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Open Access

Anti-high-density lipoprotein antibodies and lipoprotein characteristics in systemic lupus erythematosus-related cardiovascular disease

  • J Su1,
  • A Cederholm1,
  • E Hurt-Camejo1,
  • E Svenungsson1 and
  • J Frostegård1
Arthritis Research & Therapy20057(Suppl 1):P105

https://doi.org/10.1186/ar1626

Received: 11 January 2005

Published: 17 February 2005

Keywords

Systemic Lupus ErythematosusTumor Necrosis FactorParticle Size DeterminationSystemic Lupus Erythematosus CaseLipoprotein Particle Size

Background

The risk of cardiovascular disease (CVD) in systemic lupus erythematosus (SLE) is exceedingly high. Previously, a lupus pattern of dyslipidemia has been described (raised triglycerides, and low high-density lipoprotein [HDL]) and we recently reported that these lipid abnormalities were associated with tumor necrosis factor (TNF) activity.

Methods

Twenty-three women (52 ± 8.2 years) with SLE and a history of CVD (SLE cases) were compared with 26 age-matched women with SLE and no clinical manifestations of CVD (SLE controls) and 26 age-matched healthy women (controls). Lipoprotein-related measurements included lipoprotein particle size determination by use of NMR spectroscopy and affinity of low-density lipoprotein (LDL) to proteoglycans. Antibodies against apolipoprotein A1 (apoA1) in HDL and TNF was determined by ELISA. Common carotid intima-media thickness was measured by B-mode ultrasound as a surrogate measure of atherosclerosis.

Results

Anti-apoA1 were raised in SLE cases as compared with SLE controls (P = 0.03) and controls (P = 0.001), and in SLE controls as compared with controls (P = 0.01). Among SLE cases, anti-apoA1 was associated with TNF (P = 0.01). Small dense LDL were more common among SLE controls and controls than in SLE cases (P = 0.036 and 0.086, respectively). Small HDL was more common among controls than in SLE cases and SLE controls (P = 0.001). LDL association with proteoglycans did not differ between groups Activity in the TNF system was significantly associated with triglycerides and negatively with HDL (P < 0.01).

Conclusion

SLE-related dyslipidemia showed a surprising pattern with large LDL and HDL rather than small; that is, not an expected 'atherogenic' lipid profile. Anti-apoA1 antibodies where strongly associated with CVD in SLE. Whether they may play a pathogenic role (e.g. by inhibiting anti-inflammatory properties of HDL) is presently under investigation.

Declarations

Acknowledgements

Supported by the Swedish Heart Lung Foundation, the King Gustav V 80th Birthday Fund, the Torsten and Ragnar Söderberg Foundation, and the Swedish Science Fund.

Authors’ Affiliations

(1)
Department of Medicine, Karolinska University Hospital, Stockholm, Sweden

Copyright

© BioMed Central Ltd 2005

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