Pattern of familial aggregation of vitiligo

Majumder, P. P.

doi:10.1001/archderm.129.8.994

Cited by 95 publications

(137 citation statements)

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“…For all types of vitiligo, the interval of onset ages with the highest prevalence was 10 to 14 years (Table I). No statistically significant difference was found in the distributions of ages of onset between male and female probands (Mann-Whitney test, P = 0.243), which was consistent with the findings of Majumder et al 7 In contrast, there was a significant difference (Kruskal-Wallis test, chi-square = 25.55, P \ .001) in the distributions of ages of onset among different types of vitiligo. The distributions of ages of onset observed in this study and in a previous study conducted in the United States 7 are presented in Fig 1 for comparison.…”

Section: Proband Characteristicssupporting

confidence: 90%

“…20 Relative risks of vitiligo among relatives of probands were calculated as described. 7 Heritabilities in relatives of probands were derived using Falconer's method. 21 A level of P \ .05 (2-sided) was considered statistically significant.…”

Section: Methodsmentioning

confidence: 99%

“…4,5 Although vitiligo aggregates in families, it does not appear to segregate in a simple mendelian pattern. [6][7][8][9][10][11] Previously, an autosomal recessive model of vitiligo that took the variability of the age of onset into account was proposed that suggested there might be genes at 3 or 4 autosomal loci controlling vitiligo. 8,9 In recent years, increasing attention has been paid to exploring the genetics of vitiligo and more than 4 loci are thought to be associated with vitiligo.…”

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confidence: 99%

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Characteristics of genetic epidemiology and genetic models for vitiligo

Zhang

Liu

Gui

et al. 2004

Journal of the American Academy of Dermatology

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Section: Proband Characteristicssupporting

confidence: 90%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Characteristics of genetic epidemiology and genetic models for vitiligo

Zhang

Liu

Gui

et al. 2004

Journal of the American Academy of Dermatology

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“…Vitiligo in children represents an important entity since in 50% of patients the onset is before the age of 20 [11, 14]and in 25% before the age of 10 [15]. The disease has a significant psychological impact on the patients and their parents [16, 17].…”

Section: Introductionmentioning

confidence: 99%

Relevance of Thyroiditis and of Other Autoimmune Diseases in Children with Vitiligo

et al. 2005

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Background: Studies that clearly define the possible association of childhood vitiligo with autoimmune and/or endocrine diseases are lacking. Objective: To examine the presence of autoimmune disorders, in particular of thyroid disease, in paediatric patients with vitiligo and investigate the utility of such screening in these patients. Methods: One hundred and twenty-one paediatric patients (40 males, 81 females) with vitiligo were grouped in segmental and non-segmental vitiligo. All patients were screened for thyroid disease. Results: 13 out of 121 patients had different degrees of thyroid parameter alterations. These patients were all affected by the non-segmental type while none of those with the segmental form presented thyroid alterations. Conclusion: In paediatric patients with non-segmental vitiligo, a significant incidence of thyroid dysfunction was found. Since vitiligo usually appears before the development of the thyroid disease, it may be useful to screen thyroid autoantibodies in all paediatric patients with non-segmental vitiligo who present symptoms related to thyroid disease.

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“…It has a variable age-of-onset and a variable clinical spectrum both in severity and in localization (El-Mofty and El-Mofty 1980; Goudie et al 1980;Lorincz 1985;Kovacs 1998). Familial clustering of vitiligo has been largely observed (Goudie et al 1983;Hafez et al 1983;Das et al 1985;Majumder et al 1988Majumder et al , 1993Nath et al 1994). In general, family studies have shown that vitiligo does not segregate as a simple Mendelian trait, and the available data fit the multifactorial model (Goudie et al 1983), a dominant model with incomplete penetrance (Hafez et al 1983), and a multilocus recessive model postulating that recessive alleles, at a set of four unlinked diallelic loci, are involved in the predisposition to vitiligo (Majumder et al 1988).…”

Section: Introductionmentioning

confidence: 99%

Vitiligo: complex segregation and linkage disequilibrium analyses with respect to microsatellite loci spanning the HLA

et al. 2002

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Familial clustering and linkage disequilibrium studies suggest that genetic factors predispose to vitiligo, although a clear transmission pattern and cosegregation of vitiligo with specific mutations have not been demonstrated. We collected pedigree data on vitiligo from a set of 56 multigeneration families belonging to the Paisa community from Antioquia, Colombia, with the goal of applying the unified model of complex segregation and linkage disequilibrium analyses to test the hypotheses of the existence of a major gene predisposing to vitiligo and that allelic or haplotype polymorphisms of microsatellite loci at 6p21.3-21.4 spanning HLA (D6S276, D6S265, D6S273, and D6S291) are associated with this predisposition. Minimum sibship sample size to discriminate dominant and recessive inheritance models was largely accomplished. Between the 15 models of complex segregation used, the one that best fitted the data was that of a major dominant gene and the existence of strong environmental effects acting on the recessive genotype. The penetrance and risk estimations discriminated two sets of vitiligo patients: those with early onset of vitiligo cosegregating with a dominant mode of inheritance without environmental effects, and those with late onset of vitiligo cosegregating with the recessive genotype and being influenced by environmental effects. After establishing the normal distribution of allelic frequencies and performing multiple comparisons correction, the linkage disequilibrium analysis suggested that a major genetic factor could be located at 6p21.3-21.4, because we detected significant case-control differences for allele 122 at D6S265 (Pc=0.0264) and significant linkage disequilibrium between loci D6S276 and D6S273 in the cases but not in the controls. We cannot explain these results as a consequence of evolutionary forces or as genetic stratification acting differentially on cases and controls, because there was neither deviation from the Hardy-Weinberg expectations nor genetic subdivision between cases and controls, as θ (non-biased F ST ) was not significantly different from 0.

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Pattern of familial aggregation of vitiligo

Cited by 95 publications

References 0 publications

Characteristics of genetic epidemiology and genetic models for vitiligo

Characteristics of genetic epidemiology and genetic models for vitiligo

Relevance of Thyroiditis and of Other Autoimmune Diseases in Children with Vitiligo

Vitiligo: complex segregation and linkage disequilibrium analyses with respect to microsatellite loci spanning the HLA

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