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Rheumatology Advance Access originally published online on July 12, 2005
Rheumatology 2005 44(10):1299-1302; doi:10.1093/rheumatology/kei013
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Influence of VEGF gene polymorphisms on the severity of ankylosing spondylitis

J. S. Seo, S.-S. Lee1, S. I. Kim2, W. H. Ryu3, K. H. Sa, S. U. Kim, S. W. Han, E. J. Nam, J. Y. Park, W. K. Lee4, S. Y. Kim5 and Y. M. Kang

Department of Internal Medicine, School of Medicine, Kyungpook National University, 1 Chonnam National University, 2 Pusan National University, 3 Chonbuk National University, 4 Health Promotion Research Center and 5 Department of Orthopedic Surgery, School of Medicine, Kyungpook National University, Republic of Korea.

Correspondence to: Y. M. Kang, Department of Internal Medicine, Kyungpook National University Hospital, Samduk 2-Ga, Junggu, Daegu, 700-721, Republic of Korea. E-mail: ymkang{at}knu.ac.kr

Objectives. To investigate the role of polymorphisms of the vascular endothelial growth factor (VEGF) gene in susceptibility to ankylosing spondylitis (AS), and their relationship to clinical features and radiographic severity.

Methods. This study included 157 patients with AS and 140 healthy unrelated controls. Polymorphisms of the VEGF gene were analysed by the polymerase chain reaction (PCR)–restriction fragment length polymorphism assay and amplification refractory mutation system–PCR. Haplotypes were reconstructed using the Bayesian algorithm. Radiographic severity was assessed by the Bath Ankylosing Spondylitis Radiological Index (BASRI).

Results. The genotype frequencies of the polymorphisms were in Hardy–Weinberg equilibrium. The distributions of genotypes and alleles did not differ between AS patients and controls. Among the six haplotypes reconstructed based on the tight linkage disequilibrium at positions –2578, –1154 and –634 (pairwise linkage disequilibrium coefficient, r = 0.361–0.706), no haplotype was associated with susceptibility to AS. Clinical features were analysed for the four haplotypes (CGC, CGG, AAG, AGG) which were prevalent. In carriers of the AGG haplotype, the frequency of cervical spine involvement was significantly higher (P = 0.002, Pcorr = 0.036) and that of patients showing a BASRI score >6 was also higher (P = 0.025, Pcorr = 0.45).

Conclusions. This study demonstrates that polymorphisms of the VEGF gene may contribute to disease severity in AS.

KEY WORDS: Vascular endothelial growth factor, Ankylosing spondylitis, Polymorphism


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