末端补体SC5b-9抗C1q抗体及补体C3 C4在狼疮疾病活动性判定中的价值

目的 探讨末端补体SC5b-9、抗C1q抗体及补体C3和C4在狼疮疾病活动性判定中的价值.方法 采用酶联免疫吸附试验(ELISA)检测系统性红斑狼疮(SLE)组62例、疾病对照组35例和健康对照组35名血清中的末端补体SC5b-9和抗C1q抗体水平,并检测血清中补体C3和C4的水平,并与SLE患者临床表现、病情活动度及狼疮肾炎(LN)的病理分型进行相关性分析.结果 在SLE活动组中末端补体SC5b-9和抗C1q抗体水平均显著高于各对照组(均P<0.05).末端补体SC5b-9和抗C1q抗体与补体C3、C4呈负相关(P<0.05),与SLE疾病活动指数(SLEDAI)呈正相关(P<0.05).联合检测对疾病活动的判断的敏感性和特异性分别为95%和98%.末端补体SC5b-9及抗C1q抗体在狼疮增殖件肾炎中表达明显高于膜性肾炎(均P<0.05).结论 联合检测可提高疾病诊断和活动性判断的特异性和敏感性;末端补体SC5b-9和抗C1q抗体参与了狼疮增殖性肾炎的免疫发病机制.

The significance of serum SC5b-9, anti-Clq antibody, C3 and C4 levels in assessing lupus disease activity

Objective To explore the value of serum SC5b-9, anti-C1q antibody, C3 and C4 levels in the assessment of lupus activity. Methods The enzyme linked immunosorbent assay (ELISA) was used to measure SC5b-9 and anti-C1q antibody, rate nepheiometry was used to detect the serum level of C3 and C4 in sera of 62 SLE patients, 35 patients with other rheumatic diseases (including rheumatoid arthritis, ankylosing spondylitis, primary Sjogren' s syndrome, mixed connective tissue disease, dermatomyositis, polymyositis, systemic sclerosis and vasculitis) and 35 healthy controls. And the correlation between above-mentioned parameters and lupus clinical manifestations, disease activity and histological type of lupus nephritis were analyzed. Results In SLE patients, the levels of SC5b-9 and anti-C1q antibody were significantly higher than those in patients with other rheumatic diseases and healthy controls (P<0.05). The titers of SC5b-9 and anti-C1q antibody negatively correlated with C3 and C4 (P<0.05), and positively correlated with SLEDAI (P<0.05). The sensitivity and specificity of the combination of these three measurements for SLE was 95.37% and 98.46 respectively. SC5b-9 and anti-C1q antibody were associated with the presence of proliferative glomerulonephritis (P <0.05). Conclusion Taking the evaluation of all these three measurements simultaneously is valuable for the diagnosis of lupus flare. SC5b-9 and anti-C1q antibody may play major roles in the immunopathogenesis of lupus nephritis.