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Co-morbidities
Original research
Association of lipoprotein subfractions and glycoprotein acetylation with coronary plaque burden in SLE
  1. Monica M Purmalek1,
  2. Philip M Carlucci1,
  3. Amit K Dey2,
  4. Maureen Sampson3,
  5. Yenealem Temesgen-Oyelakin1,
  6. Simantini Sakhardande1,
  7. Joseph B Lerman2,
  8. Alice Fike1,
  9. Michael Davis1,
  10. Jonathan H Chung2,
  11. Taufiq Salahuddin2,
  12. Zerai Manna1,
  13. Sarthak Gupta1,
  14. Marcus Y Chen2,
  15. Sarfaraz Hasni1,
  16. Nehal N Mehta2,
  17. Alan Remaley2 and
  18. Mariana J Kaplan1
  1. 1National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA
  2. 2National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA
  3. 3National Institutes of Health Clinical Center, Bethesda, Maryland, USA
  1. Correspondence to Dr Mariana J Kaplan; mariana.kaplan{at}nih.gov

Abstract

Objective Subjects with SLE display an enhanced risk of atherosclerotic cardiovascular disease (CVD) that is not explained by Framingham risk. This study sought to investigate the utility of nuclear MR (NMR) spectroscopy measurements of serum lipoprotein particle counts and size and glycoprotein acetylation (GlycA) burden to predict coronary atherosclerosis in SLE.

Methods Coronary plaque burden was assessed in SLE subjects and healthy controls using coronary CT angiography. Lipoproteins and GlycA were quantified by NMR spectroscopy.

Results SLE subjects displayed statistically significant decreases in high-density lipoprotein (HDL) particle counts and increased very low-density lipoprotein (VLDL) particle counts compared with controls. Non-calcified coronary plaque burden (NCB) negatively associated with HDL subsets whereas it positively associated with VLDL particle counts in multivariate adjusted models. GlycA was significantly increased in SLE sera compared with controls. In contrast to high-sensitivity C reactive protein, elevations in GlycA in SLE significantly associated with NCB and insulin resistance (IR), though the association with NCB was no longer significant after adjusting for prednisone use.

Conclusions Patients with SLE display a proatherogenic lipoprotein profile that may significantly contribute to the development of premature CVD. The results demonstrate that NMR measures of GlycA and lipoprotein profiles, beyond what is captured in routine clinical labs, could be a useful tool in assessing CVD risk in patients with SLE.

  • systemic lupus erythematosus
  • atherosclerosis
  • lipoproteins
  • glyca
  • insulin resistance
  • cardiovascular disease

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/lupus-2019-000332

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    Footnotes

    • MMP and PMC are joint first authors.

    • Contributors MMP, PMC, SS, MS performed experiments; AKD, JBB, JHC, TS, MYC and NNM were involved in statistical analysis and/or coronary CT quantification; YT-O, SS, AF, MC, SG, SH,were involved in patient assessment and recruitment and clinical phenotyping; ZM managed the database; AR and MS were involved in interpretation of lipoprotein data; MMP, PMC and MJK designed the study and wrote the manuscript.

    • Funding This study was supported by the Intramural Research program at NIAMS/NIH (ZIAAR041199) and by the Lupus Research Institute.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Ethics approval The study was approved by the Institutional Review Board of National Institute of Arthritis and Muskuloskeletal and Skin Diseases/National Institute of Diabetes and Digestive and Kidney Diseases (NIAMS/NIDDK), Bethesda, Maryland, under protocol 94-AR-0066.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data availability statement All data relevant to the study are included in the article or uploaded as supplementary information.