Ann Rheum Dis

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Published Online First: 17 August 2007. doi:10.1136/ard.2007.074666
Annals of the Rheumatic Diseases 2008;67:485-488
Copyright © 2008 BMJ Publishing Group Ltd & European League Against Rheumatism

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EXTENDED REPORTS

–463 G/A myeloperoxidase promoter polymorphism in giant cell arteritis

C Salvarani 1, B Casali 2, E Farnetti 2, N Pipitone 1, D Nicoli 2, P L Macchioni 1, L Cimino 3, G L Bajocchi 1, M G Catanoso 1, L Pattacini 2, A Ghinoi 1, G Restuccia 1, L Boiardi 1

1 Unitè Operativa di Reumatologia, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy
2 Laboratorio di Biologia Molecolare, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy
3 Unitè Operativa di Oculistica, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy

Correspondence to:
Carlo Salvarani, Unitè Operativa di Reumatologia, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy; salvarani.carlo{at}asmn.re.it

Objective: To investigate potential associations between–463 G/A myeloperoxidase (MPO) promoter polymorphism and susceptibility to, and clinical features of giant cell arteritis (GCA).

Methods: A total of 156 patients with biopsy-proven GCA who were residents of Reggio Emilia, Italy, and 235 population-based controls from the same geographic area were genotyped for–463 G/A promoter polymorphism of the MPO gene by molecular methods. The patients were subgrouped according to the presence or absence of polymyalgia rheumatica and severe ischaemic complications (visual loss and/or cerebrovascular accidents).

Results: The distribution of the MPO-G/A genotype differed significantly between patients with GCA and the controls (pcorr = 0.003). Allele G was significantly more frequent in patients with GCA than in the controls (pcorr = 0.0002, OR 2.0, 95% CI 1.4 to 2.9). Homozygosity for the G allele was significantly more frequent in patients with GCA than in controls (pcorr = 0.0002, OR 2.2, 95% CI 1.4 to 3.4). No significant associations were found when patients with GCA with and without polymyalgia rheumatica or with and without severe ischaemic complications were compared.

Conclusions: Our findings show that the–463 G/A promoter polymorphism of the MPO gene is associated with GCA susceptibility and support a role for MPO in the pathophysiology of GCA.








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