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–463 G/A myeloperoxidase promoter polymorphism in giant cell arteritis
  1. C Salvarani1,
  2. B Casali2,
  3. E Farnetti2,
  4. N Pipitone1,
  5. D Nicoli2,
  6. P L Macchioni1,
  7. L Cimino3,
  8. G L Bajocchi1,
  9. M G Catanoso1,
  10. L Pattacini2,
  11. A Ghinoi1,
  12. G Restuccia1,
  13. L Boiardi1
  1. 1
    Unitè Operativa di Reumatologia, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy
  2. 2
    Laboratorio di Biologia Molecolare, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy
  3. 3
    Unitè Operativa di Oculistica, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy
  1. Carlo Salvarani, Unitè Operativa di Reumatologia, Arcispedale S. Maria Nuova, Viale Risorgimento n 80, Reggio Emilia, 42100, Italy; salvarani.carlo{at}asmn.re.it

Abstract

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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Footnotes

  • Competing interests: None.

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