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Platelet activation, as measured by plasma soluble glycoprotein VI, is not associated with disease activity or ischaemic events in giant cell arteritis
  1. Richard Conway1,2,
  2. Anne Madigan1,
  3. Niamh Redmond3,
  4. Laura Helbert1,
  5. Eamonn S Molloy4,
  6. Eimear Dunne5,
  7. Dermot Kenny5,
  8. Geraldine McCarthy1
  1. 1Department of Rheumatology, Mater Misericordiae University Hospital, Dublin Academic Medical Centre, Dublin, Ireland
  2. 2CARD Newman Research Fellow, University College Dublin, Dublin, Ireland
  3. 3Clinical Research Centre, Mater Misericordiae University Hospital, Dublin Academic Medical Centre, Dublin, Ireland
  4. 4Centre for Arthritis and Rheumatic Diseases, Dublin Academic Medical Centre, St Vincent’s University Hospital, Dublin, Ireland
  5. 5Cardiovascular Biology and Clinical Research Centre, Royal College of Surgeons in Ireland, Dublin, Ireland
  1. Correspondence to Dr Richard Conway, Department of Rheumatology, Mater Misericordiae University Hospital, Dublin Academic Medical Centre, Dublin D07 R2WY, Ireland; drrichardconway{at}gmail.com

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Giant cell arteritis (GCA) is associated with cranial ischaemic complications (CIC) including vision loss and stroke.1 British Society of Rheumatology and European League against Rheumatism guidelines recommend platelet inhibition with aspirin for most patients with GCA; on the basis of two retrospective studies showing a reduction in CICs, these results were not replicated in two other retrospective studies.2 3 There are no data from prospective or randomised controlled trials to support aspirin use in GCA.4 The glycoprotein VI (GPVI) receptor is found exclusively on platelets and megakaryocytes.5 GPVI is proteolytically cleaved following platelet activation and is detectable in plasma as soluble GPVI (sGPVI).6 Elevated plasma sGPVI signifies platelet activation and an increased risk of cardiovascular events.7 We have recently demonstrated enhanced platelet reactivity as measured by sGPVI in gout and rheumatoid arthritis, …

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