skin.
  • Removing the remaining color (depigmentation): This therapy is considered if the vitiligo is widespread and other treatments have failed. A medication containing monobenzone is applied on normal areas of skin. Because of this, the normal skin gradually lightens and blends with discolored skin.
  • Surgery is the last option for those in whom light therapy and drugs do not have any effect. Various procedures like skin grafting, blister grafting or tattooing are used to cover the patches.


Generally, limited vitiligo involving the face and trunk in children of recent onset is very receptive to treatment. Wide-spread disease in adults and disease affecting the hands and feet is resistant to therapy.


The cause of vitiligo is not known, but studies suggest that it may develop due to viral infections, oxidative stress and autoimmune, genetic or neural causes [1].


The incidence worldwide is less than 1% [2]. Around 30% of the cases are seen within a group of members in a family. Appearance of the vitiligo is independent of the age, although the onset is usually observed in persons aged 10-30 years. In most of the cases, the person suffers from vitiligo at early age in life.

Sex distribution
Age distribution


Vitiligo can be caused by both genetic and non-genetic factors. Even though the actual cause remains unknown, commonly considered factors are that there are no functional melanocytes left in the affected skin and there is damage of histochemically identified melanocytes, leading to their destruction. Theories regarding destruction of melanocytes include the following:

Autoimmune destruction of melanocytes

The autoimmune theory [3] suggests changes in humoral and cellular immunity in the devastation of melanocytes of vitiligo. The most assuring data of an autoimmune involvement is the existence of circulating antibodies in persons suffering from vitiligo [4]. Substantial data points towards link between cellular immunity and vitiligo.

Intrinsic defect of melanocytes

Vitiligo melanocytes might have an intrinsic defect causing death of melanocyte. These melanocytes exhibit different abnormalities like unusual, harsh endoplasmic reticulum and inadequate synthesis and transformation of melanocytes.

Disruption in oxidant-antioxidant mechanism in vitiligo

Studies suggest that piling up of free radicals lethal to melanocytes results in their devastation. Current investigations are deployed to figure out the action of oxidative stress by calculating the levels of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in the affected as well as the unaffected skin of patients suffering from vitiligo and in the skin of totally unaffected control persons. It was proved that oxidative stress is raised in vitiligo, as determined by increased levels of SOD and decreased levels of CAT in the skin of people suffering from vitiligo [5].

Neural theory

Case reports portray that patients suffering from an injury to nerve along with having vitiligo, are also suffering from hypopigmentation or depigmentation in those denervated regions. In addition, segmental vitiligo regularly develops in a dermatomal pattern, which indicates that some chemical mediators are liberated from nerve endings affecting the melanin production. Additionally, sweating and vasoconstriction are raised in depigmented patches of vitiligo, suggesting high adrenergic activity. Ultimately, increased excretion of homovanillic acid and vanillylmandelic acid in urine has been recorded in patients suffering from vitiligo. This can be a basic or trivial episode [6].

Genetics of vitiligo

Vitiligo is characterized by partial penetrance, many sensitive areas, and genetic heterogeneity [7]. Vitiligo caused due to inheritance can be due to involvement of genes related to the biosynthesis of melanin, reaction to oxidative stress, and control of autoimmunity [8].


There is no way to prevent vitiligo, but using sunscreens with a minimum sun protection factor (SPF) of 15 to protect the skin from the sun is always a healthy decision.


Vitiligo is a condition that causes depigmentation of segments of the skin. It develops due to death or malfunctioning of melanocytes, the cells that are in charge for skin pigmentation. This condition is often associated with disorders of autoimmune origin and thyroid abnormalities.

Patient Information

Vitiligo is a condition that causes depigmentation of segments of the skin. Being a genetic disorder there is no way of preventing this disease; it is advised to start the treatment as early as possible. As the disease is associated with various other autoimmune diseases, care must be taken to diagnose and treat them too. Emotional support is another important part of vitiligo therapy as the skin changes caused by vitiligo can affect people emotionally and socially.

Even in today’s world due to unawareness people feel that vitiligo can also spread due to close contact but that is not true, vitiligo is not a communicable disease. It does not cause any disability and the patient is fit for any type of work. Now due to progress in cosmetic industry there are many local applications that are available to hide small areas of vitiligo on the exposed area. The creams camouflages with the skin such that no one can make out the difference.



  1. Halder RM, Chappell JL. Vitiligo update. Semin Cutan Med Surg. 2009 Jun;28(2):86-92.
  2. Nath SK, Majumder PP, Nordlund JJ. Genetic epidemiology of vitiligo: multilocus recessivity cross-validated. Am J Hum Genet. 1994 Nov;55(5):981-90.
  3. Le Poole IC, Luiten RM. Autoimmune etiology of generalized vitiligo. Curr Dir Autoimmun. 2008;10:227-43.
  4. Toussaint S, Kamino H. Noninfectous papular and squamous diseases. In: Elder D, Elenitas R, Jaworsky D, Johnson B Jr. Lever's Histopathology of the Skin. Philadelphia, Pa: Lippincot-Raven; 1997:154-5.
  5. Sravani PV, Babu NK, Gopal KV, Rao GR, Rao AR, Moorthy B. Determination of oxidative stress in vitiligo by measuring superoxide dismutase and catalase levels in vitiliginous and non-vitiliginous skin. Indian J Dermatol Venereol Leprol. 2009 May-Jun;75(3):268-71.
  6. Kovacs SO. Vitiligo. J Am Acad Dermatol. 1998 May;38(5 Pt 1):647-66; quiz 667-8.
  7. Spritz RA. The genetics of generalized vitiligo. Curr Dir Autoimmun. 2008;10:244-57.
  8. Halder R, Taliaferro S. Vitiligo. In: Wolff K, Goldsmith L, Katz S, Gilchrest B, Paller A, Lefell D, eds.Fitzpatrick's Dermatology in General Medicine. Vol 1. 7th ed. New York, NY: McGraw-Hill; 2008:72.
  9. Ortonne J. Vitiligo and other disorders of Hypopigmentation. In: Bolognia J, Jorizzo J, Rapini R, eds.Dermatology. Vol 1. 2nd. Spain: Elsevier; 2008:65.
  10. Matz H, Tur E. Vitiligo. Curr Probl Dermatol. 2007;35:78-102.

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Last updated: 2019-07-11 22:45