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PubMed2003

Melanocyte-keratinocyte cell transplantation for stable vitiligo.

BACKGROUND: Vitiligo is a common disorder with a worldwide prevalence of 1-2%. In India the psychological and social impact of the disease is significant and is detrimental to patients. OBJECTIVE: To evaluate the usefulness of epidermal cell transplantation in the treatment of vitiligo. METHODS: A simpler and modified method based on that of Olsson and Juhlin has been used. It utilizes a shave biopsy skin sample of up to one-tenth the size of the recipient area. The skin sample is incubated, the cells mechanically separated using trypsin EDTA solution, and then centrifuged to prepare a suspension. The cell suspension is then applied to the derm-abraded depigmented skin area and collagen dressing is applied to keep it in place. RESULTS: One hundred and twenty-two patients with generalized vitiligo, 43 with segmental and 19 with focal vitiligo were treated and observed for a period of 1 year. In the generalized vitiligo group 65 (53%) showed excellent pigmentation, 10 (8%) showed good pigmentation, 11 (9%) showed fair pigmentation and 28 (23%) patients showed poor pigmentation. Eight (7%) patients did not follow up. Thirty-six (84%), five (12%) and two (4%) patients showed excellent, good and poor pigmentation, respectively, in the segmental vitiligo group. Thirteen (69%) and five (26%) patients showed excellent and poor results, respectively, in the focal vitiligo group. One (5%) patient did not appear for follow up. Recurrence was observed in 15 patents. CONCLUSION: This surgical treatment gives its best results in segmental and focal vitiligo, even with large affected areas, and in at least 50% of patients with generalized vitiligo, thus improving their appearance.

Adolescent↗
PubMedDate not supplied

Characteristics of vitiligo in Korean children.

Eighty Korean children (ages 8 months-12 years) with clinical and/or histopathologic diagnoses of vitiligo were evaluated; 39 boys and 41 girls. The mean age at first visit was 7.9 years and the mean age at onset was 5.6 years. The most common site of onset was the head/neck area (58.8%), followed by the trunk and lower limbs. The children were compared with a control group of 422 adults with vitiligo. Children comprised 16% of the total vitiligo patients and adults comprised 84%. A family history of vitiligo was found in 11 (13.8%) children, compared to 10.7% in the adult group; poliosis in 20 (25. 0%); halo nevi in 2 (2.5%), compared to 4.0% in the adult group; combined autoimmune and endocrine diseases in 1 (1.3%), compared to 7.6% in the adult group; and segmental vitiligo in 26 (32.5%), compared to 13.0% in the adult group. The combined diseases were significantly less often found in children than adults (p < 0.01), and segmental vitiligo was significantly more often associated with children (p < 0.0001). Our study did not show a higher prevalence of vitiligo in girls as reported in other studies, which may indicate racial differences. Of the total 502 patients, only 1 patient with segmental vitiligo had halo nevi. Sixty-four percent of the children with vitiligo responded to treatment, compared to 57% of the adults.

Adult↗
PubMed2002

Treatment of vitiligo with the 308-nm excimer laser: a pilot study.

BACKGROUND: Present vitiligo therapies require many months of treatment and often result in disappointing outcomes. Common therapeutic options include phototherapy with psoralens plus ultraviolet A (UVA) radiation and broadband or narrowband UVB radiation phototherapy. Some of these modalities require regular phototherapy sessions several times a week for up to a year to achieve a therapeutic response. Targeted phototherapy with single-wavelength laser light is a treatment alternative that may prove to be a time-efficient and effective therapeutic option for the management of vitiligo. METHODS: This intervention study was designed as a before and after trial with a single arm. Twenty-nine patches of vitiligo from 18 patients (6 males and 12 females) were treated at the start of the study. Vitiligo patches were treated by using a 308-nm xenon-chloride excimer laser. Lesions were treated 3 times a week for a maximum of 12 treatments. Treatment was withheld if sunburn was observed and held until resolution. All patients had untreated vitiligo patches that served as control sites. RESULTS: Twenty-three vitiligo patches from 12 patients received at least 6 treatments and resulted in some repigmentation in 57% of the treated patches. Eleven vitiligo patches from 6 patients received all 12 treatments and resulted in some repigmentation in 82% of the treated patches. Untreated control patches remained unchanged. CONCLUSION: This degree of repigmentation in a period of 2 to 4 weeks is much higher than that achieved with any other present vitiligo therapy. The xenon-chloride excimer laser may represent a new treatment modality for the management of stable vitiligo.

Adult↗
PubMed2004

T cell subpopulations and IL-2R in vitiligo.

Immunological alterations have been implicated in the etiopathogenesis of vitiligo. The aim of this study was to determine peripheral lymphocyte subpopulations and interleukin-2 receptor (IL-2R) in patients with vitiligo. Forty-five vitiligo patients (24 female, 21 male) and 34 healthy controls (11 female, 23 male) were included into the study. Eight (17.8%) of the patients had the segmental type, and 37 (82.2%) had generalized vitiligo. The disease was active in 25 (55.6%) patients; the other 20 (44.4%) patients had static vitiligo. Flow cytometry was used to determine the percentages of total T-lymphocytes, B-lymphocytes, helper/inducer T cells, suppressor/cytotoxic T cells, natural killer (NK) cells, activated T cells and interleukin-2 receptor (IL-2R) with the use of CD3, CD19, CD4, CD8, CD16, HLA-DR and CD25 monoclonal antibodies, respectively. The mean value of helper T cells showed a significant difference (p=0.01) between the two groups with the value being 32.5% in patients and 38.1% in control subjects. CD4/CD8 was significantly lower in vitiligo patients (p=0.04). There was also a statistically significant difference in the mean percentage of activated T cells between vitiligo patients and control subjects (4.7 and 8.1, respectively; p=0.001). No statistically significant differences were found when the values were compared between segmental and generalized vitiligo patients, or between active and static cases. In conclusion, T helper/inducer cells, CD4/CD8 ratio and activated (HLA-DR+) T cells are decreased in vitiligo patients, suggesting a role for changes in cellular immunity.

Adolescent↗
PubMed2007

Effects of psoralen plus ultraviolet A irradiation on cultured epidermal cells in vitro and patients with vitiligo in vivo.

BACKGROUND: Both psoralen plus ultraviolet (UV) A (PUVA) and narrowband UVB (NB-UVB) irradiation are effective treatments for vitiligo vulgaris. However, the mechanisms of PUVA and NB-UVB in repigmentation are not thoroughly clarified. Our previous results showed that NB-UVB irradiation directly promotes melanocyte (MC) migration and stimulates MC proliferation via keratinocytes (KCs). OBJECTIVES: In the present study, we used NB-UVB as a reference for comparison to investigate the immediate effects of PUVA on MC proliferation and migration. METHODS: Cultured MCs and KCs were treated with PUVA or irradiated with NB-UVB. The direct impact of PUVA treatment on MCs was assessed in terms of its effect on MC proliferation and migration. The indirect effect of PUVA treatment and NB-UVB irradiation on MC proliferation via KCs was also investigated. The activities of matrix metalloproteinase (MMP)-2 and MMP-9, known for their influence on cell migration, were evaluated in the PUVA-treated MC and KC supernatants. The concentrations of MC mitogens/growth factors in the PUVA-treated KC supernatants were also determined. In addition, the serum levels of MC mitogens/growth factors in healthy controls, in patients with active vitiligo and in patients with repigmenting vitiligo after PUVA treatment were determined to elucidate the mechanisms of how PUVA induces vitiligo repigmentation in vivo. RESULTS: Our results demonstrated that PUVA treatment did not significantly stimulate the release of MC mitogens/growth factors from KCs. The migration of MCs was also not enhanced after PUVA treatment. The expression of MMP-2 activity in supernatants derived from PUVA-treated MCs was significantly increased as compared with the control group. However, neither MMP-2 nor MMP-9 activity in KC supernatants was stimulated by PUVA treatment. In contrast to NB-UVB, immediate effects of PUVA on MC proliferation and migration were not observed in this study. Sera from patients with repigmenting vitiligo after PUVA treatment contained higher levels of basic fibroblast growth factor, stem cell factor and hepatocyte growth factor as compared with healthy controls and patients with active vitiligo. CONCLUSIONS: Our results indicate that in addition to immune suppression, PUVA treatment creates a favourable milieu for promoting the growth of MCs in patients with vitiligo instead of directly stimulating the regrowth of MCs. Based on our results, we propose that in the active stage of vitiligo, PUVA treatment is the therapy of choice to slow down the destruction of MCs and to create a favourable environment for MCs to survive. In the stable stage of vitiligo, NB-UVB irradiation should be used to stimulate the proliferation and migration of MCs directly.

Cell Movement↗
PubMed2006

Vitiligo associated with other autoimmune diseases: polyglandular autoimmune syndrome types 3B+C and 4.

Vitiligo is a common skin disease characterized by depigmented maculae resulting from a reduction of the number and function of melanocytes. Many studies suggest that vitiligo might be an autoimmune disease. Vitiligo has been frequently described in association with other autoimmune diseases. Among the diseases described in association with vitiligo are the so-called autoimmune polyglandular syndromes (APS). Vitiligo can be present in all types of APS but the most frequent association appears to be in APS-3. APS-3 was defined as the association between autoimmune thyroiditis and another autoimmune disease. Here we report one patient with thyroiditis, vitiligo and autoimmune gastritis (APS-3B+C), one patient with chronic autoimmune thyroiditis, vitiligo and alopecia (APS-3C), and one case of a young patient with type 1 diabetes mellitus and vitiligo (APS-4), according to the newest classification. We stress the importance of a thorough assessment for autoimmune diseases in selected patients with vitiligo.

Adult↗
PubMed2007

Vitiligo prevalence study in Shaanxi Province, China.

BACKGROUND: Recent publications, especially those based on population surveys, show that the presumed vitiligo prevalence of 1-2% is overestimated. OBJECTIVE: To obtain the vitiligo prevalence in Shaanxi Province, China, through a population survey. METHODS: Approximately one-thousandth of the 36.05 million people in Shaanxi Province, China, were selected through stratified four-stage cluster sampling. They lived in 180 investigation units and all were investigated in a door-to-door survey. Vitiligo and suspected vitiligo patients were marked in the basic questionnaire. They were encouraged to complete a well-prepared questionnaire and send it back to the investigation center. The questionnaire assigned to the investigators contained questions about vitiligo characteristics, such as the area affected, number of areas, and whether or not the affected areas were covered by scurf. Professional dermatologists verified these results. RESULTS: There were 42,833 people in 180 investigation units. The sex, residence, and educational level of these individuals were representative of the population of Shaanxi Province. The investigation team reported 43 vitiligo patients and 14 with suspected vitiligo. During the verification period, three patients and all those with suspected vitiligo were excluded. In total, there were 40 patients (17 women and 23 men). Eleven lived in urban areas and 29 in rural areas. CONCLUSIONS: The prevalence of vitiligo in Shaanxi Province is 0.093% (95% confidence interval, 0.067-0.127%). No significant difference was found between males and females or between urban and rural residents.

Adolescent↗
PubMed2004

On the etiology of contact/occupational vitiligo.

Vitiligo is an acquired depigmentary disorder of the skin that results from the selective destruction of melanocytes, generally during the second decade of life and affecting approximately 1% of the population worldwide. Loss of cutaneous pigment appears to render the skin susceptible to premature aging and cancer. In addition this disease can be socially devastating for afflicted individuals. The etiology of vitiligo is poorly understood. The present dogma suggests that genetic factors render the melanocyte fragile thus predisposing individuals to developing vitiligo. When subjected to instigating factors, these susceptible, fragile melanocytes undergo apoptosis. Autoimmune factors then perpetuate the removal of the melanocyte component from the skin. In the majority of cases the instigating factors are not known (idiopathic vitiligo), however a small sub-set of individuals develop contact/occupational vitiligo following exposure to particular chemicals. Many of these chemicals have been implicated in both contact/occupational vitiligo and chemical leukoderma. Both conditions present with well-defined, depigmented skin lesions that develop following exposure. Only in the case of vitiligo does the depigmentation spread beyond the areas of contact, probably via an immune-mediated mechanism. The largest class of chemicals known to trigger contact/occupational vitiligo is the phenolic/catecholic derivatives. Many have been demonstrated to be preferentially cytotoxic to melanocytes, with high-dose exposure resulting in the initiation of apoptosis. Phenolic/catecholic derivatives are structurally similar to the melanin precursor tyrosine, and therefore tyrosinase was originally implicated as a mediator of cytotoxicity. However, our data suggests that tyrosinase-related protein-1, rather than tyrosinase, facilitates toxicity, possibly by catalytic conversion of the compounds, which results in the generation of radical oxygen species. The ensuing oxidative stress then triggers activation of cellular free radical scavenging pathways to prevent cell death. Genetic inability of melanocytes to tolerate and/or respond to the oxidative stress may underlie the etiology of contact/occupational vitiligo.

Catechols↗
PubMedDate not supplied

Melanocyte destruction and repigmentation in vitiligo: a model for nerve cell damage and regrowth.

Melanocytes (MCs) are melanin-producing cells of the skin that are derived from neural crest cells. Vitiligo vulgaris is a common depigmentation disorder resulting from the destruction of functional MCs in the affected skin. The three prevailing pathomechanisms of vitiligo are the immune hypothesis, the neural hypothesis and the autocytotoxic hypothesis. None of these mechanisms has been conclusively proven. Melanoblasts (MBs) in the outer root sheath of the hair follicles are the reservoir cells for repigmentation. Recovery from vitiligo is initiated by activation and proliferation of these MBs, followed by upward migration to the nearby epidermis that forms perifollicular pigmentation islands. Migration, proliferation and differentiation of MCs and MBs are regulated by keratinocyte-derived factors and some coat color genes. Any therapy for vitiligo must explain not only the repopulation of MCs but also their functional development. In patients with vitiligo, MCs are destroyed in the skin, the eyes, and possibly the ears. However, the concept of vitiligo as a systemic disease will be clearly established only when the mechanisms involved in vitiligo are identified. Recent advances in the fields of neural crest cell culture and molecular genetics have opened new perspectives in the understanding of vitiligo. Not only will this result in better treatments for vitiligo patients, but possibly will also provide a key to triggering nerve cell regrowth in other nervous diseases.

Animals↗
PubMed1976

Treatment of vitiligo with oral corticosteroids.

17 patients with generalized vitiligo and 5 patients with localized vitiligo were treated with oral corticosteroids. Six patients with generalized vitiligo showed over 75% repigmentation in at least one of the patches. Two patients with generalized vitiligo and 1 patient with localized vitiligo showed a partial repigmentation of 25-75%, while 5 patients with generalized vitiligo and 1 patient with localized vitiligo showed a minimal repigmentation of less than 25%. Four patients with generalized vitiligo and 3 patients with localized vitiligo failed to respond. Repigmentation became evident within 4 weeks in most cases, and in general was more markedly noted in exposed areas.

Administration, Oral↗
PubMed2005

New treatment modalities for vitiligo: focus on topical immunomodulators.

The development of effective treatment modalities for vitiligo is dependent on an understanding of the events leading to depigmentation. However, the exact pathogenesis of vitiligo is still mostly unknown. Abnormalities in both humoral and cell-mediated immunity have been documented in vitiligo patients and they present a basis for using immunomodulating agents, such as corticosteroids and macrolide immunomodulators, in the treatment of vitiligo. Macrolide immunomodulators, such as tacrolimus and pimecrolimus, which can be used topically, are known as topical immunomodulators (TIMs). TIMs inhibit the action of calcineurin, and consequently inhibit T-cell activation and the production of various cytokines; this is considered the working mechanism of action of TIMs in vitiligo. Several small studies and case reports on the use of TIMs in vitiligo have been published so far. Tacrolimus achieves better results on the face and neck than on other body areas. Particular advantages of TIMs are safety in treating these areas because of lack of skin atrophy and good tolerability. The incidence of application site adverse events in vitiligo seems to be lower than in the treatment of atopic dermatitis. On the face and neck, TIMs may become a useful tool in the treatment of adults and children with vitiligo despite possibly lower efficacy than topical corticosteroids. Further, larger, controlled clinical studies are warranted to determine the definite role of TIMs as monotherapy or in combination with other modalities in the treatment of vitiligo.

Administration, Topical↗
PubMed1996

Detection of antibodies to melanocytes in vitiligo by western immunoblotting.

To more fully define the nature of the antibody response to melanocytes which is associated with vitiligo, a Western immunoblot assay was used to test the sera of 28 patients with vitiligo (21 with active non-segmental, and 7 with stable segmental diseases) and 26 normal individuals for antibodies to antigens in detergent extracts of melanocyte membrane fractions. Antibodies to melanocytes were found in 26 (93%) of the patients with vitiligo, and in 16 (62%) of the control individuals. Patients with vitiligo and control individuals both had antibodies to an 80 approximately 83 kD antigen. The patient with vitiligo, in addition, had antibody responses to antigens with MWs of 45, 65, and 110 kD. Antibodies to these antigens were present in 46, 25, and 31% of vitiligo patients, but in only 19%. 0%, amd 0%, respectively, of the normal individuals. The heterogeneity of the antibody responses to melanocytes in vitiligo was further confirmed by the presence of antibodies to at least 3 distinct antigens in one-third of vitiligo patients but in none of the normal individuals. There was no difference in antibody response between patients with generalized and segmental vitiligo, suggesting that the pathogenesis of diseases was similar in both cases.

Antibodies↗
PubMed2004

Serum concentrations of interleukin-2 soluble receptor (IL-2 sR) in patients with vitiligo: relationship with type and extent of the disease.

Vitiligo is a disorder of melanin pigmentation, affecting 1-2% of general population. The etiopathogenesis of the disease is not clear, but probably includes the interaction among nervous system, cytotoxic factors, and immune mechanisms. The aim of the study was to evaluate serum concentrations of interleukin-2 soluble receptor (IL-2 sR) in patients with vitiligo and assess a possible association between IL-2 sR and clinical type, extent, and duration of the disease. The study included 51 patients with vitiligo aged 7-70 years and 29 healthy controls aged 10-60 years. Serum concentrations of IL-2 sR were determined by ELISA method. The serum concentration of IL-2 sR in patients with vitiligo was lower than that in the control group (1,164.2+/- 357.2 vs. 1,301.6+/-404.1 pg/mL, respectively). Significantly decreased serum IL-2 sR concentrations were noticed in patients with non-dermatomal type A vitiligo (1,137.5+/-356.7 pg/mL), especially those suffering from type A1 (active lesions) of the disease (959.4+/-251.7 pg/mL), compared with both healthy controls and patients with type B (dermatomal) vitiligo (1,105.2+/-346.5 pg/mL). In patients with more extensive vitiliginous changes of the skin, IL-2 sR serum concentrations were significantly lower. Moreover, patients with type A1 vitiligo had significantly decreased serum IL-2 sR concentrations compared with type A2 (non-active lesions) patients. There was no difference in serum IL-2 sR concentrations between patients with dermatomal distribution of vitiligo and control group. Serum IL-2 sR concentrations in patients with vitiligo were decreased and depended on the activity and intensity of the disease process.

Adult↗
PubMed2001

Immunological pathomechanisms in vitiligo.

Vitiligo is a depigmenting disorder characterised by the loss of melanocytes from the cutaneous epidermis. Although the exact aetiology of vitiligo has not yet been established, the abnormal immune responses frequently observed in vitiligo patients have led to the suggestion that, in some cases, the condition has an autoimmune component. Briefly, circulating autoantibodies and autoreactive T cells that recognise pigment cell antigens have been detected in the sera of a significant proportion of vitiligo patients compared with healthy individuals. In addition, vitiligo is often associated with other disorders that have an autoimmune origin, including Hashimoto's thyroiditis, Graves' disease, type 1 insulin-dependent diabetes mellitus and Addison's disease. Furthermore, effective use of immunosuppressive therapies to treat vitiligo, the association of vitiligo with certain major histocompatibility complex antigens, and evidence from animal models of the disease have all added credence to the hypothesis that immune reactions play a role in vitiligo pathogenesis. This review presents and discusses the evidence for immunological pathomechanisms in vitiligo.

Journal Article↗
PubMed1989

Growth defects of melanocytes in culture from vitiligo subjects are spontaneously corrected in vivo in repigmenting subjects and can be partially corrected by the addition of fibroblast-derived growth factors in vitro.

Melanocytes cultured from uninvolved skin of untreated vitiligo subjects have decreased initial seeding capacities, manifest a lag period for the onset of the growth phase, and cannot be passaged. In contrast, melanocytes obtained from uninvolved and perilesional skin of vitiligo subjects actively repigmenting under 8-methoxy psoralen plus sunlight (PUVA) therapy have higher initial seeding capacities, grow faster without a lag period, and can be passaged to more than 12 passages. Extracts of a fetal lung fibroblast cell line (PMR-GF) that promote the growth rates and passage capacities of melanocytes from normal adult donors have been found also to promote the growth rates and passage capacities of melanocytes from the uninvolved skin of vitiligo subjects. Extracts of a fetal lung fibroblast cell line (PMR-GF), however, did not have any further stimulatory effect on the growth of melanocytes obtained from repigmenting vitiligo subjects. Melanocytes cultured from normal and untreated vitiligo subjects grew individually dispersed in the absence of PMR-GF, but tended to grow in clusters in its presence. Melanocytes from the repigmenting vitiligo subjects, however, tended to grow in clusters even in the absence of PMR-GF. These results indicate that the defective in vitro growth characteristics of melanocytes from vitiligo subjects may be related to the pathogenesis of this disease. It is possible that growth factors may be involved in the process of repigmentation in vitiligo subjects.

Adolescent↗
PubMed1983

New observations on vitiligo and ocular disease.

We examined 223 consecutive patients with vitiligo for ocular disease and 154 consecutive patients with uveitis for vitiligo to better determine the nature of the relationship between vitiligo and ocular disease. Of the 129 patients whose uveitis had an unknown cause, seven (5.4%) had cutaneous depigmentation, poliosis, or early graying of hair. The incidence is 0.5% in the general population (P less than .02). None of the 25 patients whose uveitis had a known cause had vitiligo. Eleven (4.8%) of 223 patients with vitiligo had uveitis at the time of the study or had had it within the previous two years. Of 27 patients in whom vitiligo was associated with cutaneous melanoma, five (18.5%) had had uveitis within the previous two years. In three of these five, the uveitis began within one month of the appearance of cutaneous changes. Evidence of old chorioretinal scars were present in 69 of 223 patients with vitiligo (30.9%) but in only two of 148 control patients (P less than .001). Sixty of 223 patients with vitiligo (26.9%) had evidence of hypopigmentation or atrophy of the retinal pigment epithelium, or both, not related to old chorioretinitis or macular degeneration but only six of 148 controls did (P less than .001).

Adolescent↗
PubMed1986

Aberrations in T lymphocytes and natural killer cells in vitiligo: a flow cytometric study.

Twenty-five patients with vitiligo and twenty-five healthy control subjects were evaluated with the use of flow cytometry to compare percentages of peripheral T lymphocytes and natural killer cells. The percentages of total T lymphocytes, helper T cells, suppressor T cells, and natural killer cells were evaluated with the use of OKT3, OKT4, OKT8, and Leu-7 monoclonal antibodies, respectively. Mean total T lymphocytes and helper T cells were markedly depressed; mean natural killer cells were markedly elevated and mean suppressor T cells were moderately elevated in patients with vitiligo in comparison with control subjects. These results indicate that cell-mediated immunity is subject to some defect in regulation in patients with vitiligo. It remains to be determined whether these abnormalities are a direct cause or a result of vitiligo. Antibody-dependent cytotoxicity, utilizing killer cells with recently reported antimelanocyte antibodies found in patients, may be responsible for pigment cell destruction in vitiligo. Helper T cells may be reduced because of low levels or faulty production of T lymphocyte-stimulating factors in patients or because of a serum factor in patients that is toxic to helper T cells. The presence or absence of autoimmune and/or endocrine disease in patients with vitiligo had no effect on lymphocyte populations. There seemed to be a trend toward lower levels of helper T cells in patients having vitiligo for the shortest amount of time. In summary, the data indicate immunologic abnormalities in patients with vitiligo.

Adult↗
PubMed2000

Intrinsic and extrinsic pathomechanisms in vitiligo.

Vitiligo is the most commonly acquired hypomelanosis, and is restricted to a limited cutaneous territory (focal/segmental vitiligo [SV]) or generalized in symmetric patches (nonsegmental vitiligo [NSV]). In the majority of cases, vitiligo corresponds to a loss of melanocytes, first in the epidermal compartment, and later in the follicular reservoir where most melanocytic stem cells are probably situated. There are many data currently supporting an impaired redox status of the epidermal melanin unit as a primary defect leading to inappropriate immune responses in NSV. SV is probably a mosaic developmental predisposition to melanocytic loss, with similar mechanisms at work on a limited scale, as suggested by its cutaneous distribution and success of autografting. In NSV, engraftment of autologous melanocytes is less durable, especially in areas prone to repeated trauma or pressure. Although melanocytes are the obvious target of the disease, keratinocytes, as providers of antioxidant molecules to melanocytes as well as cofactors in the synthesis of melanin, are probably involved. The production of autoantibodies and specific cytotoxic T cells is not surprising in the context of the massive uptake of melanocytic antigens by Langerhans cells in unstable vitiligo vulgaris, thereby allowing the self-perpetuation of lesions. This article reviews the recent data on the pathophysiology of vitiligo, on the basis of clinical classification and the intrinsic/extrinsic nature of proposed pathomechanisms. Unfortunately, basic issues like pathological staging, clinical scoring, and eliciting factors have not yet been fully resolved. More genetic studies in vitiligo-prone families and in specific genetic disorders associated with vitiligo are also needed.

Humans↗