Vitiligo is an acquired disorder of skin pigmentation in which functioning melanocytes are lost from affected areas, producing well-demarcated depigmented macules and patches. Melanocytes are specialised cells responsible for producing melanin, the pigment that contributes to skin, hair and eye colour. Vitiligo can affect people of any skin colour and may become particularly visually apparent in individuals with darker baseline pigmentation because the contrast between affected and unaffected skin is greater. Lesions commonly occur on the face, hands, around body openings and over areas subject to repeated trauma, but virtually any skin surface can be involved. The condition is not contagious and is not caused by poor hygiene or ordinary physical contact.
The principal biological mechanism in most non-segmental vitiligo is believed to involve immune-mediated destruction or dysfunction of melanocytes in genetically susceptible individuals. Genetic factors influence susceptibility, but vitiligo is not inherited through a simple single-gene pattern. Oxidative stress, cellular stress responses, innate immune signalling and adaptive T-cell responses have all been implicated in melanocyte loss and persistence of inflammation. Melanocytes can also be affected by interactions between the epidermis, immune system and local tissue environment. The exact initiating event remains incompletely understood, and different forms of vitiligo may involve different pathogenic processes.
Vitiligo is classified clinically into patterns including non-segmental and segmental disease. Non-segmental vitiligo is generally bilateral or more widely distributed and may involve multiple body regions, while segmental vitiligo often affects one side or a specific anatomical segment and can follow a more limited course. Other descriptive classifications concern the extent and location of depigmentation. Lesions are typically sharply demarcated and completely depigmented, although early lesions can be less conspicuous. Hair growing within affected areas can also lose pigment, producing white or prematurely depigmented hair. Mucosal surfaces and areas around the eyes or mouth may be involved, and genital involvement is possible.
Diagnosis is usually clinical, but examination under a Wood's lamp can make depigmented lesions more conspicuous and help distinguish vitiligo from some causes of hypopigmentation. Differential diagnoses include post-inflammatory hypopigmentation, pityriasis alba, tinea versicolor and other pigmentary disorders. The distribution, degree of depigmentation, history of progression and presence of other autoimmune conditions can help establish the diagnosis. Vitiligo is associated statistically with several autoimmune disorders, particularly autoimmune thyroid disease, but an individual with vitiligo does not necessarily have another autoimmune condition. Investigation should therefore be clinically directed rather than assuming that every patient has multiple systemic diseases.
The course of vitiligo is unpredictable. Some individuals have stable, localised patches, whereas others experience periods of progression separated by relative stability. New lesions may appear at sites of skin trauma through a phenomenon known as the Koebner phenomenon, although this is not universal. Spontaneous repigmentation can occur, particularly around hair follicles where melanocyte reservoirs may remain. Treatment aims either to restore pigment or to reduce contrast and prevent progression, depending on disease extent and patient preference. Options include topical corticosteroids, topical calcineurin inhibitors, phototherapy such as narrowband ultraviolet B and, in selected stable cases, surgical techniques that transfer melanocytes or melanocyte-containing tissue to depigmented areas.
Phototherapy is particularly important for more extensive disease because it can stimulate residual melanocytes and melanocyte precursors to repopulate affected epidermis. Response varies by body site, disease duration, extent and individual biology, with facial lesions often responding more readily than certain acral areas. Surgical approaches are generally considered when disease is stable and localised because ongoing progression can compromise graft survival or produce new lesions elsewhere. Cosmetic camouflage, self-tanning products and depigmentation of remaining pigmented skin in exceptional circumstances can be considered according to the extent and impact of disease. Sun protection is important because depigmented skin contains less melanin and is more vulnerable to ultraviolet injury and sunburn.
Vitiligo can have substantial psychosocial effects, particularly when lesions involve the face, hands or other visible areas. These effects are not a sign that the disease is medically more severe, but they are clinically relevant when determining treatment priorities. Vitiligo itself does not usually cause pain or itching, although affected skin can experience ordinary dermatological problems and associated autoimmune conditions may produce unrelated symptoms. The condition is sometimes incorrectly attributed to diet, infection or contact with another person, none of which explains the usual pathogenesis. Psychological stress may affect coping and perceived burden and may sometimes coincide with disease activity, but it should not be presented as a simple cause.
Vitiligo must be distinguished from albinism, which is a group of inherited disorders involving reduced melanin production from birth and affecting multiple tissues, and from temporary hypopigmentation after inflammation. Vitiligo can affect hair and mucosal surfaces, but it primarily represents acquired melanocyte loss rather than a generalised congenital absence of pigmentation. There is currently no universally effective treatment that permanently restores normal pigmentation in every affected person, and recurrence can occur after successful repigmentation. Nevertheless, several treatments can produce meaningful repigmentation or reduce the visual contrast between affected and unaffected skin. Understanding its autoimmune and melanocyte-specific biology is important for distinguishing vitiligo from superficially similar pigmentary conditions and for selecting appropriate treatment strategies.
