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MCP-1 Gene Haplotype Association in Biopsy Proven Giant Cell Arteritis
MAHSA M. AMOLI, FIONA SALWAY, ELEFTHERIA ZEGGINI, WILLIAM E.R. OLLIER, and MIGUEL A. GONZALEZ-GAY
ABSTRACT. Objective. Giant cell arteritis (GCA) is the most frequent vasculitis in European and North American countries. Increased expression of monocyte chemoattractant protein 1 (MCP-1) has been observed within the inflammatory infiltrates of blood vessels and serum of patients with GCA and in other autoimmune and inflammatory conditions. MCP-1 gene polymorphisms have been reported to contribute to susceptibility to several immune and inflammatory conditions. To investigate the clinical implication of MCP-1 polymorphisms in GCA, we examined the association of 3 single nucleotide polymorphisms (SNP) in a series of patients with GCA from Northwest Spain. Methods. Seventy-nine patients with biopsy proven GCA and 99 ethnically matched controls were studied. Patients and controls were genotyped for MCP-1 polymorphisms. SNP included in this study (rs2857657, rs4586, rs139000) were located in intron 1(G/C), exon 2(T/C), and 3'UTR(C/T) region of MCP-1 gene. Results. The distribution of the alleles and genotypes for each MCP-1 polymorphism showed no significant differences between GCA patients and controls. When we compared the overall distribution of haplotype frequencies between GCA cases and controls a significant difference was observed (p = 0.005, by chi-square test from 4 ´ 2 contingency table). In addition, haplotype C-C was significantly increased in GCA patients compared with controls (p = 0.03, OR 2.09, 95% CI 1.09–4.02). Similarly, haplotype T-T was overrepresented in GCA patients (p = 0.005). Conclusion. Significant differences in haplotype frequencies between GCA patients and controls may indicate a role for MCP-1 gene in susceptibility to GCA. (J Rheumatol 2005;32:507-10) Key Indexing Terms:
GIANT CELL ARTERITIS
From the Centre for Integrated Genomic Medical Research, School of Epidemiology and Health Sciences, the University of Manchester, Manchester, United Kingdom; and Division of Rheumatology, Hospital Xeral-Calde, Lugo, Spain. M.M. Amoli, MD, PhD; F. Salway, MPhil; E. Zeggini, PhD; W.E.R. Ollier, PhD, FRCPath, Centre for Integrated Genomic Medical Research, School of Epidemiology and Health Sciences, University of Manchester; M.A. Gonzalez-Gay, MD, PhD, Rheumatology Division, Hospital Xeral-Calde. Address reprint requests to Dr. M.A. Gonzalez-Gay, Rheumatology Division, Hospital Xeral-Calde, c) Dr. Ochoa s/n, 27004 Lugo, Spain. E-mail: miguelaggay@hotmail.com Submitted November 25, 2003; revision accepted November 19, 2004. |