Impact of short-term therapies with biologics on prothrombotic biomarkers in rheumatoid arthritis

Clin Exp Rheumatol. May-Jun 2009;27(3):491-4.


Background: Imbalance of haemostasis in patients with rheumatoid arthritis (RA) contributes to future risk of cardiovascular diseases (CVD). Prothrombotic molecules, e.g. fibrinogen, D-dimer, and tPA are elevated in plasma of RA patients, being associated to CVD. There is no imformation about the influence of biological drugs, e.g. anti-CD20 and tumor necrosis factor (TNF) antibodies on these prothrombotic molecules.

Objective: To assess whether anti-TNF and anti-CD20 therapies modify the profiles of cardiovascular risk factors in patients with RA.

Methods: The expression of prothrombotic molecules in plasma was investigated in 10 RA patients before and after treatment with TNF-alpha antibodies and in another 12 RA patients before and after anti-CD20 treatment.

Results: Both anti-TNF and anti-CD20 infusions gave rise to clear clinical improvement. However, only anti-CD20 infusion significantly (p=0.05) reduced concentration of fibrinogen (p=0.05), D-dimer (p<0.001), as well as tPA levels (p<0.01). In contrast, in TNF antibody treated patients only tPA levels were significantly decreased following the treatment (p<0.05).

Conclusions: Infusion of CD20 antibodies to the patients with active RA led to a clearly reduced plasma levels of predictors of CVD indicating that this treatment, apart from its anti-inflammatory properties, may reduce the risk for future CVD in RA.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antibodies / therapeutic use
  • Antibodies, Monoclonal / therapeutic use*
  • Antibodies, Monoclonal, Murine-Derived
  • Antigens, CD20 / immunology
  • Antirheumatic Agents / therapeutic use
  • Arthritis, Rheumatoid / blood*
  • Arthritis, Rheumatoid / drug therapy*
  • C-Reactive Protein / metabolism
  • Cardiovascular Diseases
  • Dose-Response Relationship, Drug
  • Female
  • Fibrin Fibrinogen Degradation Products / metabolism*
  • Fibrinogen / metabolism*
  • Humans
  • Infliximab
  • Male
  • Middle Aged
  • Plasminogen Activator Inhibitor 1 / blood*
  • Risk Factors
  • Rituximab
  • Tissue Plasminogen Activator / blood*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / immunology


  • Antibodies
  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Murine-Derived
  • Antigens, CD20
  • Antirheumatic Agents
  • Fibrin Fibrinogen Degradation Products
  • Plasminogen Activator Inhibitor 1
  • Tumor Necrosis Factor-alpha
  • fibrin fragment D
  • Rituximab
  • Fibrinogen
  • C-Reactive Protein
  • Infliximab
  • Tissue Plasminogen Activator