Evidence map›Paper›PMID 31413851›Full record

ArticleLupus science & medicine2019

Association of lipoprotein subfractions and glycoprotein acetylation with coronary plaque burden in SLE.

Monica M Purmalek, Philip M Carlucci, Amit K Dey, Maureen Sampson, Yenealem Temesgen-Oyelakin, Simantini Sakhardande, Joseph B Lerman, Alice Fike, Michael Davis, Jonathan H Chung and 8 more

Open access · goldAbstract read
In one paragraph

Article in Lupus science & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024
    Review
  9. Article
  10. Review
  11. Glycosylation and Cardiovascular Diseases.Advances in experimental medicine and biology · 2021
    Article
  12. Review
  13. Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 2 institutions in 1 country.

Monica M PurmalekNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Philip M CarlucciNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Amit K DeyNational Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA.
Maureen SampsonNational Institutes of Health Clinical Center, Bethesda, Maryland, USA.
Yenealem Temesgen-OyelakinNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Simantini SakhardandeNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Joseph B LermanNational Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA.
Alice FikeNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Michael DavisNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Jonathan H ChungNational Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA.
Taufiq SalahuddinNational Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA.
Zerai MannaNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Sarthak GuptaNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Marcus Y ChenNational Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA.
Sarfaraz HasniNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Nehal N MehtaNational Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA.
Alan RemaleyNational Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland, USA.
Mariana J KaplanNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland, USA.ORCID 0000-0003-2968-0815
National Institutes of Health · USNational Institutes of Health Clinical Center · US

Funding

Cardiovascular CT Clinical ResearchZIAHL006220 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CHEN, MARCUS · 2017 to 2025
$22.5M
6 · The paper itself

Abstract

objectiveSubjects 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.

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

resultsSLE 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.

conclusionsPatients 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.

Indexed as

atherosclerosiscardiovascular diseaseglycainsulin resistancelipoproteinssystemic lupus erythematosus

Identifiers

PMID31413851
PMCPMC6667837
OpenAlexW2956183823

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.