title: Impact of short-term therapies with biologics on prothrombotic biomarkers in rheumatoid arthritis.
abstract: 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.
authors: Department of Rheumatology and Inflammation Research, Sahlgrenska University Hospital, S-413 46 Göteborg, Sweden. tao.jin@rheuma.gu.se
authors: T
authors: T
authors: Jin
authors: M
authors: M
authors: Bokarewa
authors: S
authors: S
authors: Amu
authors: A
authors: A
authors: Tarkowski
mesh_terms: D000328:Adult; D000368:Aged; D000906:Antibodies / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D058846:Antibodies, Monoclonal, Murine-Derived; D018951:Antigens, CD20 / Q000276:immunology; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy*; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases; D004305:Dose-Response Relationship, Drug; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism*; D005340:Fibrinogen / Q000378:metabolism*; D006801:Humans; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D012307:Risk Factors; D000069283:Rituximab; D010959:Tissue Plasminogen Activator / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000276:immunology
chemical_list: D000906:Antibodies; D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D018951:Antigens, CD20; D018501:Antirheumatic Agents; D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; D014409:Tumor Necrosis Factor-alpha; C036309:fibrin fragment D; D000069283:Rituximab; D005340:Fibrinogen; D002097:C-Reactive Protein; D000069285:Infliximab; D010959:Tissue Plasminogen Activator