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Author Spotlight: Assessing the Cardiovascular Profile of Patients with Metabolic Syndrome
Published on: September 27, 2024
Systemic lupus erythematosus patients have unique changes in serum metabolic profiles across age associated with
Elizabeth C Jury1, Junjie Peng2, Alexandra Van Vijfeijken1
1Centre for Rheumatology Research, Division of Medicine, University College London, London, UK.
Insights
Systemic lupus erythematosus (SLE) patients show age-related metabolic changes, including altered lipoproteins and glycolysis. Interventions to increase high-density lipoprotein (HDL) and manage disease activity may improve cardiovascular outcomes in SLE.
Area of Science:
- Metabolomics
- Systemic Lupus Erythematosus (SLE)
- Cardiovascular Disease
Background:
- Cardiovascular disease (CVD) is a primary cause of mortality in SLE patients, driven by accelerated atherosclerosis.
- Chronic inflammation and cardiometabolic defects contribute to CVD risk in SLE patients with increasing age.
- Understanding age-associated metabolomic shifts is crucial for managing CVD in SLE.
Purpose of the Study:
- To investigate age-associated changes in serum metabolomic profiles of female patients with SLE compared to healthy controls (HCs).
- To identify specific metabolites and pathways affected by age in SLE.
- To explore the association of these metabolites with disease activity, treatments, and cardiovascular outcomes.
Main Methods:
- Serum Nuclear Magnetic Resonance (NMR) metabolomic profiling was performed on 164 female SLE patients and 123 HCs across a wide age range.
- Data were analyzed using linear regression and stratified by age groups (≤25, 26-49, ≥50) with multiple t tests.
- Impact of inflammation, disease activity, and medications (prednisolone, hydroxychloroquine) was assessed; UK Biobank disease-wide association analysis was conducted.
Main Results:
- Age-specific metabolomic differences were observed, including altered amino acids, very-low-density lipoproteins, and low-density lipoproteins in SLE patients.
- Twenty-five metabolites were significantly altered across all SLE age groups, notably decreased high-density lipoprotein (HDL) subsets and apolipoprotein (Apo)A1, and increased glycoprotein acetyls (GlycA).
- Glycolysis pathway metabolites uniquely increased with age in SLE, influenced by prednisolone and hydroxychloroquine, and associated with diabetes risk.
Conclusions:
- Increasing HDL (ApoA1) levels and maintaining low disease activity from a young age could improve cardiometabolic outcomes in SLE patients.
- Metabolites from the glycolytic pathway may serve as biomarkers for adverse metabolic effects of current SLE therapies.
- Targeting HDL and monitoring glycolytic metabolites could be key strategies for CVD prevention in SLE.
Objectives:
Cardiovascular disease through accelerated atherosclerosis is a leading cause of mortality for patients with systemic lupus erythematosus (SLE), likely due to increased chronic inflammation and cardiometabolic defects over age. We investigated age-associated changes in metabolomic profiles of SLE patients and healthy controls (HCs).
Methods:
Serum NMR metabolomic profiles from female SLE patients (n = 164, age = 14-76) and HCs (n = 123, age = 13-72) were assessed across age by linear regression and by age group between patients/HCs (Group 1, age ≤ 25, n = 62/46; Group 2, age = 26-49, n = 50/46; Group 3, age ≥ 50, n = 52/31) using multiple t tests. The impact of inflammation, disease activity and treatments were assessed, and UK Biobank disease-wide association analysis of metabolites was performed.
Results:
Age-specific metabolomic profiles were identified in SLE patients vs HCs, including reduced amino acids (Group 1), increased very-low-density lipoproteins (Group 2), and increased low-density lipoproteins (Group 3). Twenty-five metabolites were significantly altered in all SLE age groups, dominated by decreased atheroprotective high-density lipoprotein (HDL) subsets, HDL-bound apolipoprotein (Apo)A1 and increased glycoprotein acetyls (GlycA). Furthermore, ApoA1 and GlycA were differentially associated with disease activity and serological measures, as well as atherosclerosis incidence and myocardial infarction mortality risk through disease-wide association. Separately, glycolysis pathway metabolites (acetone/citrate/creatinine/glycerol/lactate/pyruvate) uniquely increased with age in SLE, significantly influenced by prednisolone (increased pyruvate/lactate) and hydroxychloroquine (decreased citrate/creatinine) treatment and associated with type 1 and type 2 diabetes by disease-wide association.
Conclusions:
Increasing HDL (ApoA1) levels through therapeutic/nutritional intervention, whilst maintaining low disease activity, in SLE patients from a young age could improve cardiometabolic disease outcomes. Biomarkers from the glycolytic pathway could indicate adverse metabolic effects of current therapies.
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