OBJECTIVE: To investigate potential associations between interleukin-10 (IL-10) promoter polymorphisms and susceptibility to, and clinical features of, giant cell arteritis (GCA). METHODS: A total of 140 patients with biopsy-proven GCA who were residents of Reggio Emilia, Italy, and 200 population-based controls from the same geographic area were genotyped for promoter polymorphisms of the IL-10 gene, by molecular methods. The patients were subgrouped according to the presence or absence of polymyalgia rheumatica (PMR) and ischemic complications (any or all of the following: vision loss, jaw claudication, cerebrovascular accidents, or aortic arch syndrome). RESULTS: The distribution of the C/A 592 genotype differed significantly between the GCA patients and the controls (P(corr) = 0.003). Carriers of the A592 allele (A/A or C/A) were significantly more frequent among the GCA patients than among the controls (P(corr) = 0.004, odds ratio [OR] 2.0 [95% confidence interval (95% CI) 1.3-3.1]). Homozygosity for the A592 allele was significantly more frequent among the GCA patients than among the controls (P(corr) = 0.002, OR 3.4 [95% CI 1.6-7.2]). The distribution of the A/G 1082 genotype was similar in GCA patients and controls. In the haplotype analysis, the frequency of the ATA haplotype was significantly higher in GCA patients than in the controls (P = 0.0001), whereas the frequencies of the ACC and GTA haplotypes were significantly lower (P = 0.0001 for both comparisons). No significant associations were found for comparisons of GCA patients with and those without PMR or GCA patients with and those without ischemic complications. CONCLUSION: Our findings show that the -592 C/A promoter polymorphism of the IL-10 gene is associated with susceptibility to GCA.
OBJECTIVE: To investigate potential associations between interleukin-10 (IL-10) promoter polymorphisms and susceptibility to, and clinical features of, giant cell arteritis (GCA). METHODS: A total of 140 patients with biopsy-proven GCA who were residents of Reggio Emilia, Italy, and 200 population-based controls from the same geographic area were genotyped for promoter polymorphisms of the IL-10 gene, by molecular methods. The patients were subgrouped according to the presence or absence of polymyalgia rheumatica (PMR) and ischemic complications (any or all of the following: vision loss, jaw claudication, cerebrovascular accidents, or aortic arch syndrome). RESULTS: The distribution of the C/A 592 genotype differed significantly between the GCA patients and the controls (P(corr) = 0.003). Carriers of the A592 allele (A/A or C/A) were significantly more frequent among the GCA patients than among the controls (P(corr) = 0.004, odds ratio [OR] 2.0 [95% confidence interval (95% CI) 1.3-3.1]). Homozygosity for the A592 allele was significantly more frequent among the GCA patients than among the controls (P(corr) = 0.002, OR 3.4 [95% CI 1.6-7.2]). The distribution of the A/G 1082 genotype was similar in GCA patients and controls. In the haplotype analysis, the frequency of the ATA haplotype was significantly higher in GCA patients than in the controls (P = 0.0001), whereas the frequencies of the ACC and GTA haplotypes were significantly lower (P = 0.0001 for both comparisons). No significant associations were found for comparisons of GCA patients with and those without PMR or GCA patients with and those without ischemic complications. CONCLUSION: Our findings show that the -592 C/A promoter polymorphism of the IL-10 gene is associated with susceptibility to GCA.
Authors: K Cremin; P Leo; J E Harris; E De Smit; L Bradbury; P McKelvie; C L Hill; M A Brown; A W Hewitt Journal: Genes Immun Date: 2014-05-15 Impact factor: 2.676
Authors: Rogelio J Palomino-Morales; Tomas R Vazquez-Rodriguez; Orlando Torres; Inmaculada C Morado; Santos Castañeda; Jose A Miranda-Filloy; Jose L Callejas-Rubio; Benjamin Fernandez-Gutierrez; Miguel A Gonzalez-Gay; Javier Martin Journal: Arthritis Res Ther Date: 2010-03-23 Impact factor: 5.156