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Antioxidant Vitamins and Lipid Peroxidation in Patients with Rheumatoid Arthritis: Association with Inflammatory Markers

SILVIA PAREDES, JOSEFA GIRONA, EVA HURT-CAMEJO, JOAN CARLES VALLVÉ, SILVIA OLIVÉ, MERCEDES HERAS, PERE BENITO, and LLUÍS MASANA

ABSTRACT.

Objective.
We evaluated vitamin status in relation to inflammatory markers and lipid peroxidation measures in patients with rheumatoid arthritis (RA).

Methods. Thirty patients with RA and 30 controls were studied. Lipid profile, vitamin A, vitamin E, and inflammatory markers were analyzed in all subjects. Susceptibility to low density lipoprotein (LDL) oxidation was evaluated in both groups by measuring the kinetics of conjugated dienes induced by hemin.

Results. Patients and controls had similar lipid profiles, except with LDL cholesterol, which was lower in the patients (p < 0.05). Patients had significantly higher plasma levels of inflammatory markers with respect to controls (p < 0.01). Plasma levels of vitamin A were lower in patients, and similar levels of vitamin E were observed in both groups. Oxidative variables, measured as the different phases of conjugated diene formation, were similar in patients and controls. We found a significant inverse correlation between vitamin A, vitamin E, and secretory type II phospholipase A2 in patients. We found a positive correlation between the affinity constant of LDL binding to glycosaminoglycans (GAG), Kd-LDL, and the lag phase of LDL oxidation (p < 0.05) in patients.

Conclusion. This report supports the hypothesis that chronic inflammation affects antioxidant vitamin levels in RA. Combined with the presence of a chronic inflammatory process and high LDL affinity for GAG, this may explain the high risk of cardiovascular disease in patients with RA. (J Rheumatol 2002;29:2271-7)

Key Indexing Terms:

RHEUMATOID ARTHRITIS
CARDIOVASCULAR DISEASES
INFLAMMATION
VITAMINS
LIPID PEROXIDATION


From the Unitat de Recerca de Lípids i Arteriosclerosi, Facultat de Medicina, Universitat Rovira i Virgili, Reus, Spain; Cell Biology and Biochemistry, AstraZeneca, Mölndal, Sweden; and Hospital del Mar y de la Esperanza, IMAS, Barcelona, Spain.

Supported by a grant from the Service of Rheumatology, Hospital del Mar, Barcelona, Spain.

S. Paredes, MD, Hospital del Mar y de la Esperanza; J. Girona, PhD; J.C. Vallvé, PhD; S. Olivé; M. Heras; L. Masana, MD, PhD, Unitat de Recerca de Lípids i Arteriosclerosi, Universitat Rovira i Virgili; E. Hurt-Camejo, PhD, Cell Biology and Biochemistry, AstraZeneca; P. Benito, MD, PhD, Hospital del Mar y de la Esperanza.

S. Paredes and J. Girona contributed equally to this article.

Address reprint requests to Prof. L. Masana, Unitat de Recerca de Lípids i Arteriosclerosi, IRCIS, Universitat Rovira i Virgili, C/Sant Llorenç, 21, 43201 Reus, Spain. E-Mail: lmm@fmcs.urv.es.

Submitted December 19, 2001; revision accepted May 16, 2002.




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