机构地区:[1]青岛大学医学院附属医院感染科,山东青岛266003 [2]青岛大学医学院附属医院消化科,山东青岛266003 [3]青岛市传染病医院肝病三区,山东青岛266003 [4]青岛大学医学院附属医院中心实验室,山东青岛266003
出 处:《现代生物医学进展》2011年第9期1730-1733,共4页Progress in Modern Biomedicine
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HBVDNA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±3252.27COI、5494.35±2129.84COI和6921.25±1957.60COI,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HBVDNA、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HBVDNA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HBVDNA、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HBVDNA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。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 cir- rhosis 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 con- trol 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 con- trol 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 (P0.05). In compensat- ed cirrhosis group, the pearson correlation in HBsAg vs. HBV DNA and HBsAg vs. HBeAg were significantly reverse correlation (P0. 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 cir- rhosis group than in compensated cirrhosis group, it is also higher in compensated cirrhosise group than in control group. With the pro- gression 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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