title: Higher genetic susceptibility to inflammation in mild disease activity of systemic lupus erythematosus.
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.
authors.affiliation: College of Engineering, National Taiwan University of Science and Technology, Taipei, 10672, Taiwan.
authors.forename: Li-Jen
authors.initials: LJ
authors.lastname: Tsai
authors.forename: Sheng-Hsiung
authors.initials: SH
authors.lastname: Hsiao
authors.forename: Jaw-Ji
authors.initials: JJ
authors.lastname: Tsai
authors.forename: Ching-Yuang
authors.initials: CY
authors.lastname: Lin
authors.forename: Lih-Min
authors.initials: LM
authors.lastname: Tsai
authors.forename: Joung-Liang
authors.initials: JL
authors.lastname: Lan
mesh_terms: D000328:Adult; D000483:Alleles; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D053583:Interleukin-1beta / Q000235:genetics; D007674:Kidney Diseases / Q000473:pathology; D008180:Lupus Erythematosus, Systemic / Q000235:genetics*; D008233:Lymphotoxin-alpha / Q000235:genetics; D008297:Male; D009422:Nervous System Diseases / Q000473:pathology; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D012720:Severity of Illness Index; D013624:Taiwan
chemical_list: D053583:Interleukin-1beta; D008233:Lymphotoxin-alpha