title: Effects of 14 weeks of TNF alpha blockade treatment on lipid profile in ankylosing spondylitis.
abstract: OBJECTIVE
  Cardiovascular morbidity and mortality seem to be increased in ankylosing spondylitis, perhaps as the result of biological inflammation and consecutive dyslipidemia. This study aims to investigate the impact of TNF alpha-inhibitors, an effective treatment, on lipid profile.
  
  
  METHODS
  Thirty-four ankylosing spondylitis (AS) patients with active disease undergoing anti-TNF alpha therapy (n=20, infliximab; n=7, etanercept; n=7, adalimumab) were recruited. Disease activity parameters, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were assessed at baseline and after 14 weeks of treatment.
  
  
  RESULTS
  After 14 weeks of TNF alpha blockade treatment, there was a significant increase in levels of total cholesterol (5.08+/-1.20 vs. 4.73+/-1.12 mmol/l; p=0.01) and HDL-cholesterol (1.61+/-0.47 vs. 1.47+/-0.35 mmol/l; p=0.008), but no resulting change in the atherogenic index (3.43+/-1.13 vs. 3.35+/-0.93; p=0.87). There was also no change in concentrations of triglycerides (1.33+/-1.22 vs. 1.27+/-0.98 mmol/l; p=0.794) and LDL-cholesterol (3.15+/-0.99 vs. 2.91+/-0.93 mmol/l; p=0.24). TNF alpha inhibitor treatment was followed by a significant improvement in all disease activity parameters: VAS pain or VAS disease activity, BASDAI or BASFI and systemic inflammation. Sub-group analysis showed that monoclonal antibodies increased total and LDL-cholesterol levels but did not change the atherogenic index. Conversely, 14 weeks of etanercept treatment was followed by no change in lipid profile.
  
  
  CONCLUSIONS
  TNF alpha inhibitors may be successful in reducing cardiovascular risk in AS, as in RA, but not by affecting lipid profile. However, there is insufficient documented evidence, and long-term investigations are needed to define the possible protective mechanisms of TNFalpha inhibitor treatment in spondylarthropathies.
authors.affiliation: Rheumatology department, G.-Montpied Hospital, 58, rue Montalembert, 63003 Clermont-Ferrand, France. smathieu@chu-clermontferrand.fr
authors.forename: Sylvain
authors.initials: S
authors.lastname: Mathieu
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Dubost
authors.forename: Anne
authors.initials: A
authors.lastname: Tournadre
authors.forename: Sandrine
authors.initials: S
authors.lastname: Malochet-Guinamand
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Ristori
authors.forename: Martin
authors.initials: M
authors.lastname: Soubrier
mesh_terms: D000328:Adult; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D002784:Cholesterol / Q000097:blood; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D050356:Lipid Metabolism / Q000187:drug effects* / Q000502:physiology; D008055:Lipids / Q000097:blood*; D008297:Male; D010146:Pain; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012720:Severity of Illness Index; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000097:blood
chemical_list: D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D008055:Lipids; D018124:Receptors, Tumor Necrosis Factor; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol; D000068800:Etanercept