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Cell adhesion molecules and plasminogen activator inhibitor type-1 (PAI-1) in patients with rheumatoid arthritis: influence of metabolic syndrome

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Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory and systemic disease characterized by endothelial activation. The main objective of this study was to verify the profile of cell adhesion molecules (CAM) in RA patients, and the influence of metabolic syndrome (MetS) and drugs used in the treatment of RA in this profile. A second objective was to propose models of prediction of activity in RA using these biomarkers. A total of 115 healthy individuals and 144 RA patients were enrolled. Disease activity was determined by DAS28 (disease activity score 28) based on erythrocyte sedimentation rate (DAS28-ESR) or C-reactive protein (DAS28-CRP). Serum CAM and plasminogen activator inhibitor type-1 (PAI-1), anthropometric and immunological parameters were measured. Vascular cell adhesion molecule-1 (VCAM-1) was significantly decreased, and PAI-1 was significantly higher in RA patients as compared to controls. Binary logistic regression analysis showed that VCAM-1, CRP, and tumor necrosis factor-α (TNF-α) predicted RA with a sensitivity of 95.9% and a specificity of 89.5%. 42.9% of the variance in DAS28-ESR and 49.2% of the variance in DAS28-CRP are explained by increased PAI-1, TNF-α, body mass index (BMI) and decreased platelet endothelial cell adhesion molecule 1 (PECAM-1). Our data show that lower levels of VCAM-1 are associated with RA independently of MetS, while increased PAI-1 levels were associated with both RA and MetS and increased selectins (E-selectin and P-selectin) were exclusively associated with MetS and not with RA. A model to predict disease activity based on PECAM-1, PAI-1, TNF-α, age and BMI is proposed.

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Acknowledgements

This study was supported by the National Council of Brazilian Research-CNPq and by Araucária Foundation from the state of Paraná. We thank the University Hospital of State University of Londrina and HUTec Foundation for technical and administrative supports.

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Authors and Affiliations

  1. Post-Graduate Program in Clinical and Laboratory Pathophysiology, University of Londrina, Londrina, PR, Brazil

    Marcelo Cândido de Sá & Fabiano Aparecido de Medeiros

  2. Department of Pathology, Clinical Analysis and Toxicology, University of Londrina, Robert Koch Avenue, 60, Londrina, PR, CEP 86038-440, Brazil

    Andréa Name Colado Simão, Marcell Alysson Batisti Lozovoy & Edna Maria Vissoci Reiche

  3. Department of Rheumatology, Pontifical Catholic University of Paraná (PUC/PR), Londrina, PR, Brazil

    Tatiana Mayumi Veiga Iriyoda

  4. Department of Rheumatology, University of Londrina, Londrina, PR, Brazil

    Neide Tomimura Costa

  5. Post-Graduate Program in Health Sciences, University of Londrina, Londrina, PR, Brazil

    Daniela Frizon Alfieri & Tamires Flauzino

  6. Post-Graduate Program in Experimental Pathology, University of Londrina, Londrina, PR, Brazil

    Bruno Alexandre Sekiguchi

  7. IMPACT Strategic Research Centre, School of Medicine, Deakin University, Geelong, VIC, Australia

    Michael Maes

  8. Department of Internal Medicine, University of Londrina, Londrina, PR, Brazil

    Isaias Dichi

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  1. Marcelo Cândido de Sá
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  5. Neide Tomimura Costa
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  10. Edna Maria Vissoci Reiche
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  11. Michael Maes
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Correspondence to Andréa Name Colado Simão.

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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards.

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de Sá, M.C., Simão, A.N.C., de Medeiros, F.A. et al. Cell adhesion molecules and plasminogen activator inhibitor type-1 (PAI-1) in patients with rheumatoid arthritis: influence of metabolic syndrome. Clin Exp Med 18, 495–504 (2018). https://doi.org/10.1007/s10238-018-0516-3

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