Effects of 14 weeks of TNF alpha blockade treatment on lipid profile in ankylosing spondylitis.
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.
Mathieu
Sylvain
S
Rheumatology department, G.-Montpied Hospital, 58, rue Montalembert, 63003 Clermont-Ferrand, France. smathieu@chu-clermontferrand.fr
Dubost
Jean-Jacques
JJ
Tournadre
Anne
A
Malochet-Guinamand
Sandrine
S
Ristori
Jean-Michel
JM
Soubrier
Martin
M
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
D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D008055:Lipids; D018124:Receptors, Tumor Necrosis Factor; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol; D000068800:Etanercept