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Cell adhesion molecules and plasminogen activator inhibitor type-1 (PAI-1) in patients with rheumatoid arthritis: influence of metabolic syndrome
Authors:Marcelo Cândido de Sá  Andréa Name Colado Simão  Fabiano Aparecido de Medeiros  Tatiana Mayumi Veiga Iriyoda  Neide Tomimura Costa  Daniela Frizon Alfieri  Tamires Flauzino  Bruno Alexandre Sekiguchi  Marcell Alysson Batisti Lozovoy  Edna Maria Vissoci Reiche  Michael Maes  Isaias Dichi
Affiliation:1.Post-Graduate Program in Clinical and Laboratory Pathophysiology,University of Londrina,Londrina,Brazil;2.Department of Pathology, Clinical Analysis and Toxicology,University of Londrina,Londrina,Brazil;3.Department of Rheumatology,Pontifical Catholic University of Paraná (PUC/PR),Londrina,Brazil;4.Department of Rheumatology,University of Londrina,Londrina,Brazil;5.Post-Graduate Program in Health Sciences,University of Londrina,Londrina,Brazil;6.Post-Graduate Program in Experimental Pathology,University of Londrina,Londrina,Brazil;7.IMPACT Strategic Research Centre, School of Medicine,Deakin University,Geelong,Australia;8.Department of Internal Medicine,University of Londrina,Londrina,Brazil
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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