ArticleRheumatology international2009
Higher genetic susceptibility to inflammation in mild disease activity of systemic lupus erythematosus.
Article in Rheumatology international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Polymorphisms in the TNFA and IL6 genes represent risk factors for autoimmune thyroid disease.PloS one · 2014Article
- Interleukin-1 gene cluster and IL-1 receptor polymorphisms in Iranian patients with systemic lupus erythematosus.Rheumatology international · 2013Article
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Authors and funding
6 authors.
Funding
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Abstract
In order to test the hypothesis that stratification of Mexican Modification of the Systemic Lupus Erythematosus Disease Activity Index (MEX-SLEDAI) simplifies the genetic study of SLE, we evaluated the genetic susceptibility to inflammation and defects in clearance of immune complexes among SLE patients in Taiwan. SLE phenotypes were stratified according to the MEX-SLEDAI scores into two subgroups (<or=10 and >10), and then according to renal disorder and neurological disorder, aiming to minimize any loss of power associated with disease heterogeneity. Upon stratification, IL1-beta polymorphism and LTA were significantly associated with SLE within the MEX-SLEDAI <or=10 subgroup. When SLE patients were classified into two subgroups with or without renal disorder to stratify the genetic study, we could find that the stratification with renal disorder could partially confirm the hypothesis that stratification of MEX-SLEDAI score simplifies the genetic study of complex diseases such as SLE. So we concluded that in the mild disease state of SLE, stratification of disease phenotypes, especially IL1-beta and LTA, according to MEX-SLEDAI scores could reveal new associations between candidate genes and disease activity index of SLE.
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