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Table 6 Association between IL-10 and TNFα genotypes and response to antimalarial treatment

From: Cytokine polymorphisms influence treatment outcomes in SLE patients treated with antimalarial drugs

Genotype Healthy controls n (%) SLE patients Univariate analysis Multivariate analysisa
   Good responders to antimalarials n (%) Others n (%) OR (95% CI) p OR (95% CI) p
-1,082 IL-10        
   Low (AA/AG) 292 (85.1) 34 (85.0) 119 (78.8) Referent   Referent  
   High (GG) 51 (14.9) 6 (15.0) 32 (21.2) 0.66 (0.25–1.70) 0.386 0.59 (0.20–1.78) 0.354
-308 TNFα        
   Low (GG) 265 (77.3) 17 (42.5) 95 (62.5) Referent   Referent  
   High (AA/GA) 78 (22.7) 23 (57.5) 57 (37.5) 2.25 (1.11–4.58) 0.024 2.67 (1.20–5.97) 0.016
Combined IL-10/TNFα        
   Low/Low 224 (65.3) 12 (30.0) 75 (49.7) Referent   Referent  
   Low/High 68 (19.8) 22 (55.0) 44 (29.1) 3.13 (1.41–6.92) 0.005 4.20 (1.66–10.63) 0.002
   High/Low 41 (12.0) 5 (12.5) 19 (12.6) 1.64 (0.52–5.24) 0.400 1.77 (0.47–6.63) 0.397
   High/High 10 (2.9) 1 (2.5) 13 (8.6) 0.48 (0.06–4.02) 0.499 0.43 (0.04–4.21) 0.472
Trend test     0.021   0.011  
  1. Association was calculated by unconditional logistic regression modeling using good response to antimalarial treatment as the dependent variable. aAdjusted for sex, age, disease duration and clinical parameters: malar rash, discoid lesions, subacute cutaneous lesions, photosensitivity, oral ulcers, arthritis, serositis, renal disorder, neurological disorder, hematological disorder and age at systemic lupus erythematosus (SLE) diagnosis (continuously). CI, confidence interval; OR, odds ratio; TNF, tumor necrosis factor.