Postprandial Hyperlipidemia: Association with Inflammation and Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis

To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial...

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Published inBiomedicines Vol. 10; no. 1; p. 133
Main Authors Mena-Vázquez, Natalia, Redondo-Rodríguez, Rocío, Rioja, José, Jimenez-Nuñez, Francisco Gabriel, Manrique-Arija, Sara, Lisbona-Montañez, Jose Manuel, Cano-García, Laura, Rojas-Gimenez, Marta, Ureña, Inmaculada, Valdivielso, Pedro, Fernández-Nebro, Antonio
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 08.01.2022
MDPI
Subjects
apolipoprotein B48
Apolipoproteins
Arteriosclerosis
Atherosclerosis
Body mass index
C-reactive protein
Cholesterol
Cytokines
Diabetes
Disease
Dyslipidemia
Enzymes
Fasting
Fatty acids
High density lipoprotein
Hyperlipidemia
Inflammation
Laboratories
Lipids
Lipoproteins
Multivariate analysis
Physical activity
postprandial lipemia
Questionnaires
Rheumatoid arthritis
subclinical atherosclerosis
Triglycerides
Tumor necrosis factor-α
Ultrasonic imaging
Variables
Spain
apolipoprotein B48
triglycerides
inflammation
rheumatoid arthritis
subclinical atherosclerosis
postprandial lipemia
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Abstract To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09-12.11); = 0.037), TNF-α (OR (95% CI) 2.00 (1.00-3.98); = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01-1.19); = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00-1.04); = 0.049). PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.
AbstractList Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. Results: A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09–12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00–3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01–1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00–1.04); p = 0.049). Conclusion: PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.
Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. Results: A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09–12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00–3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01–1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00–1.04); p = 0.049). Conclusion: PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.
To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity.OBJECTIVETo describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity.Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA.METHODSObservational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA.A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09-12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00-3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01-1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00-1.04); p = 0.049).RESULTSA total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09-12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00-3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01-1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00-1.04); p = 0.049).PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.CONCLUSIONPPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.
To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09-12.11); = 0.037), TNF-α (OR (95% CI) 2.00 (1.00-3.98); = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01-1.19); = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00-1.04); = 0.049). PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.
Author Lisbona-Montañez, Jose Manuel
Fernández-Nebro, Antonio
Rojas-Gimenez, Marta
Manrique-Arija, Sara
Redondo-Rodríguez, Rocío
Jimenez-Nuñez, Francisco Gabriel
Cano-García, Laura
Ureña, Inmaculada
Valdivielso, Pedro
Mena-Vázquez, Natalia
Rioja, José
AuthorAffiliation 1 Instituto de Investigación Biomédica de Málaga (IBIMA), 29010 Malaga, Spain; rocio.redondo.sspa@juntadeandalucia.es (R.R.-R.); jose.rioja@uma.es (J.R.); franciscop.jimenez.sspa@juntadeandalucia.es (F.G.J.-N.); sara.manrique.sspa@juntadeandalucia.es (S.M.-A.); laura.cano.sspa@juntadeandalucia.es (L.C.-G.); inmaculada.urena.sspa@juntadeandalucia.es (I.U.); valdivielso@uma.es (P.V.); afernandezn@uma.es (A.F.-N.)
5 UGC de Medicina Interna, Hospital Universitario Virgen de la Victoria, 29010 Malaga, Spain
4 UGC de Reumatología, Instituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Hospital Universitario Reina Sofia, 14004 Cordoba, Spain; marta.rojas.gimenez.sspa@juntadeandalucia.es
3 Departamento de Medicina y Dermatología, Universidad de Málaga, 29010 Malaga, Spain
2 UGC de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain; josemanuellisbona@uma.es
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/35052812$$D View this record in MEDLINE/PubMed
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Keywords apolipoprotein B48
triglycerides
inflammation
rheumatoid arthritis
subclinical atherosclerosis
postprandial lipemia
Language English
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These authors contributed equally to this work.
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Publisher MDPI AG
MDPI
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Snippet To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory...
Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and...
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SubjectTerms apolipoprotein B48
Apolipoproteins
Arteriosclerosis
Atherosclerosis
Body mass index
C-reactive protein
Cholesterol
Cytokines
Diabetes
Disease
Dyslipidemia
Enzymes
Fasting
Fatty acids
High density lipoprotein
Hyperlipidemia
Inflammation
Laboratories
Lipids
Lipoproteins
Multivariate analysis
Physical activity
postprandial lipemia
Questionnaires
Rheumatoid arthritis
subclinical atherosclerosis
Triglycerides
Tumor necrosis factor-α
Ultrasonic imaging
Variables
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Title Postprandial Hyperlipidemia: Association with Inflammation and Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis
URI https://www.ncbi.nlm.nih.gov/pubmed/35052812
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