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. 2013 Aug 14;19(30):4935–4943. doi: 10.3748/wjg.v19.i30.4935

Table 4.

Inflammatory bowel disease-phenotypes were investigated by performing family-based and case-control approach in genetic association studies

rs7620166 (CLDN1)
rs12014762 (CLDN2)
rs8629 (CLDN4)
allelic OR (95%CI) P value allelic OR (95%CI) P value allelic OR (95%CI) P value
IBD Swedish case-control 1.33 (1.04-1.72) 0.025 1.39 (0.95-2.01) 0.083 1.21 (0.89-1.65) 0.225
Non-Swedish families 0.87 (0.72-1.06) 0.177 1.25 (0.89-1.77) 0.195 1.09 (0.88-1.33) 0.432
CD Swedish case-control 1.17 (0.86-1.60) 0.319 1.98 (1.17-3.35) 0.007 1.25 (0.84-1.85) 0.258
Non-Swedish families 0.80 (0.64-1.00) 0.052 1.37 (0.91-2.07) 0.126 1.14 (0.89-1.46) 0.287
UC Swedish case-control 1.35 (0.98-1.84) 0.064 1.27 (0.80-2.02) 0.304 1.18 (0.80-1.73) 0.409
Non-Swedish families 1.19 (0.77-1.84) 0.436 0.91 (0.39-2.14) 0.827 1.15 (0.75-1.77) 0.512

The family-based association studies included a total of 463 families. For the single nucleotide polymorphism -markers rs7620166 [claudin (CLDN)1], rs12014762 (CLDN2) and rs8629 (CLDN4) genotyping failed for 5 [including 2 Crohn’s disease (CD)], 9 (including 3 CD) and 7 (including 2 CD) samples, respectively. Results were based on 191, 103 and 102 cases of inflammatory bowel disease (IBD), CD and ulcerative colitis (UC), respectively and 333 controls. OR (and its associated 95%CI) and P values (based on log likelihood ratio χ2 statistics) were calculated for the T allele of rs7620166, the C allele of rs12014762, and the C allele of rs8629.