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Dysfunctional antioxidant capacity of high-density lipoprotein in rheumatoid arthritis.
European Journal of Clinical Investigation 2023 March 31
BACKGROUND: High-density lipoprotein (HDL) present atheroprotective functions not readily reflected by plasma HDL-cholesterol levels. The aim of this study was to investigate HDL antioxidant function in patients with rheumatoid arthritis (RA).
METHODS: This pilot and cross-sectional study included 50 RA patients and 50 controls matched by age, gender, cardiovascular risk factors and drug therapy. The antioxidant capacity of HDL was assessed by the total radical-trapping antioxidative potential test (TRAP-assay) and the susceptibility of low-density lipoprotein (LDL) to oxidation by the Conjugated Dienes Assay (Dmax). A carotid ultrasound was performed in all participants to detect subclinical atherosclerosis.
RESULTS: HDL from RA patients showed lower antioxidant capacity than those from controls [oxidized-LDL%: 35.8(27-42) vs. 24.4(20-32), p<0.001] when analysed with the TRAP-assay. In addition, the time to achieve 50% of maximal LDL oxidation (Lag-time) was shorter in RA-patients than in matched controls [57.2(42-71) vs. 69.5(55-75) minutes, (p=0.003)]. RA patients showed a higher atherosclerotic burden than controls. The pro-oxidant pattern in RA was irrespective of the presence of carotid atherosclerosis. On the contrary, there was a positive correlation between inflammatory parameters (erythrocyte sedimentation rate, ultrasensitive C-reactive protein and fibrinogen) and the loss of HDL-anti-oxidant capacity measured by the TRAP-assay (rho=0.211, p=0.035; rho=0.231, p=0.021 and rho=0.206, p=0.041, respectively). Furthermore, the glucocorticoid dose at recruitment was negatively associated with the Lag-time in RA patients (rho=-0.387, p=0.026).
CONCLUSION: RA patients present reduced HDL antioxidant capacity and a lower resistance of LDL particles to oxidation, mainly related to the degree of inflammation.
METHODS: This pilot and cross-sectional study included 50 RA patients and 50 controls matched by age, gender, cardiovascular risk factors and drug therapy. The antioxidant capacity of HDL was assessed by the total radical-trapping antioxidative potential test (TRAP-assay) and the susceptibility of low-density lipoprotein (LDL) to oxidation by the Conjugated Dienes Assay (Dmax). A carotid ultrasound was performed in all participants to detect subclinical atherosclerosis.
RESULTS: HDL from RA patients showed lower antioxidant capacity than those from controls [oxidized-LDL%: 35.8(27-42) vs. 24.4(20-32), p<0.001] when analysed with the TRAP-assay. In addition, the time to achieve 50% of maximal LDL oxidation (Lag-time) was shorter in RA-patients than in matched controls [57.2(42-71) vs. 69.5(55-75) minutes, (p=0.003)]. RA patients showed a higher atherosclerotic burden than controls. The pro-oxidant pattern in RA was irrespective of the presence of carotid atherosclerosis. On the contrary, there was a positive correlation between inflammatory parameters (erythrocyte sedimentation rate, ultrasensitive C-reactive protein and fibrinogen) and the loss of HDL-anti-oxidant capacity measured by the TRAP-assay (rho=0.211, p=0.035; rho=0.231, p=0.021 and rho=0.206, p=0.041, respectively). Furthermore, the glucocorticoid dose at recruitment was negatively associated with the Lag-time in RA patients (rho=-0.387, p=0.026).
CONCLUSION: RA patients present reduced HDL antioxidant capacity and a lower resistance of LDL particles to oxidation, mainly related to the degree of inflammation.
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