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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.