Epidemiology of Systemic Lupus Erythematosus: Time Trend and Racial Differences

Siegel, Morris; Reilly, Edith Bramwell; Lee, Stanley L.; Fuerst, Harold T.; Seelenfreund, Morton H.

doi:10.2105/ajph.54.1.33

Cited by 29 publications

(6 citation statements)

References 8 publications

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“…Epidemiologic studies of SLE, performed as early as the 1960s, have noted that SLE is not only more common but also more severe among minority populations in the US (23). Subsequent studies have confirmed this finding and have generated vigorous debate over whether environmental or genetic factors might account for these differences.…”

Section: Discussionmentioning

confidence: 99%

European genetic ancestry is associated with a decreased risk of lupus nephritis

Richman

Taylor

Chung

et al. 2012

Arthritis & Rheumatism

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Objective African Americans, East Asians, and Hispanics with systemic lupus erythematosus (SLE) are more likely to develop renal disease than SLE patients of European descent. We investigated whether European genetic ancestry protects against the development of lupus nephritis and explored genetic and socioeconomic factors that might explain this effect. Methods This was a cross-sectional study of 1906 adults with SLE. Participants were genotyped for 126 single nucleotide polymorphisms (SNPs) informative for ancestry. A subset of participants was also genotyped for 80 SNPs in 14 candidate genes for renal disease in SLE. We used logistic regression to test the association between European ancestry and renal disease. Analyses adjusted for continental ancestries, socioeconomic status, and candidate genes. Results Participants (n=1906) had on average 62.4% European, 15.8% African, 11.5% East Asian, 6.5% Amerindian, and 3.8% South Asian ancestry. Among participants, 34% (n=656) had renal disease. A 10% increase in European ancestry was associated with a 15% reduction in the odds of having renal disease after adjustment for disease duration and sex (OR 0.85, 95% CI 0.82-0.87, p=1.9 × 10−30). Adjusting for other genetic ancestries, measures of socioeconomic status, or SNPs in genes most associated with renal disease (IRF5 (rs4728142), BLK (rs2736340), STAT4 (rs3024912), ITGAM (rs9937837) and HLA-DRB1*0301 and DRB1*1501, p<0.05) did not substantively alter this relationship. Conclusion European ancestry is protective against the development of renal disease in SLE, an effect independent of other genetic ancestries, common risk alleles, and socioeconomic status.

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Section: Discussionmentioning

confidence: 99%

European genetic ancestry is associated with a decreased risk of lupus nephritis

Richman

Taylor

Chung

et al. 2012

Arthritis & Rheumatism

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“…2-4 Recent studies, particularly in Latino populations, have examined genetic admixture in relation to SLE severity, and have shown a trend toward more severe disease with increasing Amerindian ancestry or decreasing European ancestry. 5, 6 …”

Section: Introductionmentioning

confidence: 99%

European population substructure correlates with systemic lupus erythematosus endophenotypes in North Americans of European descent

et al. 2009

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Previous work has demonstrated that northern and southern European ancestries are associated with specific systemic lupus erythematosus (SLE) manifestations. Here, 1855 SLE cases of European descent were genotyped for 4965 single nucleotide polymorphisms and principal components analysis of genotype information was used to define population substructure. The first principal component (PC1) distinguished northern from southern European ancestry, PC2 differentiated eastern from western European ancestry, and PC3 delineated Ashkenazi Jewish ancestry. Compared to northern European ancestry, southern European ancestry was associated with autoantibody production (OR=1.40, 95% CI 1.07-1.83) and renal involvement (OR 1.41, 95% CI 1.06-1.87), and was protective for discoid rash (OR=0.51, 95% CI 0.32-0.82) and photosensitivity (OR=0.74, 95% CI 0.56-0.97). Both serositis (OR=1.46, 95% CI 1.12-1.89) and autoantibody production (OR=1.38, 95% CI 1.06-1.80) were associated with Western compared to Eastern European ancestry. Ashkenazi Jewish ancestry was protective against neurologic manifestations of SLE (OR=0.62, 95% CI 0.40-0.94). Homogeneous clusters of cases defined by multiple PCs demonstrated stronger phenotypic associations. Genetic ancestry may contribute to the development of SLE endophenotypes and should be accounted for in genetic studies of disease characteristics.

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“…1 The annual incidence of well-defined cases of SLE was found to be highest for Negroes followed in descending order by Puerto Ricans and then by other whites living in an area of Manhattan in New York with a popu¬ lation of about 750,000. These differences in rates were in sharp contrast to the presumed higher sus¬ ceptibility of females with fair skin noted by some clinicians, or the apparent lack of racial difference reported by others."…”

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confidence: 96%