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Interleukin‐10 promoter polymorphisms in giant cell arteritis

2006; Wiley; Volume: 54; Issue: 12 Linguagem: Inglês

10.1002/art.22218

1529-0131

Luigi Boiardi, Bruno Casali, Enrico Farnetti, Nicolò Pipitone, Davide Nicoli, Pierluigi Macchioni, Luca Cimino, Gianluigi Bajocchi, Mariagrazia Catanoso, Laura Pattacini, Carlo Salvarani,

Systemic Lupus Erythematosus Research

Abstract 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.