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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.