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Ann Rheum Dis 2006;65:952-954 doi:10.1136/ard.2005.043562
  • Concise report

Low plasma protein nitrotyrosine levels distinguish primary Raynaud’s phenomenon from scleroderma

  1. E J Kingdon1,
  2. A R Mani2,
  3. M T Frost3,
  4. C P Denton3,
  5. S H Powis1,
  6. C M Black3,
  7. K P Moore2
  1. 1Royal Free and University College Medical School, University College London, UK
  2. 2The UCL Institute of Hepatology, University College London, UK
  3. 3Centres for Nephrology and Rheumatology, University College London, UK
  1. Correspondence to:
    Professor K P Moore
    The UCL Institute of Hepatology, Royal Free and University College Medical School, University College London (UCL), Rowland Hill Street, London NW3 2PF, UK; kmoore{at}medsch.ucl.ac.uk
  • Accepted 18 November 2005
  • Published Online First 24 November 2005

Abstract

Objective: To investigate the hypothesis that increased formation of reactive nitrogen species may contribute to the vascular pathology that develops in patients with connective tissue disease such as scleroderma.

Patients and methods: The level of protein-bound nitrotyrosine in plasma was measured by stable isotope dilution gas chromatography/negative ion chemical ionisation mass spectrometry in 11 patients with primary Raynaud’s phenomenon, 37 with scleroderma, 13 with chronic renal impairment, and in 23 healthy controls.

Results: Plasma protein-bound nitrotyrosine was markedly decreased in patients with primary Raynaud’s phenomenon (mean (SEM) 0.60 (0.06) ng/mg dry protein) compared with patients with scleroderma (1.78 (0.21) ng/mg protein), chronic renal impairment (1.42 (0.17) ng/mg protein) or healthy controls (1.63±0.15 ng/mg protein, ANOVA p<0.001).

Conclusion: These data suggest that there is decreased nitration of plasma proteins, or increased degradation of nitrated proteins from the circulation of patients with primary but not secondary Raynaud’s phenomenon.

Footnotes

  • Published Online First 24 November 2006

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