Skip to main content

Table 3 Lack of replication of epistasisa as the described by Briggs et al. [22]

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

SNP RORi(95%CI) P SNP carriers SNP noncarriers Anti-CCP+patients
OR PTPN22 (95% CI) OR PTPN22 (95%CI) RORi(95% CI) P
rs7726839 1.08 (0.75 to 1.55) 0.70 1.56 (1.18 to 2.07) 1.45 (1.15 to 1.83) 1.23 (0.8 to 1.9) 0.34
rs12573019 0.74 (0.49 to 1.12) 0.15 1.19 (0.83 to 1.71) 1.61 (1.31 to 1.98) 0.63 (0.38 to 1.04) 0.07
rs1168587 0.84 (0.58 to 1.22) 0.35 1.40 (1.11 to 1.76) 1.68 (1.24 to 2.24) 0.92 (0.59 to 1.43) 0.71
rs1895535 0.66 (0.36 to 1.20) 0.17 1.02 (0.58 to 1.80) 1.56 (1.25 to 1.92) 0.84 (0.39 to 1.8) 0.66
rs7200573 1.14 (0.8 to 1.63) 0.47 1.60 (1.24 to 2.07) 1.40 (1.10 to 1.80) 1.26 (0.82 to 1.93) 0.28
rs11865624 1.15 (0.68 to 1.94) 0.59 1.69 (1.04 to 2.75) 1.47 (1.21 to 1.78) 1.35 (0.72 to 2.53) 0.36
  1. aData show lack of replication between the six single-nucleotide polymorphisms (SNPs) and the PTPN22 rheumatoid arthritis (RA) locus in the whole set of RA patients and controls (left) and in the comparison of anti–cyclic citrullinated peptide–positive (anti-CCP+) patients with controls (last two columns on the right). PTPN22, Protein tyrosine phosphatase nonreceptor type 22; RORi, Ratio of odds ratios of the interaction.