Article Text

THU0228 Reduction of Inflammation Drives Lipid Changes in Ankylosing Spondylitis
  1. S.C. Heslinga1,
  2. M. Peters2,
  3. M. Ter Wee3,
  4. A. Van Sijl1,
  5. Y. Smulders2,
  6. I. van der Horst-Bruinsma3,
  7. M. Nurmohamed1
  1. 1Rheumatology, Amsterdam Rheumatology and immunology Center, Reade
  2. 2Internal Medicine, VU University Medical Center
  3. 3Rheumatology, Amsterdam Rheumatology and immunology Center, VU University Medical Center, Amsterdam, Netherlands


Background In inflammatory diseases, including ankylosing spondylitis (AS), systemic inflammation induces secondary dyslipidaemia with lower total cholesterol (TC) and lower high density cholesterol (HDL-C) levels. Effective anti-inflammatory treatment with tumor necrosis factor (TNF) alpha-blocking therapy has been shown to increase lipid levels, which as a result, may affect cardiovascular (CV) risk. It is still unclear whether lipid changes following TNF-alpha blocking therapy are due to suppressed inflammation, or due to a specific effect of TNF-alpha blocking therapy.

Objectives We investigated the effects of changing inflammation levels during treatment with TNF-alpha blocking therapy on the lipid profile in AS patients.

Methods 230 consecutive AS patients with an indication for TNF-alpha blocking therapy with etanercept or adalimumab were enrolled. Data was collected at baseline and after 52 weeks of treatment. Serum C-reactive protein (CRP) was measured at each visit. High inflammatory status was defined as CRP≥10mg/L. Non-fasting lipid samples were collected at baseline and at 52 weeks.

Results CRP decreased significantly during treatment from 8 (3-22) to 2 (1-6) mg/l (p<0.01). TC, HDL-C and low density lipoprotein cholesterol (LDL-C) increased significantly with 4.6%, 3.7%, and 4.3% respectively. Apolipoprotein A-1 increased with 5.3%, while apolipoprotein B did not change. The TC/HDL-C ratio was not significantly changed after 52 weeks of TNF-alpha blocking therapy.

Regression analyses yielded an inverse association between changes in CRP and changes in TC (+0.104 mmol/l per 10mg/l reduction in CRP) and HDL-C (+0.024mmol/l per 10mg/l reduction in CRP) but not TC/HDL-C ratio. Significant changes in TC (+8.2%) and HDL-C (+8.3%) levels were only seen in patients whom CRP levels decreased during treatment from ≥10 mmol/l to <10mmol/l, but again, the TC/HDL-C ratio did not change.

Conclusions TNF-alpha blocking therapy is associated with a modest, but broadly parallel increase in TC, LDL-C, and HDL-C that might affect CV risk. Also, our data show, for the first time, that lipid changes following TNF-alpha blocking therapy are mostly due to suppressing inflammation and not to a specific TNF-alpha blocking therapy effect. Finally, consistent with previous findings, our data illustrate that the TC/HDL-C ratio is not appreciably altered by TNF-alpha blocking therapy and is therefore currently the most appropriate marker to determine CV risk in patients with an inflammatory condition.

Disclosure of Interest None declared

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