title: Modulation of lipoprotein plasma concentrations during long-term anti-TNF therapy in patients with active rheumatoid arthritis.
abstract: OBJECTIVE
  Durable blockade of tumour necrosis factor-alpha (TNF-alpha) in patients with rheumatoid arthritis (RA) suppresses disease activity and its progression. Cardiovascular diseases are 1.5-2-fold more frequent in RA patients than in the general population. Although TNF-alpha has well-established effects on lipid metabolism, the long-term effects of TNF-alpha blockade on lipid pattern are still unclear. In the present study, we investigated the effects of 1-year therapy with anti-TNF on the lipid profile of RA patients.
  
  
  METHODS
  Disease activity (DAS28) and plasma lipoproteins concentrations (total, HDL and LDL-cholesterol, triglycerides, ApoA, ApoB) were assessed in 55 RA patients and 55 controls. The whole RA group was followed up for 6 months, and 31 of the patients were followed up for 1 year.
  
  
  RESULTS
  In RA patients, DAS28 decreased after 2 weeks from the start of therapy (p<0.001) and remained low during the entire study duration. Short-term effects of anti-TNF on plasma lipid concentrations seemed beneficial and anti-atherogenic. However, these changes did not persist: plasma concentrations of total and LDL-cholesterol and the atherogenic index increased after 6 months and 1 year from the start of therapy. During therapy, the changes in disease activity and inflammatory status were inversely correlated with changes in plasma total and HDL cholesterol levels and positively correlated with the variation of atherogenic index.
  
  
  CONCLUSIONS
  We conclude that one-year therapy with infliximab is likely to lead to a more pro-atherogenic pattern of the plasma lipids concentrations. However, the overall impact of these changes on the cardiovascular risk is more complex, considering the strong anti-inflammatory effects of anti-TNF drugs.
authors.affiliation: Department of General Internal Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. c.popa@aig.umcn.nl
authors.forename: Calin
authors.initials: C
authors.lastname: Popa
authors.forename: Frank H J
authors.initials: FH
authors.lastname: van den Hoogen
authors.forename: Timothy R D J
authors.initials: TR
authors.lastname: Radstake
authors.forename: Mihai G
authors.initials: MG
authors.lastname: Netea
authors.forename: Agnes E
authors.initials: AE
authors.lastname: Eijsbouts
authors.forename: Martin
authors.initials: M
authors.lastname: den Heijer
authors.forename: Jos W M
authors.initials: JW
authors.lastname: van der Meer
authors.forename: Piet L C M
authors.initials: PL
authors.lastname: van Riel
authors.forename: Anton F H
authors.initials: AF
authors.lastname: Stalenhoef
authors.forename: Pilar
authors.initials: P
authors.lastname: Barrera
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000494:pharmacology* / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy; D001799:Blood Sedimentation; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D000069285:Infliximab; D008074:Lipoproteins / Q000097:blood* / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D008076:Cholesterol, HDL; D008074:Lipoproteins; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol; D000069285:Infliximab