Abstract:
BACKGROUND:There is no report about the association between GATA3 rs3824662 polymorphism and systemic lupus erythematosus (SLE). OBJECTIVE:To investigate the possible role of GATA3 rs3824662 polymorphism as a susceptibility risk factor for either adult SLE (aSLE) or pediatric SLE (pSLE) and to evaluate its role in the development of lupus nephritis (LN) in pSLE. METHODS:Typing of GATA3 rs3824662 polymorphism was done using real-time polymerase chain reaction for three groups; 104 pSLE patients, 140 aSLE patients and 436 age- and sex-matched healthy controls. RESULTS:Non-significant differences were found between SLE patients and healthy controls for the allele and genotype frequencies of GATA3 rs3824662 ( p > 0.05). In pSLE; the AC genotype was associated with LN ( p = 0.04); the A allele and AC genotype were associated with persistent proteinuria ( p = 0.036 and 0.01, respectively) and both the A allele and AA genotype were associated with higher chronicity index ( p = 0.031 and 0.04, respectively). In aSLE; the C allele was associated with cellular cast ( p = 0.03) and thrombocytopenia ( p = 0.01). Logistic regression analysis revealed significant association between the AC+AA genotypes and the prediction of LN and renal active disease in pSLE ( p = 0.04 and 0.01, respectively). CONCLUSION:GATA3 rs3824662 is not associated with susceptibility to SLE either in adult or in pediatric patients; however, in pSLE patients, the heterozygous AC genotype could be considered a risk factor for LN. At the same time, the AC and AA genotypes could be considered as predictors for LN and active renal disease. However, the small sample size is a limiting factor of the present study when interpreting the positive association.
journal_name
Lupusjournal_title
Lupusauthors
Mosaad YM,Hammad A,Elghzaly AA,Tawhid ZME,Hammad EM,Showma A,Abdelsalam R,Elmoughy A,Fawzy IM,Anber Ndoi
10.1177/0961203318804894subject
Has Abstractpub_date
2018-11-01 00:00:00pages
2112-2119issue
13eissn
0961-2033issn
1477-0962journal_volume
27pub_type
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