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Ann Rheum Dis 73:1144-1150 doi:10.1136/annrheumdis-2012-203028
  • Clinical and epidemiological research
  • Extended report

Suppression of inflammation reduces endothelial microparticles in active systemic lupus erythematosus

Open Access
  1. Ian N Bruce1,6
  1. 1Arthritis Research UK Epidemiology Unit, Institute of Inflammation and Repair, Manchester Academic Health Sciences Centre, University of Manchester, Manchester, UK
  2. 2Specialist Assay Laboratory, Central Manchester University Hospitals NHS Foundation Trust, Manchester, UK
  3. 3Kellgren Centre for Rheumatology, Central Manchester University Hospitals NHS Foundation Trust, Manchester, UK
  4. 4Department of Rheumatology, East Lancashire Hospitals NHS Trust, Blackburn, UK
  5. 5Institute for Cardiovascular Science, University of Manchester, Manchester, UK
  6. 6NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK
  1. Correspondence to Professor Ian N Bruce, Arthritis Research UK Epidemiology Unit, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester M13 9PT, UK; ian.bruce{at}manchester.ac.uk
  • Accepted 14 April 2013
  • Published Online First 5 May 2013

Abstract

Background In a prospective observational study, we investigated whether patients with active systemic lupus erythematosus (SLE) had higher indices of endothelial damage and dysfunction than healthy controls and whether improved disease control was associated with improvement in these indices.

Methods Twenty-seven patients with active SLE (four or more American College of Rheumatology (ACR) criteria) and 22 age-matched controls were assessed. Endothelial microparticles (EMPs; CD31+/annexin V+/CD42b−) were quantified using flow cytometry. Brachial artery flow-mediated dilatation (FMD) was measured using automated edge-tracking software. Twenty-two patients had a second assessment at a median (IQR) of 20 (16, 22) weeks after initiating new immunosuppressive therapy.

Results SLE patients had a median (IQR) baseline global British Isles Lupus Assessment Group Disease Activity Index (BILAG-2004) score of 14 (12, 22). CD31+/annexin V+/CD42b− EMPs were higher (157 548/ml (59 906, 272 643) vs 41 025(30 179, 98 082); p=0.003) and endothelial-dependent FMD was lower (1.63% (−1.22, 5.32) vs 5.40% (3.02, 8.57); p=0.05) in SLE patients than controls. CD31+/annexin V+/CD42b− EMPs correlated inversely with FMD (%) (r2 −0.40; p=0.006). At follow-up, the median (IQR) change in global BILAG-2004 score was −11 (−18, −3). CD31+/annexin V+/CD42b− EMP levels were reduced (166 982/ml (59 906, 278 775 vs 55 655(29 475, 188 659; p=0.02) and FMD had improved (0.33% (−2.31, 4.1) vs 3.19% (0.98, 5.09); p=0.1) at the second visit.

Conclusions Active SLE is associated with evidence of increased endothelial damage and endothelial dysfunction, which improved with suppression of inflammation. Better control of active inflammatory disease may contribute to improved cardiovascular risk in patients with SLE.

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