Key result
Rheumatoid arthritis is linked to a ~295 ng/ml increase in ANGPTL4 versus controls.
Why the study?
Patients with rheumatoid arthritis present changes in lipid profiles and accelerated cardiovascular disease, but the status of the ANGPTL4, ApoC3, and LPL axis in RA compared to controls was unclear.
Is the ANGPTL4, ApoC3, and LPL axis disrupted in patients with rheumatoid arthritis compared to controls, and is it associated with subclinical atherosclerosis?
Cross-Sectional (n=569)
Yes
Is the ANGPTL4, ApoC3, and LPL axis disrupted in patients with rheumatoid arthritis compared to controls, and is it associated with subclinical atherosclerosis?
Answers are grounded in this paper and cite their sources.
The ANGPTL4, ApoC3, and LPL axis is disrupted in rheumatoid arthritis and higher ANGPTL4 levels are independently associated with increased carotid intima-media thickness, suggesting a mechanism for accelerated atherosclerosis in this population.
BACKGROUND: Modulators of triglyceride metabolism include lipoprotein lipase (LPL), angiopoietin-like protein 4 (ANGPTL4), and apolipoprotein C-3 (ApoC3). There is evidence on the influence of this triangle of molecules on an increased risk of atherosclerotic cardiovascular disease (CV) in the general population. Patients with rheumatoid arthritis (RA) present changes in lipid profiles and accelerated CV disease. In the present study, we set out to study whether the ANGPTL4, ApoC3, and LPL axis differs in subjects with RA compared to controls. In a further step, we investigated the relationship of this axis with subclinical atherosclerosis in patients with RA. METHODS: Cross-sectional study that included 569 individuals, 323 patients with RA and 246 age-matched controls. ANGPTL4, ApoC3 and LPL, and standard lipid profiles were analyzed in patients and controls. Carotid intima-media thickness (cIMT) and carotid plaques were assessed in RA patients. A multivariable analysis was performed to assess whether the ANGPTL4, ApoC3, and LPL axis was altered in RA and to study its relationship with RA dyslipidemia and subclinical carotid atherosclerosis. RESULTS: Most lipid profile molecules did not differ between patients and controls. Despite this, and after fully multivariable analysis including CV risk factors, use of statins, and changes in the lipid profile caused by the disease itself, patients with RA showed higher serum levels of ANGPTL4 (beta coef. 295 [95% CI 213-376] ng/ml, p<0.001) and ApoC3 (beta coef. 2.9 [95% CI 1.7-4.0] mg/dl, p<0.001), but lower circulating LPL (beta coef. -174 [95% CI -213 to -135] ng/ml, p<0.001). ANGPTL4 serum levels were positively and independently associated with a higher cIMT in patients with RA after fully multivariable adjustment. CONCLUSION: The axis consisting in ANGPTL4, ApoC3, and LPL is disrupted in patients with RA. ANGPTL4 serum levels are positively and independently associated with a higher cIMT in RA patients.
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Armas‐Rillo et al. (2022) conducted a cross-sectional in Rheumatoid arthritis (n=569). Rheumatoid arthritis vs. Age-matched controls without rheumatoid arthritis was evaluated on ANGPTL4 serum levels (ng/ml) (beta coef. 295, 95% CI 213-376, p=<0.001). Rheumatoid arthritis was associated with a disrupted lipid metabolism axis, showing higher serum levels of ANGPTL4 and ApoC3, and lower LPL compared to controls.
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