Vitiligo is an acquired pigmentary skin disorder by the absence of pigmentary cells from the epidermis that results in white macules and patches on the body. The condition is usually associated with few autoimmune disorders, with thyroid abnormalities are the commonest one. The etiology of vitiligo is unknown but there are different theories to explain its pathogenesis. Vitiligo presents clinically with signs and symptoms of white spots on the body distributed symmetrically and more obvious in people with dark skin. The lesions are characterized by well-demarcated pearly white or depigmented macules and patches, oval, round, or linear-shaped, and the borders are convex, range from the size of few millimeters to centimeters and enlarge centrifugally. There are different clinical variants of vitiligo which are Trichrome, Marginal inflammatory, and Quadrichrome vitiligo. Koebner phenomenon(Development of vitiligo at specific trauma prone sites, like cut, burn, or abrasion)is also a common clinical manifestation. Initial lesions occur most frequently on the hands, forearms, feet, and face, favoring a periocular or perioral distribution. On the basis of the distribution, pattern Vitiligo is classified into three types, generalized, segmental, and localized. The severity of the disease is scored by the body surface area affected. The course of the disease is often unpredictable and varies in response to the treatment. Depigmentation often the cause of psychological distress, social stigmatization, and low self-esteem.

Chemical leucoderma, an under-diagnosed common condition often mimicking idiopathic vitiligo, represents an acquired depigmentation induced by repeated exposure to specific chemical compounds in subjects with genetic susceptibility to vitiligo. This has been increasing rapidly in incidence in recent decades in developing countries like India. The term 'chemical vitiligo' was first coined by us to indicate the possible relationship between chemical leucoderma and vitiligo, which has been supported recently by other authors to designate the term 'chemical-induced vitiligo'. The largest case series showed that household chemical exposure was the major etiological factor. Causative chemicals are mostly phenolic and catecholic derivatives. Vitiligo pathogenesis is induced by genetic and environmental factors like many other autoimmune diseases. Innate immunity acts as a bridge between cellular stress and adaptive immunity. Multiple patches are commonly seen; children below 12 years are also affected in good numbers. The most common presence of confetti macules indicates these as characteristic, although not pathognomonic, of chemical leucoderma. Chemical leucoderma has been broadened into 'chemical leucoderma syndrome' with proper staging. The clinical criteria for diagnosis of chemical leucoderma have been specifically outlined. Same pathomechanism of chemical leucoderma might elucidate trigger factors and reasons for progression and chronicity in idiopathic vitiligo. Depigmentation in chemical vitiligo spreads to distant sites, in the same way as generalized idiopathic vitiligo. The study showed that chemical triggering factors played a very significant role in the induction and progression of vitiligo. Thus it should be rational to consider chemical vitiligo not as a separate entity but as a major subset of vitiligo spectrum.

Keywords: Chemical leucoderma; chemical vitiligo; contact leucoderma; vitiligo.

Vitiligo is an acquired depigmentary disorder of the skin that results from the selective destruction of melanocytes. The etiology of vitiligo is poorly understood. There appears to be a genetic predisposition, but additional factors are probably involved. The purpose of this article is to outline the factors that might play a role in the development of vitiligo. These include trauma such as vaccination, radiotherapy, and sun exposure, malignancies and treatment of malignancies like lymphoma or melanoma, bone marrow transplantation, interferon, interleukin, and other drugs, psychological factors, endocrine disease and cytotoxic compounds that cause contact vitiligo. We hope future research will shed more light on the subject and identify the precipitating factors, since in the majority of vitiligo cases the contributing factors are as yet unidentified.

Vitiligo, an acquired pigmentary disorder of unknown origin, is the most frequent cause of depigmentation worldwide, with an estimated prevalence of 1%. The disorder can be psychologically devastating and stigmatising, especially in dark skinned individuals. Vitiligo is clinically characterised by the development of white macules due to the loss of functioning melanocytes in the skin or hair, or both. Two forms of the disease are well recognised: segmental and non-segmental vitiligo (the commonest form). To distinguish between these two forms is of prime importance because therapeutic options and prognosis are quite different. The importance of early treatment and understanding of the profound psychosocial effect of vitiligo will be emphasised throughout this Seminar.

Vitiligo is a common disorder afflicting people of all ages around the world. It produces milky white patches of depigmentation that cause significant morbidity due to cosmetic disfigurement. One should distinguish segmental from nonsegmental vitiligo, and be aware the latter is associated with an extremely small risk of associated autoimmune disorders. New therapeutic options offer some additional hope to patients with vitiligo, but more progress in the understanding of its pathogenesis and therapy is still needed.

Vitiligo represents a selective destruction of the melanocytes. It is a relatively common, probably autoimmune disorder that affects people of all backgrounds and both genders. No particular group seems to be preferentially affected. Half of vitiligo patients have an onset before the age of 18 years. In regions where leprosy is endemic, individuals with vitiligo are often stigmatized due to similarities in appearance between the two diseases. We will review this important subject, emphasizing the latest therapeutic advances.

The destruction of melanocytes is the cause of depigmented maculae that clinically represent the disease vitiligo. Although the cause is unknown, various theories such as the autoimmune, autocytotoxic, and neural hypotheses have been proposed. Extensive research has provided numerous answers regarding the pathogenesis, histopathologic evidence, and treatment of vitiligo. This discussion of vitiligo summarizes the varied clinical presentations of the disease, theories attempting to explain the mechanism of melanocyte destruction, histopathologic findings, and different treatment modalities currently available.

Vitiligo involves a progressive loss of melanocytes from the epidermis and hair follicles. Milky-white patches appear resulting in cosmetic disfiguration that is most apparent in dark-skinned individuals. The disease is further classified according to distribution pattern and extent of depigmentation. The presence of several clinical subtypes may reflect the diversity in causative factors. To select appropriate therapeutic measures it is important to distinguish vitiligo from other disorders that affect melanocyte function. Although vitiligo has a characteristic clinical appearance and histological features, the presence of early or atypical lesions often requires the exclusion of other disorders such as postinflammatory hypopigmentation and piebaldism. Multiple hypotheses have been put forward to explain vitiligo. An inherited tendency to develop depigmentation may involve the inherent aberrancies that have been observed in nonlesional vitiligo melanocytes in vivo as well as in vitro. These abnormalities potentially render vitiliginous melanocytes more vulnerable to assaults from extracellular factors. Such factors include keratinocyte physiology, extracellular matrix composition, humoral and cellular immunity, and environmental agents. Therapies aimed at repopulation of lesional skin include phototherapy, application of topical corticosteroids, and transplantation of skin or skin cells. Moreover, micropigmentation or camouflage can be used to restore a pigmented appearance to lesional skin. In patients in which vitiligo affects extensive areas of the body, depigmentation may be the treatment of choice. In all, this acquired pigmentary disorder can be treated in a variety of ways and should not be regarded as an untreatable affliction.

Vitiligo is a disorder in which, owing to disappearance of melanocytes in the skin, sharply delimited, symmetrically arranged white patches develop. The condition occurs in 1-2% of the population, mostly between the ages of 10 and 30 years, and as often in males as in females. The course is usually progressive with periods of stability. A number of autoimmune diseases and dermatoses coincide with vitiligo. The cause of vitiligo is unknown. Hereditary factors, autoimmunization, neurological disorders and autodestruction have been hypothesized. Repigmentation therapy consists of photo(chemo)therapy use of corticosteroids, and transplantation of pigment cells. For patients in whom this fails and with more than 80% cutaneous involvement, total depigmentation therapy could be considered.

Vitiligo is characterized by depigmentation in large or small areas of the skin. There is a complete lack of melanin production in the hypopigmented areas, due to the destruction of previously active melanocytes. This is in contrast to albinism, in which melanocytes are present but there is little or no pigmentation because of defective or absent tyrosinase. Although the etiology of vitiligo remains unknown, an autoimmune theory is gaining acceptance.

Vitiligo is an acquired depigmenting disorder that affects 0.5% to 2% of the world population. Three different forms are classified according to the distribution of lesions; namely non-segmental, segmental and mixed vitiligo. Vitiligo is associated with polymorphisms in genes involved in the immune response and in melanogenesis. However, environmental factors are required for the development of manifest disease. In general, the diagnosis is clinical and no laboratory tests or biopsies are required. Metabolic alterations are central to current concepts in pathophysiology. They induce an increased generation of reactive oxygen species and susceptibility to mild exogenous stimuli in the epidermis. This produces a senescent phenotype of skin cells, leads to the release of innate immune molecules, which trigger autoimmunity, and ultimately causes dysfunction and death of melanocytes. Clinical management aims to halt depigmentation, and to either repigment or depigment the skin, depending on the extent of disease. New therapeutic approaches include stimulation of melanocyte differentiation and proliferation through α-melanocyte-stimulating hormone analogues and through epidermal stem cell engineering. Several questions remain unsolved, including the connection between melanocyte depletion and stem cell exhaustion, the underlying degenerative mechanisms and the biological mediators of cell death. Overall, vitiligo is an excellent model for studying degenerative and autoimmune processes and for testing novel approaches in regenerative medicine. For an illustrated summary of this Primer, visit: http://go.nature.com/vIhFSC.

BACKGROUND

Vitiligo is an acquired skin disorder characterised by white (depigmented) patches in the skin, due to the loss of functioning melanocytes. The extent and distribution of vitiligo often changes during the course of a person's lifetime and its progression is unpredictable.

METHODS

We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of medical treatments, and of ultraviolet light treatments, for vitiligo in children and in adults? We searched: Medline, Embase, The Cochrane Library and other important databases up to March 2007 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).

RESULTS

We found 25 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.

CONCLUSIONS

In this systematic review we present information relating to the effectiveness and safety of the following interventions: corticosteroids, oral levamisole, topical immunomodulators, topical Vitamin D analogues, ultraviolet A plus psoralen (PUVA), and ultraviolet B (narrowband, and broadband).

Vitiligo is a disease that affects from 1 to 3 per cent of the population. It is characterized by cutaneous white macules that often develop in cosmetically important areas such as the face, the dorsal hands, and the arms. It may be accompanied by ocular abnormalities and a number of associated disorders such as thyroid disease, diabetes, pernicious anemia, and alopecia areata. There is increasing evidence that vitiligo is an autoimmune disease. Although there is as yet no definitive cure, many patients have obtained respectable repigmentation by the use of topical or oral psoralen plus ultraviolet light. When large areas of skin are involved or when the patient is unresponsive to therapy, serious consideration should be given to depigmentation with monobenzone (Benoquin).

The authors report 2 cases of atypical vitiligo in which they observed 1) "cockade-like" lesions resembling those of "trichrome" vitiligo (from the centre to the periphery, achromic area, hypochromic ring, normal or hyperchromic border), 2) numerous linear achromic lesions corresponding to former excoriations (Koebner's phenomenon, isomorphic phenomenon). Related affections are discussed with reference to these cases; the trichrome vitiligo described by Lerner and Fitzpatrick, and the primary leukomelanodermas described in black patients by Basset and by Sarrat and Nouhouayi.