Apolipoprotein C-III in patients with systemic lupus erythematosus.


Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
10 05 2022
Historique:
received: 22 09 2021
accepted: 01 05 2022
entrez: 10 5 2022
pubmed: 11 5 2022
medline: 14 5 2022
Statut: epublish

Résumé

Systemic lupus erythematosus (SLE) has been associated with atherosclerotic cardiovascular disease (CV) and an altered lipid profile. High levels of apolipoprotein C-III (ApoC3) are associated with elevated triglyceride levels and an increased risk of CV. In the present study, we aimed to study circulating ApoC3 in patients with SLE and describe its relationship with the manifestations of the disease. This is a cross-sectional study that included 186 patients with SLE. Disease-related data, CV comorbidity, full lipid profile, and serum levels of ApoC3 were assessed. A multivariable regression analysis was performed to study how ApoC3 was related to SLE features. Classic CV risk factors were significantly and strongly associated with circulating ApoC3. After a fully multivariable analysis that included classic CV risk factors and lipid profile molecules, SLICC damage (beta coef. 0.10 [95% CI 0.02-0.19] mg/dl, 0.020) and Katz severity (beta coef. 0.11 [95% CI 0.03-0.19] mg/dl, p = 0.011) indices and SLEDAI activity score (beta coef. 0.05 [95% CI 0.05-0.08] mg/dl, p = 0.004) were all independently associated with higher levels of circulating ApoC3. Among SLE patients, disease activity, severity, and disease damage are independently associated with higher ApoC3 serum levels.

Sections du résumé

BACKGROUND
Systemic lupus erythematosus (SLE) has been associated with atherosclerotic cardiovascular disease (CV) and an altered lipid profile. High levels of apolipoprotein C-III (ApoC3) are associated with elevated triglyceride levels and an increased risk of CV. In the present study, we aimed to study circulating ApoC3 in patients with SLE and describe its relationship with the manifestations of the disease.
METHODS
This is a cross-sectional study that included 186 patients with SLE. Disease-related data, CV comorbidity, full lipid profile, and serum levels of ApoC3 were assessed. A multivariable regression analysis was performed to study how ApoC3 was related to SLE features.
RESULTS
Classic CV risk factors were significantly and strongly associated with circulating ApoC3. After a fully multivariable analysis that included classic CV risk factors and lipid profile molecules, SLICC damage (beta coef. 0.10 [95% CI 0.02-0.19] mg/dl, 0.020) and Katz severity (beta coef. 0.11 [95% CI 0.03-0.19] mg/dl, p = 0.011) indices and SLEDAI activity score (beta coef. 0.05 [95% CI 0.05-0.08] mg/dl, p = 0.004) were all independently associated with higher levels of circulating ApoC3.
CONCLUSION
Among SLE patients, disease activity, severity, and disease damage are independently associated with higher ApoC3 serum levels.

Identifiants

pubmed: 35538496
doi: 10.1186/s13075-022-02793-y
pii: 10.1186/s13075-022-02793-y
pmc: PMC9088095
doi:

Substances chimiques

APOC3 protein, human 0
Apolipoprotein C-III 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

104

Informations de copyright

© 2022. The Author(s).

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Auteurs

Candelaria Martín-González (C)

Division of Internal Medicine, Hospital Universitario de Canarias, Tenerife, Spain.

Carmen Ferrer-Moure (C)

Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.

Juan Carlos Quevedo-Abeledo (J)

Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.

Antonia de Vera-González (A)

Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.

Alejandra González-Delgado (A)

Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.

Julio Sánchez-Martín (J)

Epidemiology, Genetics and Atherosclerosis Research Group On Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain.

Miguel Á González-Gay (MÁ)

Epidemiology, Genetics and Atherosclerosis Research Group On Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain. miguelaggay@hotmail.com.
Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Santander, Spain. miguelaggay@hotmail.com.
Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. miguelaggay@hotmail.com.

Iván Ferraz-Amaro (I)

Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain. iferrazamaro@hotmail.com.

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Classifications MeSH