文章摘要
王红臻1 边城1△ 徐永红2 刘涵云1 温子荣3 李晓宇1 隋爱华4.肝硬化患者乙肝表面抗原的定量检测及意义[J].,2011,11(9):1730-1733
肝硬化患者乙肝表面抗原的定量检测及意义
Quantitation Detection of Hepatitis B Surface Antigen and Its Significancein Patients with Hepatic Cirrhosis
  
DOI:
中文关键词: HBsAg  HBV DNA  HBeAg  肝硬化
英文关键词: HBsAg  HBV DNA  HBeAg  Hepatic cirrhosis
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王红臻1 边城1△ 徐永红2 刘涵云1 温子荣3 李晓宇1 隋爱华4 青岛大学医学院附属医院感染科 
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中文摘要:
      目的:探讨HBsAg 定量测定在乙肝相关性肝硬化病程中的变化和意义。方法:选择乙肝相关性肝硬化患者60 例纳入实验 对象,根据2000 年9 月(西安)第10 次全国病毒性肝炎学术会议修订的《病毒性肝炎防治方案》中的诊断标准分为代偿期组和失 代偿期组,其中代偿期组35 例,失代偿期组25 例。另选取20 例乙型肝炎病毒携带者作为对照组。应用电化学发光免疫分析法测 定患者血清中HBsAg 和HBeAg 滴度,免疫荧光定量PCR 法检测HBV DNA 载量。结果:对照组、肝硬化代偿期组和肝硬化失代 偿期组HBsAg 滴度分别为:2574.73±3252.27 COI、5494.35±2129.84 COI 和6921.25± 1957.60 COI,三组之间差别均有统计学 意义(P<0.05)。肝硬化代偿期组中,HBsAg 滴度与HBV DNA、HBeAg 水平呈负相关性(P<0.05)(r=-0.350;r=-0.514)。肝硬化失代 偿期组中,HBsAg 滴度与HBV DNA 及HBeAg 水平均无明显相关性(r=-0.020;r=0.154)。结论:肝硬化失代偿期HBsAg 滴度明显 高于肝硬化代偿期,代偿期HBsAg 滴度高于HBV 携带者组,即HBsAg 滴度随肝脏疾病进展呈阶梯型递增。肝硬化代偿期,HBsAg 滴度与HBV DNA、HBeAg 水平呈负相关性,HBsAg 水平可以作为评估病毒复制的参考指标。肝硬化失代偿期,HBsAg 滴度与 HBV DNA 和HBeAg 无相关性,不能反映病毒复制水平,不能作为评估病毒复制的参考指标。
英文摘要:
      Objective: To assess the clinical significance of the quantitation of HBsAg in HBV-associated hepatic cirrhosis. Method: Sixty HBV-associated hepatic cirrhosis patients were included in the study. The patients were divided into the compensated cirrhosis group (n = 35) and the decompensated cirrhosis group (n = 25) based on the diagnostic criteria of hepatitis determined at the 10th National Conference on Viral Hepatitis (Xi'an, September 2000). 20 asymptomatic healthy hepatitis B carriers were recruited as the control group. The serum titers of HBsAg and HBeAg were determined using electrochemiluminescence immunoassay (ECLIA), and HBV DNA load was measured using immunofluorescence quantitative polymerase chain reaction assay(PCR). Result: HBsAg level in the control group, compensated cirrhosise group and decompensated cirrhosis group were 2574.73 ± 3252.27 COI, 5494.35 ± 2129.84 COI and 6921.25 ± 1957.60 COI, respectively. The differences among the three groups were statistically significant (P<0.05). In compensated cirrhosis group, the pearson correlation in HBsAg vs. HBV DNA and HBsAg vs. HBeAg were significantly reverse correlation (P<0. 05), with r values of -0.350 and -0.514 respectively. In decompensated cirrhosis group, HBsAg had no significant correlation with HBV DNA or HBeAg, with r values of -0.020 and 0.154 respectively. Conclusion: HBsAg level is significantly higher in decompensated cirrhosis group than in compensated cirrhosis group, it is also higher in compensated cirrhosise group than in control group. With the progression of liver disease, a rising HBsAg gradient is observed. In compensated cirrhosis group, HBsAg level has a significantly reverse correlation with HBV DNA and HBeAg, hence HBsAg is a indirect index to reflect viral replication. In decompensated cirrhosis, HBsAg has no significant correlation with HBV DNA and HBeAg, suggesting that HBsAg does not reflect the activity of viral replication.
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