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

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

SNP	ROR_i(95%CI)	P	SNP carriers	SNP noncarriers	Anti-CCP⁺patients
SNP	ROR_i(95%CI)	P	OR_PTPN22(95% CI)	OR_PTPN22(95%CI)	ROR_i(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

^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; ROR_i, Ratio of odds ratios of the interaction.

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