TY - JOUR
T1 - Inflammatory and prothrombotic biomarkers in patients with rheumatoid arthritis
T2 - Effects of tumor necrosis factor-α blockade
AU - Ingegnoli, Francesca
AU - Fantini, Flavio
AU - Favalli, Ennio Giulio
AU - Soldi, Amedeo
AU - Griffini, Samantha
AU - Galbiati, Valentina
AU - Meroni, Pier Luigi
AU - Cugno, Massimo
PY - 2008/9
Y1 - 2008/9
N2 - Objective: Increased cardiovascular (CV) risk is a rheumatoid arthritis (RA) hallmark and it has been mainly related to chronic systemic inflammation. Since inflammation is linked to coagulation perturbation, both may play a role in increasing CV risk. Treatment with tumor necrosis factor (TNF)-α blocking agents is effective in RA and reduces local and systemic inflammation but there is little information on its effect on coagulation. We therefore investigated inflammation and coagulation plasma biomarkers before and after infliximab treatment in RA patients. Methods: We studied 20 patients with active RA and 40 healthy controls. Patients were treated with: a stable dose of methotrexate (10 mg/week), and infliximab (3 mg/kg) at weeks 0, 2, 6 and 14. At baseline and week 14, we determined: disease activity score (DAS-28), visual analogue scale pain, erythrocyte sedimentation rate (ESR), and plasma levels of C-reactive protein (CRP), TNF-α, interleukin (IL)-6, prothrombin fragment 1 + 2 (F1 + 2) and D-dimer. The same inflammation and coagulation parameters were evaluated 1 h after infliximab infusion in 10 patients. Results: At baseline, ESR, CRP, TNF-α, IL-6, F1 + 2 and D-dimer levels were significantly higher in RA patients than in controls (P = 0.0001). After 14 weeks of infliximab treatment, there was a significant clinical improvement and ESR and CRP, IL-6, F1 + 2 and D-dimer level decrease (P = 0.001-P = 0.008). The levels of TNF-α, IL-6, F1 + 2 and D-dimer significantly decreased 1 h after infliximab infusion (P = 0.005). Conclusions: Infliximab decreases inflammation and coagulation biomarkers in RA patients. Such a combined effect may be pivotal in reducing the whole thrombotic risk in these patients.
AB - Objective: Increased cardiovascular (CV) risk is a rheumatoid arthritis (RA) hallmark and it has been mainly related to chronic systemic inflammation. Since inflammation is linked to coagulation perturbation, both may play a role in increasing CV risk. Treatment with tumor necrosis factor (TNF)-α blocking agents is effective in RA and reduces local and systemic inflammation but there is little information on its effect on coagulation. We therefore investigated inflammation and coagulation plasma biomarkers before and after infliximab treatment in RA patients. Methods: We studied 20 patients with active RA and 40 healthy controls. Patients were treated with: a stable dose of methotrexate (10 mg/week), and infliximab (3 mg/kg) at weeks 0, 2, 6 and 14. At baseline and week 14, we determined: disease activity score (DAS-28), visual analogue scale pain, erythrocyte sedimentation rate (ESR), and plasma levels of C-reactive protein (CRP), TNF-α, interleukin (IL)-6, prothrombin fragment 1 + 2 (F1 + 2) and D-dimer. The same inflammation and coagulation parameters were evaluated 1 h after infliximab infusion in 10 patients. Results: At baseline, ESR, CRP, TNF-α, IL-6, F1 + 2 and D-dimer levels were significantly higher in RA patients than in controls (P = 0.0001). After 14 weeks of infliximab treatment, there was a significant clinical improvement and ESR and CRP, IL-6, F1 + 2 and D-dimer level decrease (P = 0.001-P = 0.008). The levels of TNF-α, IL-6, F1 + 2 and D-dimer significantly decreased 1 h after infliximab infusion (P = 0.005). Conclusions: Infliximab decreases inflammation and coagulation biomarkers in RA patients. Such a combined effect may be pivotal in reducing the whole thrombotic risk in these patients.
KW - Coagulation
KW - Infliximab
KW - Rheumatoid arthritis
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U2 - 10.1016/j.jaut.2008.07.002
DO - 10.1016/j.jaut.2008.07.002
M3 - Article
C2 - 18707846
AN - SCOPUS:50849086145
VL - 31
SP - 175
EP - 179
JO - Journal of Autoimmunity
JF - Journal of Autoimmunity
SN - 0896-8411
IS - 2
ER -