慢性乙型肝炎及其肝硬化患者HBsAg与HBV DNA定量变化及其相关性

目的探讨慢性乙型肝炎（CHB）、乙型肝炎肝硬化（HBV-LC）患者HBsAg定量和HBVDNA定量的变化及两者的相关性。
方法采集46例CHB轻中度患者（CHB-LM组），24例CHB重度患者（CHB-S组）和28例HBV-LC患者入院时及51例患者经核
苷（酸）类似物（NA）抗病毒治疗4.08±3.06 月时的血清标本；采用化学发光法定量检测HBsAg 水平，荧光PCR 定量检测
HBVDNA载量。多组比较采用Kruskal-Wallis，两组间比较采用Mann-Whitney U检验，治疗前后比较采用Wilcoxon检测，相关
性分析采用Spearman检验。结果HBsAg和HBVDNA定量在CHB-LM组、CHB-S组和HBV-LC组中逐渐下降（χ2=12.537和
8.381，P=0.002和0.015）；CHB-LM组和CHB-S组HBsAg和HBV DNA定量值均高于HBV-LC组（P<0.05）；CHB-LM和CHB-S
两组之间差异均无统计学意义（Z=-0.649和0.032，P>0.05）。HBeAg阳性患者HBsAg和HBVDNA定量在CHB-LM组、CHB-S
组和HBV-LC 组中呈下降趋势（χ2=6.146，P=0.046 和1.009，P>0.05）；CHB-LM组HBsAg 定量高于HBV-LC 组（Z=-2.247，P=
0.025）。HBeAg阴性患者HBsAg和HBVDNA定量在CHB-LM组、CHB-S组和HBV-LC组中逐渐下降（χ2=7.196和14.658，P<
0.05）；CHB-LM 组和CHB-S 组HBsAg 和HBV DNA 定量均高于HBV-LC 组（P<0.01）。HBsAg 与HBVDNA 定量水平在
CHB-LM 组（r=0.389，P=0.009）、HBV-LC 组（r=0.431，P=0.022）中均呈正相关性；而在CHB-S 组中无相关性（r=0.348，P=
0.104）。与NA抗病毒治疗前相比，51 例患者治疗后HBsAg水平略有下降（Z=-1.050，P=0.294），而HBVDNA水平明显下降
（Z=-5.415，P<0.001）；治疗后HBsAg定量与HBVDNA定量无统计学相关性（r=0.241，P=0.111）；且两者治疗前后的差值也无统
计学相关性（r=0.257，P=0.085）。结论HBsAg和HBVDNA定量在CHB-LM、CHB-S和HBV-LC患者中逐渐降低，按照HBeAg
阳性和阴性分组后，这种趋势依然存在；HBsAg和HBVDNA之间呈正相关，但并非绝对平行。

Changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B and HBV-related liver cirrhosis

Objective To explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic
hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC). Methods Forty-six patients with mild to moderate CHB
(CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at
4.08 ± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott
chemiluminescence and fluorescence quantitative PCR, respectively. Results The serum HBsAg titer and HBV DNA load
gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC; χ2=12.537 and 8.381, respectively, P<
0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<
0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive
patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to
HBV-LC; χ2=6.146, P=0.046 and χ2=1.017, P>0.05; respectively), and CHB-LM group had significantly higher HBsAg titer than
HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually
declined with the disease severity (χ2=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and
CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels
in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral
therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415,
P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=
0.257, P=0.085). Conclusion Serum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAgpositive
and -negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.