title: Reduced paraoxonase1 activity is a risk for atherosclerosis in patients with systemic lupus erythematosus.
abstract: Excessive lipid peroxidation is a major factor of accelerated atherosclerosis, observed in patients with systemic lupus erythematosus (SLE). We aimed at the present study to determine the paraoxonasel (PON1) and arylesterase activities, and lipid-profile in 37 SLE patients and 30 age-/sex-matched controls. Association was analyzed between PON1 activity and SLEDAI, CRP, anti-oxLDL, and antiphospholipid antibody (aPL) levels, steroid dose, and atherothrombotic events. The age of patients was 40.8 +/- 13.9 year, follow-up time 6.7 +/- 6.2 year, SLEDAI 2 (0-15). PON1 and arylesterase activities were measured spectrophotometrically using paraoxon and phenyl acetate as substrates, respectively. Phenotypic distribution of PON1 was determined by dual substrate method. We measured antioxLDL and aPL levels by ELISA, the CRP by automated immunoassay. PON1 activity (121.9 +/- 65.9 U/mL) was reduced significantly (P < 0.001) in SLE as compared to control (188.1 +/- 78.9 U/mL), but arylesterase activity was not different. A negative correlation was found between PON1 activity and age. PON1 activity did not correlate with other measured parameters. Reduced PON1 activity associated with clinical atherothrombotic complications (P < 0.01). High activity BB phenotype was not present in SLE. Lipid parameters (TC, LDL-C, HDL-C, ApoAI, and ApoB) were within normal range in both groups. Results indicated reduced PON1 activity in lupus patients despite long disease duration and low inflammatory activity, and it was evidenced as a risk for atherosclerotic complications. As the arylesterase activity was normal, further examinations are required to find other mechanisms, such as anti-PON1 antibodies, genetic polymorphisms, and difference in distribution of HDL-subfractions or enzyme abnormalities in HDL remodeling.
authors: Third Department of Internal Medicine, Medical and Health Science Center University of Debrecen, Debrecen, Hungary. drkissemese@freemail.hu
authors: Emese
authors: E
authors: Kiss
authors: Ildikó
authors: I
authors: Seres
authors: Tünde
authors: T
authors: Tarr
authors: Zsolt
authors: Z
authors: Kocsis
authors: Gyula
authors: G
authors: Szegedi
authors: György
authors: G
authors: Paragh
mesh_terms: D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D043303:Aryldialkylphosphatase / Q000378:metabolism*; D050197:Atherosclerosis / Q000150:complications* / Q000378:metabolism*; D001323:Autoantibodies / Q000097:blood; D002265:Carboxylic Ester Hydrolases / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000378:metabolism*; D008297:Male; D010641:Phenotype; D012307:Risk Factors
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D001323:Autoantibodies; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D017270:Lipoprotein(a); D002265:Carboxylic Ester Hydrolases; C019734:arylesterase; D043303:Aryldialkylphosphatase