Dysfunctional antioxidant capacity of high‐density lipoprotein in rheumatoid arthritis

Author:

García‐Gómez María Carmen12ORCID,Padró Teresa34ORCID,Muñoz‐García Natàlia3ORCID,Bianchi María1,Álvarez Lorenzo5,Badimon Lina346ORCID,Corbella Emili78ORCID,Pintó Xavier789ORCID

Affiliation:

1. Department of Rheumatology Consorci Sanitari de Terrassa Carretera Torrebonica s/n, 08227 Terrassa Barcelona Spain

2. School of Physiotherapy International University of Catalonia 08017 Barcelona Spain

3. Cardiovascular‐Program‐ICCC IR‐Hospital Santa Creu i Sant Pau IIB‐Sant Pau 08041 Barcelona Spain

4. Centro de Investigación Biomédica en Red Cardiovascular Instituto de Salud Carlos III 28029 Madrid Spain

5. Division of Vascular Surgery Consorci Sanitari de Terrassa Carretera Torrebonica s/n, 08227 Terrassa Barcelona Spain

6. UAB‐Chair Cardiovascular Research Barcelona Spain

7. Cardiovascular Risk Unit Internal Medicine Department Hospital Universitari de Bellvitge‐IDIBELL 08907 L'Hospitalet de Llobregat Spain

8. CIBEROBN Fisiopatología de la Obesidad y Nutrición Instituto de Salud Carlos III 28029 Madrid Spain

9. School of Medicine Universitat de Barcelona 08907 Barcelona Spain

Abstract

AbstractBackgroundHigh‐density lipoprotein (HDL) presents 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).MethodsThis 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.ResultsHigh‐density lipoprotein from RA patients showed lower antioxidant capacity than those from controls [oxidized‐LDL%: 35.8 (27–42) vs. 24.4 (20–32), p < .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 = .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 = .211, p = .035; rho = .231, p = .021 and rho = .206, p = .041, respectively). Furthermore, the glucocorticoid dose at recruitment was negatively associated with the Lag‐time in RA patients (rho = −.387, p = .026).ConclusionRheumatoid arthritis patients present reduced HDL antioxidant capacity and a lower resistance of LDL particles to oxidation, mainly related to the degree of inflammation.

Funder

Instituto de Salud Carlos III

Publisher

Wiley

Subject

Clinical Biochemistry,Biochemistry,General Medicine

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