Kiss Emese, Seres Ildikó, Zsolt Kocsis, Tarr Tünde, Csípo István, Szegedi Gyula, Paragh György
Debreceni Egyetem Orvos- és Egészségtudományi Centrum, Altalános Orvostudományi Kar, III. Belklinika.
Orv Hetil. 2005 Nov 20;146(47):2395-402.
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.
To examine paraaoxonase activity and lipid profile in lupus patients.
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.
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.
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.
免疫炎症过程在动脉粥样硬化的发病机制中起重要作用。因此，越来越多的关注集中在伴有慢性炎症的风湿性疾病上，如系统性红斑狼疮。除了直接影响外，炎症可能通过其他机制改变动脉粥样硬化的发展。
检测狼疮患者的对氧磷酶活性和血脂谱。
作者将37例确诊的狼疮患者和30例年龄及性别匹配的正常对照纳入本研究。患者年龄为40.8±13.9岁，随访时间为6.7±6.2年，疾病活动指数为2.8±3.4。血脂参数（总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、载脂蛋白A-I和载脂蛋白B）由自动分析仪测定，对氧磷酶和芳基酯酶活性用分光光度法测量。通过双底物法测定该酶的表型分布。采用ELISA法检测抗氧化型低密度脂蛋白，采用自动化免疫分析法检测CRP。使用SPSS程序进行统计分析。
尽管病程长且炎症活动度低，但作者发现狼疮患者的对氧磷酶活性（121.9±65.9 U/mL）显著低于对照组（188.1±78.9 U/mL）（p<0.001），这与动脉粥样硬化血栓形成并发症的存在相关（p = 0.009）。狼疮患者未出现高活性BB表型。两组的血脂参数和芳基酯酶活性均在正常范围内。未发现对氧磷酶活性与疾病活动指数、糖皮质激素治疗剂量、CRP和抗氧化型低密度脂蛋白水平之间存在显著相关性。狼疮组和对照组的芳基酯酶活性无差异。
目前的结果表明，其他机制，如抗体、遗传因素、高密度脂蛋白亚组分分布改变或高密度脂蛋白重塑中的酶异常，可能是狼疮患者对氧磷酶活性降低的原因。
