Table 3 |
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|
Overall effect estimation of genotypes resulting from the classification of HLA-DRB1 alleles on rheumatoid arthritis susceptibility |
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|
Genotypes |
Genotype distribution, n (%) |
OR (95% CI) |
P values |
|
|
|
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|
RA cases, n = 758 |
Controls, n = 789 |
|||
|
|
||||
|
S2/S3P |
39 (5.1%) |
7 (0.9%) |
7.25 (3.26–16.14) |
<10-5 |
|
S3P/S3P |
74 (9.8%) |
31 (4%) |
5.15 (2.91–9.12) |
<10-5 |
|
S2/S2 |
24 (3.2%) |
8 (1%) |
4.95 (2.2–11.18) |
<10-4 |
|
S2/L |
121 (16%) |
78 (9.9%) |
2.41 (1.60–3.65) |
<10-4 |
|
S3P/L |
179 (23.6%) |
136 (17.2%) |
2.33 (1.57–3.45) |
<10-4 |
|
L/L |
321 (42.3%) |
529 (67%) |
1 |
|
|
|
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|
S1, S2, S3P, S3D, and X allele groups were defined according to the amino acid sequence at positions 70 to 74. According to the approach proposed by Michou and colleagues [9], we pooled the three low-risk allele groups (S1, S3D, and X), so called L alleles. Thus, in subsequent analyses, we considered only three allele groups (S2, S3P, and L alleles), with six corresponding genotypes [12]. The reference genotype is L/L. The combined odds ratios (ORs) and 95% confidence intervals (CIs) evaluate the significance of the global effect of the different HLA-DRB1 genotype groups on rheumatoid arthritis (RA) susceptibility over all population samples. P values were calculated with the Mantel-Haenszel method. |
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|
Barnetche et al. Arthritis Research & Therapy 2008 10:R26 doi:10.1186/ar2379 |
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