Evaluation of Paraoxonase Activity in Patients with Mixed Connective Tissue Disease

EDIT BODOLAY, ILDIKO SERES, PETER SZODORAY, ISTVAN CSÍPO, ZSANETT JAKAB, JUDIT VEGH, ANNA SZILAGYI, GYULA SZEGEDI, and GYORGY PARAGH

ABSTRACT.

Objective. Mixed connective tissue disease (MCTD) is a systemic inflammatory autoimmune disease. The connection between inflammatory measures and atherosclerosis in MCTD has not been described. Paraoxonase (PON) is known to have an antioxidant function. We evaluated lipid profiles and PON activity in patients with MCTD.

Methods. Thirty-seven patients with MCTD were enrolled. Patients had taken no antihyperlipidemic drugs in the past 2 months. Thirty healthy individuals served as controls. The mean age of patients was 51.2 ± 9.5 years; disease duration was 11.0 ± 7.2 years. PON activity was determined with spectrophotometry, von Willebrand factor (vWF) antigen was investigated with the immunoturbidimetry method, and thrombomodulin and antiendothelial cell antibody (AECA) measurements were carried out by ELISA.

Results. PON activity in patients with MCTD was significantly lower than in the controls (patients 118.5 ± 64.6 U/l, controls 188.0 ± 77.6; p < 0.001). Arylesterase activity was significantly reduced in patients (p < 0.001). Reduction of PON activity showed a close correlation with the age of the patients, duration of the disease, and vascular events (eye, cardiac, cerebral). There was a close association between the low PON activity and endothelial cell activation markers (thrombomodulin, vWF, AECA).

Conclusion. Our results indicate that in patients with MCTD there is an increased risk for atherosclerosis. In the development of atherosclerosis, besides the elevated levels of cholesterol and triglyceride, reduced PON concentrations and PON activity may play a crucial role. (First Release Dec 15 2007; J Rheumatol 2008;35:237-43)

Key Indexing Terms:

MIXED CONNECTIVE TISSUE DISEASE
PARAOXONASE
LIPID LEVELS
VASCULAR DAMAGE

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From the Division of Clinical Immunology, 3rd Department of Internal Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.

E. Bodolay, MD, PhD; P. Szodoray, MD, PhD; I. Csipo, PhD; J. Vegh, MD, PhD; A. Szilagyi, Division of Clinical Immunlogy, 3rd Department of Internal Medicine, Medical and Health Science Center, University of Debrecen; I. Seres, MD, PhD; Z. Jakab; G. Paragh, MD, PhD, 1st Department of Internal Medicine, Medical and Health Science Center, University of Debrecen; G. Szegedi, MD, PhD, Research Group of Autoimmune Diseases, Hungarian Academy of Sciences, Coordination Institute of Clinical Immunology and Allergology, Debrecen.

Address reprint requests to Dr. E. Bodolay, Division of Clinical Immunlogy, 3rd Department of Internal Medicine, Medical and Health Science Center, University of Debrecen, Moricz Zs. str 22, 4032 Debrecen, Hungary. E-mail: bodolai@iiibel.dote.hu

Accepted for publication September 28, 2007.

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