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PubMed2002

Genetic association of the catalase gene (CAT) with vitiligo susceptibility.

Vitiligo susceptibility is a complex genetic trait that may involve genes important for melanin biosynthesis, response to oxidative stress, and/or regulation of autoimmunity, as well as environmental factors. We report here case-control and family-based association studies for the catalase gene (CAT) in vitiligo patients. The CAT gene was selected as a candidate gene because of the reduction of catalase enzyme activity (EC 1.11.1.6) and concomitant accumulation of excess hydrogen peroxide observed in the entire epidermis of vitiligo patients. One of three CAT genetic markers studied was found to be informative for genotypic analysis of Caucasian vitiligo patients and control subjects. Both case/control and family-based genetic association studies of the T/C single nucleotide polymorphism (SNP) in exon 9 of the CAT gene, which is detectable with the restriction endonuclease BstX I, suggest possible association between the CAT gene and vitiligo susceptibility. The observations that T/C heterozygotes are more frequent among vitiligo patients than controls and that the C allele is transmitted more frequently to patients than controls suggest that linked mutations in or near the CAT gene might contribute to a quantitative deficiency of catalase activity in the epidermis and the accumulation of excess hydrogen peroxide (H2O2). The CAT gene may, therefore, be a susceptibility gene in some vitiligo patients, further supporting the epidermal oxidative stress model for vitiligo pathogenesis.

Biomarkers↗
PubMed2006

Function-blocking autoantibodies to the melanin-concentrating hormone receptor in vitiligo patients.

Vitiligo is a common depigmenting skin disorder resulting from the loss of melanocytes in the cutaneous epidermis. Although the cause of the disease remains obscure, autoimmune mechanisms are thought to be involved. Recently, melanin-concentrating hormone receptor (MCHR)-binding autoantibodies have been identified in vitiligo patients. In the present study, we aimed to determine if MCHR autoantibodies could also affect receptor function either by direct activation or by blocking its response to melanin-concentrating hormone. The results indicated that 10/18 (56%) vitiligo patient IgG samples inhibited the function of MCHR expressed in a Chinese hamster ovary cell line. In contrast, neither control (n=20) nor SLE patient (n=10) IgG samples blocked receptor function. Compared with healthy controls, MCHR function-blocking autoantibodies were found at a significantly increased frequency in the vitiligo patient group (P=0.0004). No MCHR-activating autoantibodies were detected in any of the vitiligo patient, SLE patient or control IgG samples that were analysed. In addition, vitiligo patient IgGs were tested for MCHR autoantibodies that could mediate antibody-dependent cell-mediated cytotoxicity via the receptor. However, this could only be demonstrated in two vitiligo patient sera. Overall, this work has provided additional evidence that MCHR is a B-cell autoantigen in vitiligo and has demonstrated the existence of MCHR function-blocking autoantibodies further to the receptor-binding autoantibodies previously reported.

Adult↗
PubMed1999

Alopecia areata and universalis in the Smyth chicken model for spontaneous autoimmune vitiligo.

The Smyth line (SL) chicken model for spontaneous, postnatal expression of vitiligo may also show varying incidences and degrees of severity ranging from alopecia areata-like to universalis-like integumental changes. Although human vitiligo patients are known to have a four times greater chance of having alopecia areata than do people without vitiligo, in the SL model, feather loss is limited to birds that show some degree of amelanosis of feather and skin tissue. Both the vitiligo and the alopecia have an autoimmune component, as shown by histologic and immunologic studies, including the correctional influences of corticosterone and cyclosporine-A. The major histocompatibility haplotype (MHC) has a major effect on the incidence and expression of the vitiligo, as well as the alopecia that occurs within vitiliginous birds. Three different MHC haplotypes were identified in the original line that was selected for vitiligo, and from these, three sublines were developed, each homozygous for a different haplotype. Of the three sublines (SL101, SL102, and SL103) the vitiligo has a significantly earlier onset and severity in the SL101 than in the other two lines. The incidence of alopecia, however, is significantly lower in the SL101 subline than in the other two. Inheritance of the vitiligo is polygenic with an additional genetic component for the alopecia trait. It is hypothesized, but as yet unproven, that a feather development defect interacts with the SL melanization and immunologic defects to initiate the partial (areata) and complete (universalis) alopecias. The alopecia universalis is rarely seen until adulthood and is characterized by short (<0.5 cm), undeveloped feathers. If feather growth resumes in these birds, the feathers dry up, cease to grow, and often break off.

Alopecia Areata↗
PubMed1999

Analysis of a microsatellite polymorphism of the cytotoxic T-lymphocyte antigen-4 gene in patients with vitiligo.

The CTLA-4 gene encodes a T-cell receptor that is involved in the regulation of T-cell activation. Recent studies have demonstrated an association of a microsatellite polymorphism [variant lengths of a dinucleotide (AT)n repeat] lying in exon 3 of the CTLA-4 gene, specifically a 106-bp allele, with autoimmune disorders, such as Graves' disease, autoimmune Addison's disease and autoimmune hypothyroidism. The aim of the present study was to determine whether the same polymorphism of the CTLA-4 gene was associated with vitiligo, a disorder that may have an autoimmune origin and can be present in patients who have one or more autoimmune diseases. CTLA-4 gene microsatellite polymorphisms were determined for 74 vitiligo patients (53 without any autoimmune disorder; 21 with one or more autoimmune disease) and 173 healthy controls, who had no clinical evidence of either vitiligo or any other autoimmune disorder, by polymerase chain reaction amplification of genomic DNA and resolution of the products on polyacrylamide sequencing gels. The frequency of the 106-bp allele was significantly increased (chi2 = 5. 2; P = 0.02) in vitiligo patients as a whole, in comparison with control subjects. However, when the patients were classified according to the absence or presence of an autoimmune disorder, the frequency of the 106-bp allele was significantly increased (chi2 = 14.8; P = 0.0001) only in the group of vitiligo patients who also had an autoimmune disease. However, the fact that 17 of 21 patients also had either autoimmune thyroiditis or autoimmune Addison's disease probably accounts for the apparent association of vitiligo and the 106-bp allele in this patient group. However, it was found that the relative risk of 3.2, conferred by the 106-bp allele in this group of vitiligo patients, was greater than that found for patients with only either Graves' disease, autoimmune hypothyroidism or autoimmune Addison's disease, with values of 2.1, 2.2 and 2.2, respectively. For the group of patients without an autoimmune disorder, there was no significant difference (chi2 = 0.2; P = 0.64) in the frequency of the 106-bp allele when compared with control subjects. These results indicate that there is no association between the 106-bp allele and vitiligo, at least when the disorder occurs in the absence of an autoimmune disease.

Abatacept↗
PubMed2001

Linkage and association of HLA class II genes with vitiligo in a Dutch population.

BACKGROUND: Serological typing of HLA has shown discrepancies in HLA associations with vitiligo in different ethnic populations. OBJECTIVES: To perform genotyping of HLA class II genes on a Dutch vitiligo population in order clearly to identify susceptible and protective HLA alleles in vitiligo. METHODS: HLA typing was carried out by amplifying genomic DNA by polymerase chain reaction (PCR) followed by dot-blot hybridization with sequence-specific oligonucleotides (SSO). Fifty Dutch vitiligo probands, and their parents (150 individuals) and 204 healthy controls were studied. RESULTS: Family-based case-control association studies and linkage disequilibrium analysis showed the linkage and association of DRB4*0101 allele with vitiligo (P(c) = 0.0016, relative risk = 2.21). The family-based association study also provided evidence for linkage and association of DQB1*0303 allele with vitiligo (chi(2) = 7.36, P = 0.006). We measured the clinical relevance of the test by calculating the prevalence corrected positive predictive values (PcPPV). The PcPPV of disease for the DRB4*0101 allele was 0.017 and for the DRB4*0101/0101 genotype was 0.0358. In other words, a DRB4*0101/0101 genotype carries a 3.58% risk of developing vitiligo. CONCLUSIONS: Both DRB4*0101 and DQB1*0303 alleles provide significant susceptibility for vitiligo.

Adolescent↗
PubMed2003

Melanocyte detachment after skin friction in non lesional skin of patients with generalized vitiligo.

BACKGROUND: In vitiligo, melanocytes are gradually lost in depigmented macules of the skin. The disappearance of melanocytes has, however, not been clearly observed and consequently the aetiology of the disease (autoimmune, neural, cytotoxic) is still elusive. The starting point of vitiligo macules is frequently determined by local conditions such as wounds and excoriations, but may also follow minor traumas such as pressure or repeated friction. This prominent feature is often neglected. OBJECTIVES: To clarify the biological consequences of repeated friction on the attachment and survival of melanocytes in non lesional vitiligo skin. METHODS: Light reproducible skin friction was performed for 4 min on the volar forearm of 18 patients with extensive vitiligo and five controls with normal healthy skin. Biopsies from the test area and control skin were taken at 1, 4, 24 and 48 h following friction. Serial sections were examined with standard light microscopy, transmission electron microscopy, histochemistry and immunohistochemistry (dihydroxyphenylalanine, HMB-45, E-cadherin and an early apoptosis marker, M30 cytoDEATH antibody). RESULTS: The observation of sections at 1 and 48 h after friction on vitiligo skin and at all time points in controls revealed no changes. In contrast, in vitiligo skin at 4 and 24 h after friction, several melanocytes had undergone detachment and were found in various suprabasal positions, including the stratum spinosum, granular layer, and within and outside the stratum corneum. 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). We propose that transepidermal elimination of melanocytes in vitiligo should be regarded as a possible mechanism of chronic loss of pigment cells, perhaps previously damaged by another process.

Adult↗
PubMed2002

Increase in total blood antioxidant status and selenium levels in black patients with active vitiligo.

BACKGROUND: Oxidative stress could be an important phenomenon leading to melanocyte death in vitiligo. The accumulation of hydrogen peroxide (H2O2) and low catalase levels have recently been demonstrated in the epidermis of vitiligo patients. Few abnormalities of antioxidants have been found in the blood of patients with vitiligo, except for an elevation of selenium. No studies on oxidative stress have been performed so far on patients with skin phototype VI (Fitzpatrick classification). AIM: To study the blood antioxidant status of black patients with active generalized vitiligo. METHODS: Randox total antioxidant status, selenium, ferritin, transferrin, ceruloplasmin, tocopherol, and retinol levels were evaluated in blood samples obtained from 11 dark-skinned patients from the French West Indies (Isle of Martinique) with recent active lesions of vitiligo and from 11 age- and sex-matched healthy volunteers. RESULTS: Total blood antioxidant status and selenium levels were significantly increased in vitiligo patients, compared to those in sex- and age-matched controls (P < 0.01 and P < 0.02, respectively). Blood levels of ferritin, transferrin, ceruloplasmin, retinol, and tocopherol were not significantly modified. CONCLUSIONS: This is the first report on the global blood antioxidant status in vitiligo. The increase in total blood antioxidant status observed in black patients was an unexpected result that needs to be confirmed and explained by further studies. The spontaneous increase in selenium levels could be of interest, as it has been recommended in the treatment of vitiligo.

Adult↗
PubMed2003

Vitiligo in the Nigerian African: a study of 351 patients in Benin City, Nigeria.

BACKGROUND: There is a paucity of reports on vitiligo in sub-Saharan Africa. AIM: To define the clinical and epidemiologic pattern of vitiligo in the Nigerian African. METHODS: We examined all new cases of vitiligo seen in the Dermatology Unit of the University of Benin Teaching Hospital (UBTH) over a 14-year period: January 1985 to December 1998. RESULTS: Three hundred and fifty-one patients with vitiligo, representing 3.2% of new dermatologic cases, were enrolled. The study group was made up of 153 males and 198 females, giving a sex ratio of 1 : 1.3. The peak incidence of vitiligo was in the second and third decades of life, and the most common form of presentation was the localized focal type (77%), followed by the segmental type (12.5%) and the generalized form (10.5%). Common sites affected were the limbs (32%), trunk (23.8%), face (18.2%), head and neck (9.1%), and the mucous membranes (7.4%). There was a positive family history of vitiligo in 18% of subjects and 3.4% had systemic diseases, such as diabetes mellitus (1.7%), anemia (0.8%), hyperthyroidism (0.6%), and leukemia (0.3%). CONCLUSIONS: Vitiligo on darkly pigmented skin is often a very striking disease. Our findings show that the pattern of vitiligo is similar to that reported from other parts of the world. The high level of social stigmatization is due to confusion with leprosy.

Adolescent↗
PubMed1993

Cytolytic antibodies to melanocytes in vitiligo.

Patients with vitiligo have been found to have circulating antibodies to pigment cells. To evaluate the functional activity of these antibodies, a highly sensitive europium release assay was used to compare complement-mediated cytolysis of human melanocytes by sera of 56 patients with vitiligo (20 with active disease, 25 with inactive disease, 11 with unidentified disease activity) and 47 control individuals. Significant melanocyte lysis was mediated by 32 (57%) of the patients with vitiligo but by only three (6%) of the control sera (p < 0.001), and by 17 (85%) of 20 patients with active vitiligo versus 11 (44%) of 25 patients with inactive disease (p < 0.025). Mean melanocyte lysis by vitiligo sera was 24% versus 6% by control sera (p < 0.0001). A subset of 12 vitiligo sera with high titers of cytolytic antibodies to melanocytes (34% mean cytolysis) reacted minimally (< 2% mean cytolysis) to a panel of control cells that included human and murine melanomas, human fibroblasts, lung carcinoma, and rhabdomyosarcoma. These findings indicate that antibodies present in patients with vitiligo have the functional ability to selectively kill melanocytes and are more common in active disease. These observations support, but do not prove, the hypothesis that vitiligo is an autoimmune disease and that anti-pigment cell antibodies have a role in inducing the disease.

Antibodies↗
PubMed1993

Coexistence and relationship of antikeratinocyte and antimelanocyte antibodies in patients with non-segmental-type vitiligo.

To test for autoantibodies in patients with vitiligo, skin biopsies from 16 patients with active vitiligo and 12 patients with stable vitiligo were examined by direct immunofluorescence. In periodate-lysine-paraformaldehyde-fixed biopsy specimens, the presence of IgG deposits in keratinocytes and the number of keratinocytes with focal IgG in active vitiligo were significantly greater than in stable vitiligo. To test whether the antibodies to normal human keratinocytes or melanocytes are present in vitiligo, we used an indirect immunofluorescent test and enzyme-linked immunosorbent assay to test the serum of 43 patients. With unfixed viable melanocytes, we found a granular pattern of IgG staining on the plasma membrane of melanocytes incubated with patients' sera but not in cells incubated with the control sera. With methanol-fixed melanocytes, however, we found a homogeneous pattern of IgG staining in the cytoplasm of melanocytes. With unfixed viable keratinocytes as targets, there was no deposit of IgG on the cells. A homogeneous pattern of IgG binding in the cytoplasm of methanol-fixed keratinocytes suggested the presence of antikeratinocyte autoantibodies to cytoplasmic keratinocyte components. The fluorescence staining for IgG binding was more prominent in active or extensive vitiligo. Vitiligo sera were cytotoxic for melanocytes but not for keratinocytes in vitro. Antimelanocytic antibodies may play a role in melanocytotoxicity, whereas antikeratinocyte antibodies may occur secondary to cellular damage.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1986

A mouse model for vitiligo.

As the result of a long search for a depigmenting mouse that could serve as a model for the study of vitiligo, we have located a strain that arose from the C57BL/6J. Its provisional genetic designation is C57BL/6J Ler-vit/vit. This vitiligo mouse has congenital dorsal and ventral white spots (piebaldism) as well as progressive replacement of pigmented hairs by white hairs with each spontaneous molt or after plucking. The lack of pigment is due to the absence of melanocytes from the amelanotic hair follicles and epidermis. As in human beings and the Smyth chicken model, there is also diminution of ocular pigment. Reciprocal skin transplants between C57BL/6J and vitiligo mice, and transplants into nude mice, suggest a programmed pigment cell death in the vitiligo mice. Like human beings with vitiligo, maximally depigmented vitiligo mice have a decreased contact sensitivity response in comparison to age-matched C57BL/6J controls. The resistance to injected B16 melanomas is lowered. Vitiligo mice show no signs of premature aging. Already at this early stage in the study of this new animal model, there are findings that open a range of new approaches to the study and treatment of patients with vitiligo and melanomas.

Animals↗
PubMed2006

Association study between catalase gene polymorphisms and the susceptibility to vitiligo in Korean population.

Vitiligo is an acquired pigmentary disorder characterized by well-circumscribed depigmented patches. Autoimmune, self-destruction, neural, and genetic theories have been proposed for the pathogenesis of vitiligo. Reactive oxygen species play an important role in the physiology of cell damage, and catalase is known to regulate oxidative stress. Reduced catalase enzyme activity and accumulation of excessive hydrogen peroxide were observed in vitiligo. To examine whether catalase gene polymorphisms are associated with vitiligo patients in Korean population, we investigated two CAT gene polymorphisms including (T/C) BstX I (A/T) Hinf I in 118 vitiligo patients and 200 healthy volunteers. The CAT gene genotype distribution and allele frequency were not significantly different between vitiligo patients and healthy controls. But, the haplotype of two polymorphisms was associated with vitiligo. This study suggests possible association between the CAT gene and the vitiligo susceptibility.

Adult↗
PubMed1993

Increased incidence of antismooth muscle antibody in Korean vitiligo patients.

To evaluate the incidence of autoimmune disorders and organ-specific autoantibodies in Korean vitiligo patients, antibodies to nuclear, mitochondrial, smooth muscle, gastric parietal cell, thyroglobulin, and microsomal antigens were screened in 226 vitiligo patients and 120 controls. Of the 226 vitiligo patients, three (1.3%) had thyrotoxicosis and two (0.8%) had diabetes mellitus. The vitiligo patients had an increased incidence of antinuclear (12.4%), antimicrosomal (7.1%), and antismooth muscle antibodies (25.7%). The increased incidence of antismooth muscle antibody was correlated with early onset (less than 15 years), a positive family history of vitiligo, and long duration of vitiligo. These results support an autoimmune origin of vitiligo and suggest that the high incidence of antismooth muscle antibody is a distinctive feature of laboratory findings in Korean vitiligo patients.

Adolescent↗
PubMed2004

Topical tacrolimus for treatment of childhood vitiligo in Asians.

Childhood vitiligo is a common disorder of pigmentation in India. Considering the lack of uniformly effective and safe treatment modalities for children with vitiligo, search for newer therapeutic agents continues. This study was designed to evaluate the role of topical tacrolimus in the treatment of childhood vitiligo. Twenty-five children with vitiligo were treated with topical 0.03% tacrolimus ointment applied twice daily for 12 weeks. Response was noted as marked to complete (> 75% repigmentation), moderate (50-75% repigmentation) and mild (< 50% repigmentation). Twenty-two children (9 boys and 13 girls) of mean age 7.2 +/- 1.4 years completed the study. Twelve (54.5%) children had vitiligo vulgaris, nine (40.9%) had focal vitiligo and one (4.5%) had segmental vitiligo. The mean duration of disease was 8 +/- 3 months. Nineteen (86.4%) children showed some repigmentation at the end of 3 months and other three had no response. Of these 19 children, repigmentation was marked to complete in 11 (57.9%), moderate in five (26.3%) and mild in three (15.7%) children. Side effects were minimal, such as the pruritus and burning noted in only three patients. Topical tacrolimus is an effective and well-tolerated treatment modality in Asian children with vitiligo.

Administration, Cutaneous↗
PubMed1995

Morphologic observations on the dermal nerves in vitiligo: an ultrastructural study.

BACKGROUND: Vitiligo is a common idiopathic skin disorder. The etiology is unknown, although various hypotheses have been advanced. These include the neuronal hypothesis, where neuronal factors are thought to play a role in the pathogenesis of this disease. METHODS: Skin biopsies were taken from marginal and central parts of four vitiligo patients. Biopsies were also taken from nonvitiliginous skin of each patient and from four normal control subjects. Sections were examined under the electron-microscope. Nerve fibers in the superficial dermis were examined. RESULTS: Subtle ultrastructural changes, including regeneration and degeneration, were consistently found in dermal nerves of vitiligo lesions. The most consistent feature, seen in all four vitiligo patients studied (in both lesional and marginal areas), was an increased thickness of the basement membrane of Schwann cells. This change was found in approximately three-quarters of all dermal nerves in vitiligo biopsies, but in only about one-quarter of dermal nerves in normal control skin. About half the abnormal dermal nerves in vitiligo skin showed minor axonal damage, although indicators of regeneration (increased mitochondria and rough endoplasmic reticulum) predominated. The dermal nerves in vitiligo showed no difference in fiber diameter or fiber density in comparison with controls. CONCLUSIONS: In vitiligo both axonal degeneration and nerve regeneration may occur, with the latter possibly being a reactive change to earlier axonal damage. These findings support the hypothesis that there is a neuronal component to this disease.

Adult↗
PubMed2006

Genetic epidemiology of vitiligo: a study of 815 probands and their families from south China.

BACKGROUND: Genetic factors are thought to be involved in the development of vitiligo. AIM: To explore the possible genetic model of vitiligo by analyzing the genetic characteristics of 815 patients and their families from south China (Zhejiang Province). METHODS: Data for 815 patients with vitiligo were obtained by questionnaire. The inheritance pattern estimation, heritability calculation, and complex segregation analysis were performed using the Penrose method, Falconer regression method, and SAGE-REGTL program, respectively. RESULTS: In 815 vitiligo probands, 128 (15.7%) had a family history. The ratio of the sibling prevalence rate to the population prevalence rate (s/q) approached 1/square root q using the Penrose calculation, and the heritability degrees of vitiligo in the first- and second-degree relatives were 59.6% and 55.2%, respectively. The complex segregation analysis suggested that the dominant model was the best-fit genetic model for vitiligo. CONCLUSIONS: Genetic factors play an important role in the occurrence of vitiligo, and the genetic model of vitiligo in this population is consistent with a polygenetic or multifactorial inheritance in a dominant major gene pattern.

Adult↗
PubMed1993

Vitiligo: where do we stand?

Vitiligo is a puzzling disorder characterized by a disappearance of epidermal and/or follicular melanocytes by unknown mechanisms. This very common disorder involving 1-4% of the world population is thus of great importance for the practicing dermatologist. The cellular and molecular mechanisms leading to the destruction of melanocytes in this disorder have not yet been elucidated, making it of major interest for the cell biologist involved in melanocyte research. Recent advances in this field, due largely to the availability of techniques for culturing normal human melanocytes, opened new perspectives in the understanding of vitiligo. Although vitiligo has long been considered a disorder confined to the skin, there is now good evidence that it also involves the extracutaneous compartment of the "melanocyte organ." It is also clear that vitiligo is not only a melanocyte disorder, but that it also involves cells, such as keratinocytes and Langerhans cells, found in the epidermis and follicular epithelium. The three prevailing theories of the pathogenesis of vitiligo are the immune hypothesis, the neural hypothesis, and the self-destruct hypothesis. New hypotheses suggest that vitiligo may be due to (1) a deficiency in an unidentified melanocyte growth factor, (2) an intrinsic defect of the structure and function of the rough endoplasmic reticulum in vitiligo melanocytes, (3) abnormalities in a putative melatonin receptor on melanocytes and (4) a breakdown in free radical defense in the epidermis. None of these hypotheses has been demonstrated, and according to the available data, it is likely that the loss of epidermal and follicular melanocytes in vitiligo may be the result of several different pathogenetic mechanisms.

Autoimmune Diseases↗
PubMed2004

Study on the antioxidant status of vitiligo patients of different age groups in Baroda.

One of the major hypotheses in the pathogenesis of vitiligo is the oxidative stress hypothesis. Pollution plays a major role in the production of free radicals. Gujarat, a highly industrialized state in India has a high prevalence of vitiligo patients. No previous studies were done on the age-dependent antioxidant status of vitiligo patients in Baroda city, Gujarat. Blood samples were collected from vitiligo patients of different age groups (5-15, 16-25, 26-35, 36-45 yr) and from age matched healthy volunteers. Antioxidant enzymes in blood such as catalase, superoxide dismutase, glutathione peroxidase and non-enzymatic antioxidants such as reduced glutathione and plasma vitamin E were estimated. Lipid peroxidation levels in erythrocytes and the reducing equivalent system, i.e. glucose-6-phosphate dehydrogenase were also measured. Significant increase in superoxide dismutase activity and lipid peroxidation levels in erythrocytes was observed in all age groups of vitiligo patients as compared with age-matched healthy controls, wherein an increase of 55% (P < 0.02) was observed in superoxide dismutase activity and lipid peroxidation levels in 36-45 yr age group. Whole blood glutathione levels, erythrocyte glutathione peroxidase and glucose-6-phosphate dehydrogenase activity were decreased significantly, whereas erythrocyte catalase activity and plasma vitamin E levels were not different in vitiligo patients as compared with age-matched healthy controls. No specific age group showed a significant difference. This is the first report on the age-dependent antioxidant status of vitiligo patients in Baroda. The disease affects individuals of any age group as shown in this study and systemic oxidative stress might precipitate the pathogenesis of vitiligo in susceptible patients.

Adolescent↗