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PubMed1994

Biologic characteristics of cultured human vitiligo melanocytes.

BACKGROUND: Vitiligo is a pigmentary disorder of unknown cause characterized by depigmented patches due to destruction of melanocytes. Recently, the inherent cellular defect theory has been discussed. To investigate the biologic characteristics of cultured melanocytes from normal and vitiligo subjects, this study had the purpose to examine the functional and ultrastructural characteristics of these melanocytes and to observe the morphologic and functional changes of melanocytes in response to ultraviolet B irradiation. METHODS: Melanocytes were isolated and cultured from foreskin and arm skin of normal and vitiligo subjects. The DNA synthesis, tyrosinase activity assay, transmission and scanning electron microscopic examination, and the effects of ultraviolet B(UVB)-irradiation on cultured melanocytes were studied. RESULTS: Vitiligo melanocytes showed no significant differences in DNA synthesis and tyrosinase activity compared with normal melanocytes, but the vitiligo melanocytes contained dilated and/or circular rough endoplasmic reticulum (RER) on transmission electron microscopic examination. Exposure of the cultured melanocytes to UVB resulted in increased protein synthesis and tyrosinase activity. Morphologic alterations and changes in DNA synthesis were also noted. Compared with normal melanocytes, the responses of vitiligo melanocyte to UVB showed no significant difference. CONCLUSIONS: Normal and vitiligo melanocytes showed similar biologic characteristics except in the changes of RERs in the vitiligo melanocytes. The ultrastructural aberrations in vitiligo subjects do not seem to be directly related to the biologic characteristics and the responses to UVB irradiation in vitiligo melanocytes.

Cell Division↗
PubMed2005

Association of HLA-DQA1 and DQB1 genes with vitiligo in Chinese Hans.

BACKGROUND: Vitiligo is an acquired depigmentary disorder of the skin and hair which results from selective destruction of melanocytes. Serological typing and genotyping of human leukocyte antigen (HLA) have shown discrepancies in HLA associations with vitiligo in different ethnic populations. METHODS: Polymerase chain reaction sequence-specific primer (PCR-SSP) method was used to analyze the distribution of HLA-DQA(1) and -DQB(1) alleles among 187 patients with vitiligo and 273 healthy controls through Epi Info version 6 package (Centers for Disease Control and Prevention, Atlanta, GA, USA). RESULTS: The frequencies of HLA-DQA1*0302 (OR = 1.98, P(c) < 0.01), -DQB1*0303 (OR = 3.14, P(c) < 0.001), and -DQB1*0503 (OR = 3.36, P(c) < 0.05) alleles were significantly increased in patients with vitiligo compared with controls, and HLA-DQA(1)*0501 (OR = 0.40, P(c) < 0.01) allele frequency was highly decreased. HLA-DQA1*0302 (OR = 5.19, P(c) < 0.001), -DQA1*0601 (OR = 2.95, P(c) < 0.05), -DQB1*0303 (OR = 4.50, P(c) < 0.001), and -DQB1*0503 (OR = 6.69, P(c) < 0.001) alleles were positively associated, whereas HLA-DQA1*0501 (OR = 0.05, P(c) < 0.001) allele was negatively associated with childhood vitiligo patients, and HLA-DQB1*0303 (OR = 2.76, P(c) < 0.001) allele was positively associated with adult vitiligo patients compared with controls. The frequency of HLA-DQB1*0303 (OR = 3.72, P(c) < 0.001) allele was significantly increased in localized vitiligo patients vs. controls, whereas HLA-DQA1*0302 (OR = 2.47, P(c) < 0.01), -DQB1*0303 (OR = 2.67, P(c) < 0.01), and -DQB1*0503 (OR = 4.46, P(c) < 0.01) allele frequencies were significantly increased and -DQA1*0501 (OR = 0.27, P(c) < 0.01) allele frequency was highly decreased in generalized vitiligo patients. CONCLUSIONS: HLA-DQA1*0302, -DQA1*0601, -DQB1*0303, and -DQB1*0503 alleles could be susceptible alleles of vitiligo, while HLA-DQA1*0501 allele could be a protective allele in Chinese Hans. There may be different genetic backgrounds between vitiligo patients of childhood and adult, localized and generalized.

Adolescent↗
PubMed2006

Vitiligo and ocular findings: a study on possible associations.

OBJECTIVE: In this study, we aimed to evaluate the ocular findings in vitiligo patients and reveal any clinical feature that might suggest an association or a risk factor. BACKGROUND: Very few reports in the literature are available about the ocular findings in vitiligo and the possible associations of the ocular findings in vitiligo patients have not been studied so far. METHODS: A total of 45 patients with previously documented cutaneous vitiligo were examined for ocular findings. Demographic features including age, gender, duration of vitiligo, presence of associated autoimmune diseases, type of vitiligo and the anatomical distributions of vitiligo were recorded to evaluate a possible relationship with the ocular findings. Univariate and multivariate analyses as well as cluster analysis were performed. After description of the clusters, the Mann-Whitney U-test and Fisher's exact test were used to determine the variables. Concordance among the variables in each group was evaluated with the McNemar test. RESULTS: Ten patients had ocular findings that included anterior segment (iris) involvement, ring-like peripapillary atrophy around the optic nerve, atrophy of pigment epithelium, focal hypopigmented spots and diffuse hypopigmentation. The presence of periorbital vitiligo was significantly related to the ocular findings. Cluster analysis revealed concordances between periorbital and genitalial localizations of vitiligo and ocular findings. CONCLUSION: The number of patients and the range of ocular findings in our study are insufficient to make definite conclusions but anatomical localizations, primarily periorbital and to a lesser extent genitalial vitiligo, seem to be the most probably alerting features for ocular findings.

Adolescent↗
PubMed2006

HLA class II haplotype DRB1*04-DQB1*0301 contributes to risk of familial generalized vitiligo and early disease onset.

Generalized vitiligo is a common autoimmune disorder characterized by white patches of skin and overlying hair caused by loss of pigment-forming melanocytes from involved areas. Familial clustering of vitiligo is not uncommon, and patients and their relatives are at increased risk for a specific complex of other autoimmune diseases. Compared with sporadic vitiligo, familial vitiligo is characterized by earlier disease onset and greater risk and broader repertoire of autoimmunity, suggesting a stronger genetic component, and perhaps stronger associations with specific alleles. To determine whether the major histocompatibility complex (MHC) contributes to the familial clustering of vitiligo and vitiligo-associated autoimmune/autoinflammatory diseases, we performed case-control and family-based association analyses of HLA class II-DRB1 and -DQB1 alleles and haplotypes in affected probands and their parents from 76 European-American Caucasian families with familial vitiligo. Affected probands showed a significantly increased frequency of DRB1*04-DQB1*0301 and a significantly decreased frequency of DRB1*15-DQB1*0602 compared with a large sample of reference chromosomes. Family-based association analyses confirmed these results. Probands with DRB1*04-DQB1*0301 developed vitiligo an average of 13.32 yr earlier than probands with DRB1*15-DQB1*0602. Overall, our results indicate that specific MHC-linked genetic variation contributes to risk of familial vitiligo, although HLA does not completely explain familial clustering of vitiligo-associated autoimmune/autoinflammatory diseases.

Adolescent↗
PubMed2004

Spontaneous vitiligo in an animal model for human melanoma: role of tumor-specific CD8+ T cells.

Tumor antigen-reactive T cells can be detected in a large proportion of melanoma patients, but their efficacy on tumor control in vivo remains unclear. On the other hand, vitiligo, a skin disorder characterized by patchy depigmented macules, may occur spontaneously or after antitumor therapies. Moreover, vitiligo is significantly associated with positive clinical response, but the mechanism is not understood. Therefore, the establishment of a relevant animal model in which melanoma and vitiligo spontaneously develop stepwise may be useful for better understanding of the parameters involved in the destruction of both benign and malignant melanocytes. In a previous work, we established a mouse model for melanoma in which MT/ret transgenic mice express the ret oncogene fused to the metallothionein promoter. Here we report that melanoma leads to spontaneous vitiligo. We further investigate, for the first time in this model, the natural antitumor T-cell response and evaluate the role of cellular immunity in the development of the disease. Interestingly, the occurrence of spontaneous tumor nodules in MT/ret mice with melanoma-associated vitiligo is significantly delayed when compared in melanoma mice without vitiligo. Moreover, a significant proportion of mice with melanoma-associated vitiligo resisted a challenge with syngeneic melanoma cells in contrast to animals without vitiligo. Our results confirm that vitiligo is associated with clinical benefit and further demonstrate the crucial role of CD8+ T cells for tumor control in melanoma-associated vitiligo.

Animals↗
PubMed1995

Detection of antibodies to human melanoma cell in vitiligo by western blot analysis.

Vitiligo is a disease in which melanocytes are selectively destroyed. The disease is thought to be an autoimmune process being there are antibodies to pigment cells in the sera of patients and animals with vitiligo. In the present study, sera from vitiligo patients were examined for reactivity with the human melanoma cell line, SK-Mel-28, by Western blot analysis of solubilized membrane antigens of these cells to identify the pigment cell antigens defined by antibodies in the patients with vitiligo. Antibody reactivity to human melanoma cells (SK-Mel-28) was investigated in 14 patients with vitiligo, and 16 with normal control individuals. Antibodies to the 116-113, 60, 40 KD antigens were associated with vitiligo being present in 79%, 86%, and 43% respectively of the patients with vitiligo, but in only 6%, 38% and 6% of the normal controls. In contrast, antibodies to the 160-155, 78 and 64 KD antigens were equally common in vitiligo and in normal individuals. The results suggest that autoreactivity to pigment cells occurs more commonly in patients with vitiligo than in the normal control and high autoreactivity to pigment cells in the vitiligo sera might be an impertinent epiphemenon to destroyed pigment cell.

Antibodies, Neoplasm↗
PubMed1997

Epidermal reconstructs in vitiligo: an extrinsic factor is needed to trigger the disease.

The primary cellular or molecular targets accounting for melanocytes loss in vitiligo are not clearly identified. To study a putative latent epidermal defect in the epidermis of vitiligo patients, we performed in vitro studies using cultured vitiligo melanocytes and keratinocytes transplanted on to a dead de-epidermized dermis according to a variant of Pruniéras' technique. Control autologous constructs were made with keratinocytes and melanocytes of normal adult epidermis and vitiligo epidermis from perilesional skin. For heterologous reconstructs we combined vitiligo-derived melanocytes or keratinocytes with their normal phototype-matched counterpart. After 15 days of culture at the air-liquid interface, epidermal reconstructs were studied macroscopically and microscopically. Immunohistochemistry was performed using antibodies to TRP-1 and NKI-beteb. All heterologous and autologous reconstructs made with melanocytes and keratinocytes from vitiligo patients had a normal histology and ultrastructure. For vitiligo melanocytes or normal melanocytes submitted to the influence of vitiligo keratinocytes, immunophenotype and function (pigment production and transfer) were similar to normal controls. So, without additional noxious stimuli, we could not discriminate between melanocytes and keratinocytes as inducers of the disease. Our data suggest that the basic abnormality in vitiligo vulgaris needs extrinsic factors to be macroscopically revealed or requires a longer period of culture to develop. Our model will allow analysis of the various pathophysiological mechanisms of vitiligo, e.g. autoantibodies or oxidative stress, at the cellular, biochemical or molecular level.

Adult↗
PubMed2006

A comparative study of oxidant-antioxidant status in stable and active vitiligo patients.

The pathogenetic mechanisms in vitiligo have not been completely clarified. One of the major hypotheses in the pathogenesis of vitiligo is the oxidative stress hypothesis. The active or stable phase of vitiligo is defined on the basis of the progression or appearance of new lesions in the last 3 months and the absence of new lesions or their progression in the last 6 months, respectively. Eighteen patients with active vitiligo, 18 patients with stable vitiligo, and 40 controls were included in this study. We examined serum levels of malondialdehyde, selenium, vitamin E and A, and the erythrocyte activities of glutathione peroxidase, superoxide dismutase, and catalase. Our results revealed a significantly higher level of serum malondialdehyde, selenium in patients with active disease compared with the controls. Significant higher increase in erythrocytes superoxide dismutase activities was observed in active vitiligo group, erythrocyte glutathione peroxidase activity was decreased significantly in active disease, whereas erythrocyte catalase activity and plasma vitamin E and A levels were not different in vitiligo patients as compared with controls. Our study shows that oxidative stress is involved in the pathophysiology of both active and stable vitiligo but increased imbalance of antioxidants was observed in the blood of active vitiligo patients.

Adolescent↗
PubMed1990

T cell subpopulations in vitiligo: a chronobiologic study.

The circadian rhythms of helper (CD4) and suppressor (CD8) T cells from the peripheral blood of 12 vitiligo patients (seven with active disease, five with static) and 12 healthy control subjects were studied. Patients with active vitiligo had a lower percentage of CD4+ cells than did control subjects at 0000 hours and at 0600 and 1200 hours; there were no differences between these values in patients with static vitiligo and those in control subjects. The percentage of CD8+ cells were lower at 1200 and 1800 hours in both active and static vitiligo patients than in control subjects. Cosinor analysis of the CD4+ cells showed a circadian rhythm in static vitiligo, whereas the rhythmicity was lost in active vitiligo. CD8+ cells did not show any circadian rhythm in either active or static vitiligo. Our data show more striking aberrations for T cell subtypes in active vitiligo than in static vitiligo. They suggest that cell-mediated immunity may play a role in the pathogenesis of the disease.

Adolescent↗
PubMed2006

Analysis of allelic variants in the catalase gene in patients with the skin depigmenting disorder vitiligo.

Vitiligo is an acquired hypomelanotic skin disorder characterised by circumscribed depigmented macules resulting from the loss of functional melanocytes from the cutaneous epidermis. Conditions that might result in epidermal oxidative stress and consequently damage to pigment cells have been reported in the skin of vitiligo patients, including low catalase activity and increases in hydrogen peroxide levels. However, the cause of the decrease in catalase activity has not been equivocally determined. Several allelic variants in the catalase gene, a number of which have deleterious effects upon the expression or function of the enzyme, have been described and the aim of the present work was to assess the relevance of catalase gene variants in patients with vitiligo. Associations between ten separate allelic variants in the catalase gene and a predisposition to vitiligo were investigated in case-control studies with 166 English patients and 169 ethnically-matched controls using DNA sequencing and restriction fragment length polymorphism-polymerase chain reaction methods. Of the ten allelic variants analysed, only a C/T single nucleotide polymorphism in exon 9 of the catalase gene was associated with vitiligo. The C/T genotype was significantly over-represented in the vitiligo patient group compared with the control cohort. Of 166 vitiligo genotypes, 66 (39.8%) had the C/T variant compared to 45/169 (26.6%) control genotypes (P = 0.030). No evidence for an association between other allelic variants in the catalase gene and vitiligo susceptibility was found. The low catalase activity in vitiligo patient epidermis is more likely to result from environmental conditions such as inhibitory levels of hydrogen peroxide rather than allelic variations in the catalase gene which affect either expression or function of the enzyme.

Adult↗
PubMed2006

The relationship between family medical history and childhood vitiligo.

BACKGROUND: The association between a family history of vitiligo and other autoimmune/endocrine diseases and increased incidence of childhood vitiligo has been described; however, the influence of family history on the clinical characteristics of childhood vitiligo has rarely been investigated. OBJECTIVE: We sought to examine the relationship between family history and the incidence, extent, and course of childhood vitiligo. METHODS: A retrospective chart review and telephone interviews were performed for 137 pediatric patients with vitiligo and 140 control patients (patients with acne, warts, or molluscum contagiosum matched in age, sex, and ethnicity to the study group). Information about the age, sex, ethnicity, age of onset and diagnosis, site of onset, distribution, treatment, course of disease, and family history was obtained. RESULTS: Patients with vitiligo and an extended family history of vitiligo were more likely to have an earlier age of onset of disease than those with a negative family history (odds ratio = 3.70, P = .024). There was no association between family history and site of onset, distribution, or course of disease. LIMITATIONS: A relatively small sample size, recall bias, disease misclassification, and confounding factors are potential limitations of this study. CONCLUSION: Earlier onset of pediatric vitiligo is linked to a family history of vitiligo. Awareness of this association can allow for closer monitoring, earlier detection, and earlier initiation of treatment.

Adolescent↗
PubMed2004

Association of estrogen receptor 1 intron 1 C/T polymorphism in Korean vitiligo patients.

BACKGROUND: Vitiligo is a common disease characterized by cutaneous white maculae due to loss of melanocytes. It is a polygenic disease, however, the exact pathogenesis of vitiligo is not yet known. The estrogen receptor (ESR) 1 gene was selected as a candidate gene because some researchers treated vitiligo successfully with the steroid-thyroid hormone mixture containing estrogen. Furthermore ESR was expressed in the melanocytes which have an important role in the pigmentation. The polymorphisms of ESR1 gene in vitiligo patients was not reported yet. OBJECTIVE: To determine whether polymorphisms of ESR1 gene were associated with susceptibility to vitiligo patients in Korean population. METHODS: We conducted case-control association study of vitiligo patients (120) and healthy controls (254). Genotypes of ESR1 gene (intron 1 C/T, exon 4 C/G, and exon 8 A/G) were determined by polymerase chain reaction followed by restriction enzyme digestion. RESULTS: Intron 1 T/C allele frequency was significantly different between patients and controls (P = 0.034). Intron 1 T/C genotype distribution (P = 0.021) and allele frequency (P = 0.013) were different between female vitiligo patients and female controls. Intron 1 T/C allele frequency showed significantly difference between generalized type of vitiligo patients and controls (P = 0.044). Genotype distributions and allele frequencies of exon 4 C/G and exon 8 A/G polymorphisms were not different between patients and controls. CONCLUSION: The present study suggests that ESR1 may be a possible risk factor for female or generalized type of vitiligo patients.

Adolescent↗
PubMed2005

The genetic concept of vitiligo.

Vitiligo is a relatively common, acquired pigmentary disorder characterized by areas of depigmented skin resulting from loss of epidermal melanocytes. The prevalence of this disease varies from 0.1 to 2% in various global populations. The genetics of vitiligo cannot be explained by simple Mendelian genetics; it is characterized by incomplete penetrance, multiple susceptibility loci and genetic heterogeneity. Unraveling the complex genetics of vitiligo is a daunting challenge but the perseverance of vitiligo gene hunters has produced commendable results in recent years. Although environmental factors are important, there is considerable evidence that genes also play a significant role in its pathogenesis. Strong evidence from twin and family studies indicates the importance of genetic factors in the development of vitiligo, although it is clear that these influences are complex. Linkage and association studies have also provided strong support for vitiligo susceptibility genes on chromosomes 4q13-q21, 1p31, 7q22, 8p12 and 17p13, while loci of interest at 6p, 6q, 14q, 9q, 13q, 19p and 22q require further follow-up. Although important obstacles to further progress will need to be overcome, the successes of the past 5 years suggest that a detailed description of the genetic basis of vitiligo is a realistic goal. In the future, dissection of the complex genetic architecture of vitiligo will provide new approaches for treatment and prevention. In this article, we will give an overview of the latest findings in the genetics of vitiligo.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

The genetics of generalized vitiligo and associated autoimmune diseases.

Generalized vitiligo is an acquired disorder in which patches of depigmented skin, overlying hair, and oral mucosa result from progressive autoimmune loss of melanocytes from the involved areas. Although vitiligo is perhaps the most common pigmentary disorder, insufficiently clear clinical definition of the disorder and lack of a good laboratory animal model have inhibited progress in understanding its pathobiology, its environmental triggers, and in developing specific and effective therapeutic approaches. Vitiligo results from a complex interaction of environmental, genetic, and immunologic factors, which ultimately contribute to melanocyte destruction, resulting in the characteristic depigmented lesions. In the past few years, studies of the genetic epidemiology of generalized vitiligo have led to the recognition that vitiligo is part of a broader, genetically-determined, autoimmune/autoinflammatory diathesis. Attempts to identify genes involved in vitiligo susceptibility have involved both allelic association studies of candidate genes and genome-wide linkage analyses to discover new genes, and these studies have begun to shed light on the mechanisms of vitiligo pathogenesis. It is anticipated that the discovery of biological pathways of vitiligo pathogenesis will provide novel therapeutic and prophylactic targets for future approaches to the treatment and prevention of vitiligo and its associated autoimmune diseases.

Autoimmune Diseases↗
PubMed1999

Serum concentration of the soluble interleukin-2 receptor in vitiligo patients.

Serum levels of sIL-2R can be used to monitor in vivo immune activation and its elevation have been shown to be correlated with T cell mediated immune disease such as atopic dermatitis, psoriasis, lymphoma and systemic sclerosis. Vitiligo is the disease of depigmentation caused by destruction of melanocytes, and there have been extensive studies on the immune pathogenesis. If the pathogenesis of vitiligo is correlated with the activation of T lymphocytes, the change of IL-2R will be detected compared with that of normal control. Therefore we sought the change in sIL-2R to determine whether T lymphocytes from patients with vitiligo show abnormal biological behavior. The quantitation of sIL-2R was done by sandwich enzyme-linked immunosorbent assay (ELISA) from the sera of 79 vitiligo patients and 40 normal controls. The results were summarized as following. The sIL-2R level in vitiligo patients (671.91 +/- 368.59 U/ml) was significantly increased compared with that of controls (370.8 +/- 71.8 U/ml; P < 0.005). According to clinical types, sIL-2R level in focal type of vitiligo patients was significantly higher than those in other types (segmental or generalized; P < 0.05). The sIL-2R level in patients less than 1 year duration was significantly higher than in patients more than 1 year duration (P < 0.05). The sIL-2R levels were not significantly different between active and inactive group. There was no significant differences among sIL-2R levels according to sex or age of onset. Our study showed that sIL-2R level was higher in vitiligo patients compared with that of normal controls, so the activation of T lymphocytes would be an important component in the pathogenesis of vitiligo. The higher sIL-2R levels in recent onset group would suggest that sIL-2R level might be an acute immunologic marker in vitiligo patients.

Adolescent↗
PubMed1998

The genetics of vitiligo in Korean patients.

BACKGROUND: Vitiligo is a common disorder whose exact cause is unknown, but genetic factors are thought to be involved. We analyzed 120 Korean proband families to clarify which genetic factors are involved in the pathogenesis of vitiligo in Korean patients. METHODS: The genetics of vitiligo were analyzed in 120 Korean proband families out of 1030 vitiligo patients. Each family was analyzed through a proband afflicted with vitiligo. RESULTS: In 51 (42.5%) of 120 proband families, at least one first-degree relative of the proband had vitiligo. The incidence of those affected among 1755 relatives (first-, second-, and third-degree) was found to be 8.0+/-0.6%. There was a statistically significant departure for segregation analysis which was inconsistent with inheritance as an autosomal or X-linked locus model. On the basis of our results, the inheritance pattern of vitiligo is more likely to tend toward the model of multifactorial inheritance. The threshold trait among first-degree relatives (7.2%) appeared to tend more toward the square root of the frequency in the general population (10%) than towards those of dominant (50%) or recessive (25%) models. CONCLUSIONS: These results indicate that there are certain genetic factors involved in the etiology of vitiligo, and that vitiligo seems to have a polygenic nature.

Female↗
PubMed2000

Recognition of melanoma cell antigens with antibodies present in sera from patients with vitiligo.

BACKGROUND: Patients with vitiligo show specific losses of integumentary melanocytes, probably due to autoimmunity against melanocytes. We attempted to determine the presence of antibodies against pigment cell antigens in the sera of vitiligo patients. METHODS: Detergent-solubilized human melanoma cells were submitted to electrophoretic separation and immunoblotted against serum samples obtained from 19 patients with vitiligo and from 20 age- and sex-matched healthy individuals. RESULTS: Eighty-nine per cent of patients with vitiligo had antibodies to one or more pigment cell antigens. Similar antibodies were detected in 20% of healthy individuals. Antigens of 165, 90, and 68 kDa were recognized by the antibodies present in sera from 11%, 26%, and 37% of vitiligo patients, respectively, and in none of the normal sera. All patients with familial vitiligo also had antibodies to these three proteins. CONCLUSIONS: Proteins of 165, 90, and 68 kDa are specifically recognized by antibodies present in the sera of vitiligo patients and in all patients with genetic vitiligo. Whether or not these proteins might be implicated in the destruction of melanocytes by the immune system in vitiligo remains to be evaluated.

Antibodies↗
PubMed2000

Epidemiology of vitiligo in the French West Indies (Isle of Martinique).

BACKGROUND: The frequency of vitiligo in white populations has been generally estimated to be about 0.5-1%. The same prevalence is expected in black populations, despite the few investigations reported. No studies have been performed in black populations living in the Caribbean Islands. Therefore, our purpose was to report an epidemiologic study of vitiligo in the French West Indies (Isle of Martinique). METHODS: We performed a prospective study between October 1995 and March 1996; 2077 outpatients of the Department of Dermatology at the Fort de France University Hospital were examined to detect vitiligo. Concurrently, 32 patients (23 women and nine men), presenting with vitiligo, were questioned about their family history, personal diseases, age, and circumstances of vitiligo occurrence. RESULTS: Vitiligo was found in seven patients (five women and two men) out of 2077. The prevalence in the studied population was 0.34%. Of the 32 patients with vitiligo who were investigated, 11 (34%) had a family history of vitiligo, two (6%) suffered from thyroid disease, two (6%) from psoriasis, and one (3%) from atopic dermatitis. The median age at vitiligo onset was 29 years. CONCLUSIONS: Despite the bias due to the recruitment of patients in the Dermatology Department, this study demonstrates a prevalence in a black population comparable, or slightly inferior, to the currently accepted data in white people. Our results concerning the age of onset and pathologic associations showed no difference with the literature data related to white populations.

Adolescent↗