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Table 2 Association of polymorphisms with rheumatoid arthritis or anti–cyclic citrullinated peptide–positive rheumatoid arthritis a

From: Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case–control study

 

RA patients

Controls

  

SNP

Genotype counts

MAF

Genotype counts

MAF

P

OR (95% CI)

PTPN22 rs2476601

1,383/325/35

0.11

1,405/235/10

0.08

4.61 × 10−7

1.53 (1.29 to 1.8)

rs7726839

1,012/631/100

0.24

959/592/88

0.23

ns

1.02 (0.91 to 1.14)

rs12573019

1,302/405/37

0.14

1,264/359/27

0.13

ns

1.11 (0.97 to 1.28)

rs1168587

652/830/260

0.39

612/762/276

0.40

ns

0.97 (0.87 to 1.05)

rs1895535

1,602/138/4

0.04

1,503/137/7

0.05

ns

0.91 (0.72 to 1.15)

rs7200573

940/687/116

0.26

890/633/127

0.27

ns

0.97 (0.87 to 1.08)

rs11865624

1,532/201/10

0.06

1,424/221/3

0.07

ns

0.92 (0.76 to 1.11)

 

Anti-CCP + patients

Anti-CCP patients

  
 

Positive/negative

 

Positive/negative

   

SE

279/174b

 

116/153b

 

1.69 × 10−6

2.11 (1.56 to 2.88)

GSTM1

402/376c

186/192c

ns

1.10 (0.86 to 1.41)

  1. aComparison of patients with rheumatoid arthritis (RA) and healthy controls for the single-nucleotide polymorphisms (SNPs) from Briggs et al.[22] in the upper rows and comparison between anti–cyclic citrullinated peptide–positive (anti-CCP+) and anti-CPP RA patients for shared epitope (SE) and glutathione S-transferase Mu 1 (GSTM1) in the lower rows. MAF, Minor allele frequency; ns, Not significant; PTPN22, Protein tyrosine phosphatase nonreceptor type 22. bPositive, SE carrier; negative, SE non-carrier. cPositive, native carrier; negative, null homozygote.