title: The Impact of Newer Biological Disease Modifying Anti-Rheumatic Drugs on Cardiovascular Risk Factors: A 12-Month Longitudinal Study in Rheumatoid Arthritis Patients Treated with Rituximab, Abatacept and Tociliziumab.
abstract: OBJECTIVE
  To assess whether treatment with one of three novel biological DMARDs; rituximab, abatacept or tocilizumab reduce cardiovascular disease (CVD) risk factors in patients with rheumatoid arthritis (RA).
  
  
  METHODS
  This is an open, observational and prospective study with visits at baseline, 3, 6, and 12 months. Patients were assigned to receive rituximab, abatacept or tocilizumab according to clinical indications assessed by an independent rheumatologist. Disease activity was quantified by the disease activity score (DAS28) and extensive ultrasonography. CVD risk was assessed by total cholesterol (TC), high-density lipoprotein cholesterol (HDL-c), blood pressure and arterial stiffness measurements [pulse wave velocity (PWV) and augmentation index (AIx)]. Within group change in disease activity and CVD risk over 3 months was explored using paired samples bivariate tests. Predictors of change in CVD risk at 3 months were identified in linear regression models. Changes in CVD risk markers over the 12- month follow-up in patients receiving rituximab were assessed by mixed models repeated analyses.
  
  
  RESULTS
  24 patients on rituximab, 5 on abatacept and 7 on tocilizumab were included. At 3 months PWV was significantly reduced in the tocilizumab group only, but at 12 months rituximab patients showed a significant reduction in PWV. Reduced inflammation at 3 months was associated with increased TC and HDL-c in the entire cohort.
  
  
  CONCLUSIONS
  Treatment with tocilizumab and rituximab reduces PWV, a marker of CVD risk, in patients with RA.
authors.affiliation: Dept. of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: Sella Aarrestad
authors.initials: SA
authors.lastname: Provan
authors.affiliation: Dept. of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: Inger Jorid
authors.initials: IJ
authors.lastname: Berg
authors.affiliation: Dept. of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: Hilde Berner
authors.initials: HB
authors.lastname: Hammer
authors.affiliation: Dept. of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: Alexander
authors.initials: A
authors.lastname: Mathiessen
authors.affiliation: Dept. of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: Tore Kristian
authors.initials: TK
authors.lastname: Kvien
authors.affiliation: Preventive Cardio-Rheuma clinic, Dept. of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: Anne Grete
authors.initials: AG
authors.lastname: Semb
mesh_terms: D000069594:Abatacept / Q000627:therapeutic use*; D000328:Adult; D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy*; D001794:Blood Pressure / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000097:blood / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D063177:Pulse Wave Analysis; D012307:Risk Factors; D000069283:Rituximab / Q000627:therapeutic use*; D059289:Vascular Stiffness / Q000187:drug effects
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D008076:Cholesterol, HDL; D000069283:Rituximab; D000069594:Abatacept; D002784:Cholesterol; C502936:tocilizumab