[Analysis of paraoxonase activity and lipid profile in lupus patients].
BACKGROUND
Immune-inflammatory processes play important role in the pathogenesis of atherosclerosis. Therefore, increasing attention is focused on rheumatic diseases with chronic inflammation, such as systemic lupus erythematosus. Besides direct influences, inflammation may modify the development of atherosclerosis by other mechanisms.


OBJECTIVE
To examine paraaoxonase activity and lipid profile in lupus patients.


METHODS
Authors entered 37 definitive lupus patients and 30 age- and sex-matched normal controls into the present study. Patients' age was 40.8 +/- 13.9 year, follow-up time 6.7 +/- 6.2 year, disease activity index 2.8 +/- 3.4. Lipid parameters (total cholesterol, LDL-C, HDL-C, Apo-AI and ApoB) were determined by an autoanalyser, paraoxonase and arylesterase activities were measured spectrophotometrically. Phenotypic distribution of the enzyme was determined by dual substrate method. Anti-oxLDL was measured by ELISA method, CRP by automatised immunoassay. Statistical analysis was performed by SPSS program.


RESULTS
Despite of long disease duration and low inflammatory activity authors found significantly (p < 0.001) decreased paraoxonase activity (121.9 +/- 65.9 U/mL) (p < 0.001) in lupus as compared to control (188.1 +/- 78.9 U/mL), which correlated with the presence of atherothrombotic complications (p = 0.009). High activity BB phenotype did not occur in lupus. Lipid parameters and arylesterase activity were within normal range in both groups. No significant correlation was found between paraoxonase activity and disease activity index, dose of corticosteroid therapy, CRP and anti-oxLDL level. Arylesterase activity did not differ in lupus and control groups.


CONCLUSIONS
Present results suggest that other mechanisms, e.g. antibodies, genetic factors, alteration in the distribution of HDL-subfractions or ensyme abnormalities in HDL remodelling may stand at the background of reduced paraoxonase activity in lupus.
Kiss
Emese
E
Debreceni Egyetem Orvos- és Egészségtudományi Centrum, Altalános Orvostudományi Kar, III. Belklinika. kiss@iiibel.dote.hu
Seres
Ildikó
I
Zsolt
Kocsis
K
Tarr
Tünde
T
Csípo
István
I
Szegedi
Gyula
G
Paragh
György
G
D000328:Adult; D001053:Apolipoproteins / Q000097:blood; D043303:Aryldialkylphosphatase / Q000097:blood*; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood*; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000150:complications / Q000201:enzymology*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
D001053:Apolipoproteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008055:Lipids; D014280:Triglycerides; D043303:Aryldialkylphosphatase