Table 1 Results of association analyses of gout.

From: Integrative Genome-Wide Association Studies of eQTL and GWAS Data for Gout Disease Susceptibility

SNP

Chr

Allele 1/2a

Stage

Cases

Controls

Additiveb

Dominantb

Recessiveb

Phet

11

12

22

RAF

11

12

22

RAF

P-value

Risk allele OR (95% CI)

P-value

Risk allele OR (95% CI)

P-value

Risk allele OR (95% CI)

rs2231142

4

T/G

Discovery

82

181

110

0.46

630

2885

3200

0.31

4.25e-18

2.00

5.27e-11

2.18

2.66e-15

3.00

0.9644

Follow-up

78

197

109

0.46

696

3202

3538

0.31

1.498e-18

1.99

2.86e-13

2.366

2.96e-12

2.65

Combinedc

160

378

219

0.46

1326

6087

6738

0.31

5.06e-35

2.00

1.10e-22

2.27

6.50e-26

2.82

rs4148155

4

G/A

Discovery

82

181

110

0.46

633

2889

3195

0.31

5.49e-18

2.00

6.27e-11

2.17

3.16e-15

2.99

0.9893

Follow-up

79

197

109

0.46

702

3204

3536

0.31

8.593e-19

2.00

2.65e-13

2.37

1.29e-12

2.68

Combinedc

161

378

219

0.46

1335

6093

6731

0.31

3.74e-35

2.00

1.21e-22

2.27

3.29e-26

2.83

rs2725211

4

T/C

Discovery

48

153

172

0.33

386

2418

3900

0.24

3.42e-09

1.64

8.52e-06

1.63

9.38e-09

2.69

0.9417

Follow-up

45

168

172

0.34

426

2764

4244

0.24

3.78e-09

1.62

1.22e-06

1.69

9.96e-07

2.35

Combinedc

93

321

344

0.33

812

5182

8144

0.24

6.88e-17

1.63

4.75e-11

1.66

5.43e-14

2.52

rs2905274

7

A/G

Discovery

12

80

279

0.14

44

1027

5640

0.083

3.91e-08

1.87

2.46e-06

1.84

4.19e-06

5.21

0.0041

Follow-up

5

71

306

0.11

58

1231

6138

0.091

0.26

1.15

0.34

1.14

0.2829

1.69

Combinedc

17

151

585

0.12

102

2258

11778

0.087

1.46e-06

1.50

4.81e-05

1.46

1.42e-05

3.50

  1. We analyzed 758 gout cases (in the GWAS and in replication) and 14,166 controls (6,721 in the GWAS and 7,445 in replication). Chr., chromosome; RAF, risk allele frequency. aAllele 1, risk allele; allele 2, non-risk allele. bP values and ORs were calculated by logistic regression analysis, with age, gender, and 10 principal components as covariates. Non-risk alleles were considered as references in the three genetic models: additive, 1 versus 2; recessive, 11 versus 12 + 22; dominant, 11 + 12 versus 22. Heterogeneity across the two stages was examined by Cochran Q test under a genetic model which provided the minimum P value in the screening stage. cORs and P values were calculated using the Mantel-Haenszel fixed-effects model.