慢性肝炎患者ECR1基因多态性、数量及活性的变化

目的　研究慢性肝炎 (CH)患者红细胞Ⅰ型补体受体 (ECR1)密度相关基因多态性、数量表达及活性的变化。方法　采用PCR和HindⅢ酶切技术测定ECR1分子基因多态性 ,采用酶联免疫法定量测定ECR1分子的数量 ,采用红细胞天然免疫粘附功能试验测定ECR1粘附活性。结果　慢性肝炎患者ECR1密度相关基因多态性与健康人群相比差异无显著性。活动性慢性肝炎、肝功能异常的肝炎后肝硬化患者ECR1的数量表达及活性明显低于健康人群 (t=9 87,P <0 0 0 0 1) ,失代偿性肝炎后肝硬化患者的ECR1分子数量明显低于代偿性肝炎后肝硬化患者 ,但肝功能正常的慢性肝炎患者ECR1数量与健康人群比较无明显变化。结论　慢性肝炎患者ECR1数量表达及活性缺陷系后天引起 ,测定慢性肝炎患者ECR1的数量对临床病情判断及发展预测有重要参考价值。

Changes of ECR1 genomic density polymorphism, quantitative expression and the activity of ECR1 natural adhesion in patients with chronic hepatitis

OBJECTIVE: To study the changes of genomic density polymorphism, quantitative expression and the adhesion activity of complement receptor type 1 (ECR1) on erythrocytes in patients with chronic hepatitis. METHODS: Polymerase chain reaction (PCR) and Hind restriction enzyme digestion, the quantitative assay of ECR1 and the activity of erythrocytes immune adhesion test were applied. RESULTS: The spot mutation rate (25.0%-30.3%) of ECR1 density gene in patients with chronic hepatitis was not significantly different from that of healthy individuals (28.0%). The amount of ECR1 in patients with chronic hepatitis, except for the diseases with normal liver function, was significantly lower than that of healthy individuals (t=9.87,P<0.000 1). The quantitative expression of ECR1 in decompensated cirrhosis was obviously lower than that of compensated cirrhosis (t=2.21,P<0.05). CONCLUSIONS: Defective expression of ECR1 in chronic hepatitis B may be acquired through central and/or peripheral mechanisms. It is very important to study the quantitative expression in the patients with chronic hepatitis.