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TNF-related apoptosis-inducing ligand and cardiovascular disease in rheumatoid arthritis

Patrick H Dessein1, Raquel Lopez-Mejias2, Begona Ubilla2

  • 1Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.

Clinical and Experimental Rheumatology
|May 13, 2015
PubMed

Insights

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) levels are lower in rheumatoid arthritis (RA) patients and linked to heart failure, independent of cardiovascular risk factors. Osteoprotegerin (OPG) may directly increase cardiovascular disease (CVD) risk in RA.

Area of Science:

  • Immunology
  • Rheumatology
  • Cardiology

Background:

  • Rheumatoid arthritis (RA) is associated with increased cardiovascular disease (CVD) risk.
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plays a role in immune regulation and apoptosis.
  • Osteoprotegerin (OPG) can act as a decoy receptor for TRAIL and has been linked to CVD in RA.

Purpose of the Study:

  • To investigate the association between TRAIL concentrations and CVD in RA patients.
  • To determine if TRAIL influences the previously documented relationship between OPG levels and atherosclerotic CVD in RA.
  • To explore the relationship between TRAIL, heart failure (HF), and C-reactive protein (CRP) in RA.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to measure TRAIL concentrations in 151 RA patients and 62 controls.
  • RA patients included those with ischaemic heart disease, cerebrovascular accident, peripheral artery disease, and/or HF.
  • Statistical analyses, including mixed regression models, were performed to assess associations, adjusting for relevant factors.

Main Results:

  • TRAIL concentrations were significantly lower in RA patients compared to controls (p<0.0001).
  • In RA patients, TRAIL levels were associated with CRP and cholesterol-HDL ratio.
  • TRAIL levels were higher in RA patients with HF compared to those without (p=0.02), an association mediated by CRP.
  • TRAIL concentrations were not related to atherosclerotic CVD, and the OPG-CVD association persisted after adjusting for TRAIL.

Conclusions:

  • TRAIL concentrations are reduced in established RA and associated with HF, with CRP levels explaining this relationship.
  • The previously observed association between OPG and atherosclerotic CVD in RA remains significant, suggesting OPG may directly contribute to CVD risk.
  • TRAIL does not appear to mediate the OPG-CVD link in RA.
Abstract

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