IκBα promoter polymorphisms in patients with rheumatoid arthritis

Abstract

To investigate the role of inhibitor of kappaBalpha promoter polymorphisms in the pathogenesis of rheumatoid arthritis (RA), 140 patients with RA and 115 healthy controls were enrolled in this study. The IkappaBalpha promoter polymorphisms were determined using the polymerase chain reaction/restriction fragment length polymorphisms method. In comparison with IkappaBalpha-826 C/C, the genotype frequency of IkappaBalpha-826 C/T was significantly higher in the patients with RA than that of the controls (P = 0.009, OR = 2.0, 95% CI = 1.2-3.4). The allele frequency of IkappaBalpha-826 T was also significantly increased in patients with RA when compared with that of the controls (P = 0.027, OR = 1.6, 95% CI = 1.1-2.4). In comparison with IkappaBalpha-550 A/A, the genotype frequency of IkappaBalpha-550 A/T was significantly decreased in patients with RA when compared with that of the controls (P = 0.02, OR = 0.2, 95% CI = 0.06-0.8). The allele frequency of IkappaBalpha-550 A was significantly increased in patients with RA (P = 0.007, OR = 5.1, 95% = 1.4-18.2). This study also revealed that the IkappaBalpha-826 T -550 A -519 C haplotype was significantly increased in patients with RA in comparison to that of controls (P = 0.01, OR = 1.8, 95% CI = 1.1-2.8). The IkappaBalpha-826 T and -550 A alleles are associated with susceptibility to RA. Moreover, the IkappaBalpha-826 T -550 A -519 C haplotype is associated with susceptibility to RA in Taiwan.

Association of the NFKBIA gene polymorphisms with susceptibility to autoimmune and inflammatory diseases: a meta-analysis

“…Characteristics of studies investigating the association of NFKBIA gene polymorphisms with autoimmune and inflammatory diseases are presented in Table 1 [14][15][16][17][18][19][20][21][22][23][24][25][26][27]. There were 41 papers relevant to the search terms.…”

“…There were 41 papers relevant to the search terms. Through the step of screening the abstract, 27 of these articles were excluded (two were review; four weren't case-control study; three didn't explore NFKBIA gene polymorphism; 18 didn't explore autoimmune and inflammatory diseases), leaving 14 studies [14][15][16][17][18][19][20][21][22][23][24][25][26][27] for full publication review. Of these, the frequencies of alleles and genotypes of three studies were unavailable [15,18,19].…”

“…One of these studies contained data on two different subpopulations and we treated them independently [22]. Four of these studies from the same population contained overlapping data in controls, so we merged them into one study [24][25][26][27]. We selected the largest controls (the study by Lin et al [25]) in these four studies as the controls of the merger study.…”

“…Meta-analysis was performed for NFKBIA gene polymorphisms at positions 2758 (5 studies [14,16,17,20,21] [22,[24][25][26][27]). Eight separate studies were used in the current meta-analysis [14,16,17,[20][21][22][24][25][26][27].…”

“…Eight separate studies were used in the current meta-analysis [14,16,17,[20][21][22][24][25][26][27]. The distribution of the genotype in control population was in Hardy-Weinberg equilibrium in eligible studies (P [ 0.05).…”