Pattern of Familial Aggregation of Vitiligo
Partha P. Majumder, PhD;
James J. Nordlund, MD;
Swapan K. Nath, MSc
Arch Dermatol. 1993;129(8):994-998.
Abstract
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Background and Design
Vitiligo is a disorder whose cause is not well understood. This study was undertaken to clarify whether genetic factors are involved in the pathogenesis of vitiligo. Data on 160 white kindreds living in the United States have been collected. Each family was ascertained through a proband afflicted with vitiligo. The nature and extent of familial aggregation and other relevant epidemiologic features have been determined.
Results
The mean age at onset of vitiligo is about 19 years in male and about 24 years in female individuals. The percentage of probands reporting one or more firstdegree relatives also afflicted with vitiligo is 20%. Children of probands are found to be afflicted about 1.7 times more commonly than other first-degree relatives. The relative risk (RR) for vitiligo is about 7 for parents, about 12 for siblings, and about 36 for children. For seconddegree relatives, the RR varies between 1 and 16. Relative risks for all first- and second-degree relatives, except uncles and grandsons, are significant at the 5% level. In families in which one or more relatives of the proband are afflicted with vitiligo, the intrafamilial correlation of ages at onset of vitiligo is moderate (0.6). No statistically significant effect (at the 5% level) of parental age at first childbirth was seen on the proportion of offspring afflicted with vitiligo. No significant association of some commonly related diseases (eg, thyroid disorder or alopecia areata) was observed with vitiligo or with a family history of vitiligo.
Conclusions
The extent of familial aggregation of vitiligo is statistically significant. The pattern of relationship between RR and degree of kinship indicates involvement of genetic factors, although it is not consistent with singlelocus mendelian transmission.
(Arch Dermatol. 1993;129:994-998)
Author Affiliations
From the Anthropometry and Human Genetics Unit, Indian Statistical Institute, Calcutta, India (Dr Majumder and Mr Nath); and the Department of Dermatology, University of Cincinnati (Ohio) College of Medicine (Dr Nordlund). Dr Thirkill is a consultant to Genica Pharmaceuticals. The other authors do not have a proprietary interest in the materials mentioned in this study.
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