Evidence map›Paper›PMID 26885490›Full record

ArticleCardiovascular diagnosis and therapy2016

HDL function and subclinical atherosclerosis in juvenile idiopathic arthritis.

Preethi Mani, Kiyoko Uno, MyNgan Duong, Kathy Wolski, Steven Spalding, M Elaine Husni, Stephen J Nicholls

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diagnosis and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 3 institutions in 2 countries.

Preethi Mani1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA ; 2 Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA ; 3 South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia ; 4 Department of Rheumatology, Cleveland Clinic, Cleveland, Ohio, USA.
Kiyoko Uno1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA ; 2 Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA ; 3 South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia ; 4 Department of Rheumatology, Cleveland Clinic, Cleveland, Ohio, USA.
MyNgan Duong1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA ; 2 Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA ; 3 South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia ; 4 Department of Rheumatology, Cleveland Clinic, Cleveland, Ohio, USA.
Kathy Wolski1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA ; 2 Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA ; 3 South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia ; 4 Department of Rheumatology, Cleveland Clinic, Cleveland, Ohio, USA.
Steven Spalding1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA ; 2 Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA ; 3 South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia ; 4 Department of Rheumatology, Cleveland Clinic, Cleveland, Ohio, USA.
M Elaine Husni1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA ; 2 Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA ; 3 South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia ; 4 Department of Rheumatology, Cleveland Clinic, Cleveland, Ohio, USA.
Stephen J Nicholls1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA ; 2 Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA ; 3 South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia ; 4 Department of Rheumatology, Cleveland Clinic, Cleveland, Ohio, USA.
Cleveland Clinic · USUniversity of Adelaide · AUThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence suggests that inflammation adversely impacts the protective properties of high-density lipoproteins (HDL) and progression of atherosclerosis. The impact of early chronic inflammatory conditions on HDL function and vascular risk has not been well investigated.

methodsWe compared measures of HDL particle distribution and functionality, in addition to measures of carotid intima-medial thickness (cIMT) in patients with juvenile idiopathic arthritis (JIA) and age matched controls.

resultsJIA patients demonstrated lower levels of HDL cholesterol [47.0 (40.0, 56.0) vs. 56.0 (53.0, 61.0) mg/dL, P=0.04], total HDL [29.5 (27.9, 32.3) vs. 32.9 (31.6, 36.3) mg/dL, P=0.05] and large HDL [5.1 (3.7, 7.3) vs. 8.0 (6.7, 9.7) mg/dL, P=0.04] particles. In association JIA patients demonstrated greater cholesterol efflux mediated via ATP binding cassette A1 (ABCA1) [17.3% (12.8, 19.7) vs. 10.0% (5.8, 16.0), P=0.05] and less efflux mediated via ATP binding cassette G-1 (ABCG1) [3.2% (2.0, 3.9) vs. 4.8% (3.5, 5.8), P=0.01] and SR-B1 [6.9% (6.0, 8.4) vs. 9.1% (8.6, 10.2), P=0.002] compared with controls. Exposure of macrophages to serum from JIA patients resulted in a smaller increase in mRNA expression of ABCA1 (2.0±0.95 vs. 7.1±5.7 fold increase, P=0.01) and greater increases in expression of ABCG1 [1.4 (0.9, 1.5) vs. 0.8 (0.7, 1.1) fold increase, P=0.04] and SR-B1 (1.3±0.47 vs. 0.7±0.3 fold increase, P=0.001) compared with controls. Arylesterase (128.9±27.6 vs. 152.0±45.2 umoles/min/mL, P=0.04) activity and endothelial cell migration (491.2±68.9 vs. 634.2±227.4 cells/field, P=0.01) were less in JIA patients. No differences in cIMT were observed between JIA patients and controls.

conclusionsThe presence of JIA was associated with alterations in HDL particle distribution, cholesterol efflux and non-lipid transporting activities. The ultimate implication of these findings for cardiovascular risk requires further investigation.

Indexed as

Arthritisatherosclerosishigh-density lipoproteins (HDL) cholesteroljuvenile

Identifiers

PMID26885490
PMCPMC4731577
OpenAlexW2268758389

What OpenQuestion holds

Textmetadata
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.