title: Influence of anti-tumour necrosis factor therapy on cardiovascular risk factors in patients with active rheumatoid arthritis.
abstract: BACKGROUND
  Tumour necrosis factor (TNF) is known to increase the concentrations of interleukin (IL) 6 and C reactive protein (CRP) and to induce proatherogenic changes in the lipid profile and may increase the cardiovascular risk of patients with rheumatoid arthritis (RA) and other inflammatory disorders.
  
  
  OBJECTIVE
  To assess whether anti-TNF therapy modifies the cardiovascular risk profile in patients with RA.
  
  
  METHODS
  The lipoprotein spectrum and the inflammation markers CRP and IL6 were investigated in 33 patients with RA treated with human anti-TNF monoclonal antibodies (D2E7, adalimumab, Humira) and 13 patients with RA given placebo, before and after 2 weeks' treatment.
  
  
  RESULTS
  In the anti-TNF treated group, the mean (SD) concentrations of HDL-cholesterol were significantly higher after 2 weeks' treatment (0.86 (0.30) mmol/l v 0.98 (0.33) mmol/l, p<0.01), whereas LDL and triglyceride levels were not significantly changed. Additionally, a significant decrease in CRP (86.1 (54.4) mg/l v 35.4 (35.0) mg/l, p<0.0001), and IL6 (88.3 (60.5) pg/ml v 42.3 (40.7) pg/ml, p<0.001) concentrations was seen in this group. No changes in lipid profile, IL6, or CRP levels were seen in the placebo group.
  
  
  CONCLUSIONS
  TNF neutralisation with monoclonal anti-TNF antibodies increased HDL-cholesterol levels and decreased CRP and IL6 levels after 2 weeks. Therefore this treatment may improve the cardiovascular risk profile of patients with RA.
authors.affiliation: Rheumatology Department, UMC St Radboud, Geert Grooteplein 8, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
authors.forename: C
authors.initials: C
authors.lastname: Popa
authors.forename: M G
authors.initials: MG
authors.lastname: Netea
authors.forename: T
authors.initials: T
authors.lastname: Radstake
authors.forename: J W M
authors.initials: JW
authors.lastname: Van der Meer
authors.forename: A F H
authors.initials: AF
authors.lastname: Stalenhoef
authors.forename: P L C M
authors.initials: PL
authors.lastname: van Riel
authors.forename: P
authors.initials: P
authors.lastname: Barerra
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004311:Double-Blind Method; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D002784:Cholesterol; D000068879:Adalimumab