No difference between UC and HC. The mutant allele C and genotype TC + CC of FokI were significantly increased in patients with mild and moderate UC compared to severe UC. The frequency of AAC haplotype was statistically lower in UC than HC (AAC haplotype formed by the VDR BsmI, ApaI, and TaqI gene might engender a reduced risk of UC attack)
ApaI: 1024 CD, 974 UC, 1551 HC FokI: 1187 CD, 1221 UC, 1746 HC BsmI: 721 CD, 813 UC, 1642 HC TaqI: 1568 CD, 1515 UC, 2152 HC
VDR: ApaI, TaqI, BsmI, FokI
FokI “ff” genotype associated with a significant risk for UC in Asians; TaqI “tt” genotype associated with an increased risk for CD in Europeans and with an increased risk for CD and UC in Asian males. ApaI “a” allele confers protection from CD
ApaI: 940 CD, 962 UC, 1468 HC FokI: 1098 CD, 1217 UC, 1676 HC BsmI: 713 CD, 799 UC, 1616 HC TaqI: 1553 CD, 1500 UC, 2145 HC
VDR: ApaI, TaqI, BsmI, FokI
ApaI, BsmI, and FokI are not significantly associated with IBD. Significant association between TaqI polymorphism and IBD risk. In subgroups, ApaI increases the overall CD risk and BsmI increases this CD risk only in East Asians, whereas TaqI reduces the risk for UC especially in Caucasians