Evidence map›Paper›PMID 28168401›Full record

ReviewImmunologic research2017

Dyslipidemia in systemic lupus erythematosus.

Melinda Zsuzsanna Szabó, Peter Szodoray, Emese Kiss

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
9.3field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 137 citations in OpenAlex.

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  14. Late-onset Systemic Lupus Erythematosus.Rheumatology international · 2025
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10 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Melinda Zsuzsanna SzabóDepartment of Clinical Immunology, Adult and Pediatric Rheumatology, National Institute of Rheumatology and Physiotherapy, Budapest, Hungary. szabo.melinda@orfi.hu.
Peter SzodorayInstitute of Immunology, Rikshospitalet, Oslo University, Oslo, Norway.
Emese KissDepartment of Clinical Immunology, Adult and Pediatric Rheumatology, National Institute of Rheumatology and Physiotherapy, Budapest, Hungary.
National Institute of Oncology · HUSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease is one of the major causes of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Accelerated atherosclerosis is related to traditional (age, hypertension, diabetes mellitus, dyslipidemia, obesity, smoking, and positive family history) and non-traditional, disease-related factors. Traditional risk factors are still more prominent in patients with lupus, as both hypertension and hypercholesterinemia were independently associated with premature atherosclerosis in several SLE cohorts. In this work, the authors summarize the epidemiology of dyslipidemia in lupus patients and review the latest results in the pathogenesis of lipid abnormalities. The prevalence of dyslipidemia, with elevations in total cholesterol (TC), low-density lipoprotein (LDL), triglyceride (TG), and apolipoprotein B (ApoB), and a reduction in low-density lipoprotein (LDL) levels are about 30% at the diagnosis of SLE rising to 60% after 3 years. Multiple pathogenetic mechanism is included, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) can suppress HDL and increase TG, auto-antibodies can cause the injury of the endothelium, lipoprotein lipase (LPL) activity can be reduced by circulating inflammatory mediators and antibodies, and increased oxidative stress may trigger a wide range of pro-atherogenic lipid modifications. As a major risk factor, dyslipidemia should be treated aggressively to minimize the risk of atherosclerosis and cardiovascular events. Randomized controlled trials with statins are controversial in the detention of atherosclerosis progression, but can be favorable by inhibiting immune activation that is the arterial wall and by decreasing lupus activity.

Indexed as

AnimalsAtherosclerosisAutoantibodiesCholesterolDyslipidemiasEndothelial CellsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsImmunomodulationLipid MetabolismLipoproteins, LDLLupus Erythematosus, SystemicOxidative StressRandomized Controlled Trials as TopicTriglyceridesAutoantibodiesCholesterolHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins, LDLTriglyceridesAccelerated atherosclerosisDyslipidemiaReverse cholesterol transportSystemic lupus erythematosus

Identifiers

PMID28168401
OpenAlexW2586057598

What OpenQuestion holds

Texttitle and abstract
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.