scholarly journals Postprandial Apolipoprotein B48 is Associated with Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis

2020 ◽  
Vol 9 (8) ◽  
pp. 2483
Author(s):  
Natalia Mena-Vázquez ◽  
Marta Rojas-Gimenez ◽  
Francisco Gabriel Jimenez Nuñez ◽  
Sara Manrique-Arija ◽  
José Rioja ◽  
...  

Objective: To describe postprandial lipemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis measured as carotid intima-media thickness (cIMT). Methods: We performed an observational study of 40 patients with RA and 40 sex and age-matched controls. Patients with dyslipidemia were excluded. Pathologically increased cIMT was defined as a carotid thickness greater than the 90th percentile (>p90) for age and sex. Fasting and postprandial plasma lipids, cholesterol, triglycerides, apolipoprotein B48 (ApoB48), and total ApoB were evaluated. The other variables included were clinical and laboratory values, Framingham score, and the 28-joint Disease Activity Score (DAS28). Two multivariate models were constructed to identify factors associated with pathologic cIMT in patients with RA. Results: Fasting lipid values were similar in patients with RA and controls, although those of postprandial ApoB48 were higher (median (IQR), 14.4 (10.8–12.1) vs. 12.1 (2.3–9,8); p = 0.042). Pathologic cIMT was recorded in 10 patients with RA (25%) and nine controls (22.5%). In patients with RA, pathologic cIMT was associated with postprandial ApoB48 (OR (95% CI), 1.15 (1.0–1.3)) and total ApoB (OR [95% CI], 1.12 [1.1–1.2]). The second model revealed a mean increase of 0.256 mm for cIMT in patients with elevated anticitrullinated protein antibodies (ACPAs). Conclusion: Postprandial ApoB48 levels in patients with RA are higher than in controls. Postprandial ApoB48 and total ApoB levels and markers of severity, such as ACPAs, are associated with pathologic cIMT in patients with RA. Our findings could indicate that these atherogenic particles have a negative effect on the endothelium.

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Mercedes García-Bermúdez ◽  
Raquel López-Mejías ◽  
Fernanda Genre ◽  
Santos Castañeda ◽  
Alfonso Corrales ◽  
...  

Rheumatoid arthritis (RA) is a polygenic disease associated with accelerated atherosclerosis and increased cardiovascular (CV) mortality. JAK/STAT signalling pathway is involved in autoimmune diseases and in the atherosclerotic process. JAK3 is a highly promising target for immunomodulatory drugs and polymorphisms inJAK3gene have been associated with CV events in incident dialysis patients. Therefore, the aim of this study was to assess the potential role ofJAK3polymorphisms in the development of CV disease in patients with RA. 2136 Spanish RA patients were genotyped for the rs3212780 and rs3212752JAK3gene polymorphisms by TaqMan assays. Subclinical atherosclerosis was evaluated in 539 of these patients by carotid ultrasonography (US). No statistically significant differences were found when each polymorphism was assessed according to carotid intima-media thickness values and presence/absence of carotid plaques in RA, after adjusting the results for potential confounders. Moreover, no significant differences were obtained when RA patients were stratified according to the presence/absence of CV events after adjusting for potential confounders. In conclusion, our results do not confirm association betweenJAK3polymorphisms and CV disease in RA.


Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 133
Author(s):  
Natalia Mena-Vázquez ◽  
Rocío Redondo-Rodríguez ◽  
José Rioja ◽  
Francisco Gabriel Jimenez-Nuñez ◽  
Sara Manrique-Arija ◽  
...  

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.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Raquel López-Mejías ◽  
Fernanda Genre ◽  
Mercedes García-Bermúdez ◽  
Begoña Ubilla ◽  
Santos Castañeda ◽  
...  

Introduction. Rheumatoid arthritis (RA) is a polygenic disease associated with accelerated atherosclerosis and increased cardiovascular (CV) mortality. Recent studies have identified theABOrs579459,PPAP2Brs17114036, andADAMTS7rs3825807 polymorphisms as genetic variants associated with coronary artery disease and thePIK3CGrs17398575 andEDNRArs1878406 polymorphisms as the most significant signals related to the presence of carotid plaque in nonrheumatic Caucasian individuals. Accordingly, we evaluated the potential relationship between these 5 polymorphisms and subclinical atherosclerosis (assessed by carotid intima-media thickness (cIMT) and presence/absence of carotid plaques) and CV disease in RA.Material and Methods. 2140 Spanish RA patients were genotyped for the 5 polymorphisms by TaqMan assays. Subclinical atherosclerosis was evaluated in 620 of these patients by carotid ultrasonography technology.Results. No statistically significant differences were found when each polymorphism was assessed according to cIMT values and presence/absence of carotid plaques in RA, after adjusting the results for potential confounders. Moreover, no significant differences were obtained when RA patients were stratified according to the presence/absence of CV disease after adjusting for potential confounders.Conclusion. Our results do not confirm association betweenABOrs579459,PPAP2Brs17114036,ADAMTS7rs3825807,PIK3CGrs17398575, andEDNRArs1878406 and subclinical atherosclerosis and CV disease in RA.


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