Lower level of complement component C3 and C3a in the plasma means poor outcome in the patients with hepatitis B virus related acute-on-chronic liver failure
Lower level of complement component C3 and C3a in the plasma means poor outcome in the patients with hepatitis B virus related acute-on-chronic liver failure
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DOI：
10.1186/s12876-020-01258-3
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发表时间：
2020-04-15
影响因子：
2.4
通讯作者：
Zheng, Jian-Ming
中科院分区：
文献类型：
--
作者：
Li, Qian;Lu, Qing;Zheng, Jian-Ming
背景本研究的目的是调查补体系统是否被系统性激活，并明确其成分在乙型肝炎病毒相关慢性肝衰竭（HBV-ACLF）期间的临床和预后意义。方法 抽取 27 名 HBV-ACLF 患者、25 名慢性乙型肝炎但无肝功能衰竭（CHB）患者和 9 名健康志愿者（对照组）的血样。用酶联免疫吸附测定法测量血浆补体成分。对补体成分水平与肝衰竭相关指标进行相关性分析。结果 HBV-ACLF组C3浓度为6568μg/ml，CHB组为8916μg/ml，对照组为15653μg/ml（P < 0.05）。 HBV-ACLF组C3a浓度为852 ng/ml，CHB组为1008 ng/ml，对照组为1755 ng/ml（P < 0.05）。 HBV-ACLF组、CHB组和对照组的C1q浓度分别为50,509 ng/ml、114,640 ng/ml和177,001 ng/ml（P < 0.05）。对照组C1q、C3、C3a、C4、C4a和sC5b-9浓度显着高于HBV-ACLF组（分别是3.5、2.4、2.1、1.4、1.3和6.0倍）。但HBV-ACLF组与对照组血浆甘露糖结合凝集素和B因子浓度差异无统计学意义。 C3和C3a水平与MELD或CLIF-C OF呈负相关（P < 0.05）。结论 我们的分析表明，C1q 介导的经典途径的激活可能在 HBV-ACLF 的发病机制中发挥重要作用。此外，C3 和 C3a 的血浆水平可能是预测 HBV-ACLF 结果的潜在新型生物标志物。
Background The purpose of this study is to investigate whether or not the complement system is systemically activated and to specify the clinical and prognostic implications of its components during hepatitis B virus related acute-on-chronic liver failure (HBV-ACLF). Methods Blood samples were taken from twenty-seven patients diagnosed with HBV-ACLF, twenty-five patients diagnosed with chronic hepatitis B but without liver failure (CHB), and nine healthy volunteers (the control group). Plasma complement components were measured with Enzyme-linked immunosorbent assay. Correlative analysis were assessed between the levels of complement components and the liver failure related index. Results The concentrations of C3 was 6568 mu g/ml in the HBV-ACLF group, 8916 mu g/ml in the CHB group and 15,653 mu g/ml in the control group, respectively (P < 0.05). The concentrations of C3a was 852 ng/ml in the HBV-ACLF group, 1008 ng/ml in the CHB group and 1755 ng/ml in the control group, respectively (P < 0.05). The concentrations of C1q was 50,509 ng/ml in the HBV-ACLF group, 114,640 ng/ml in the CHB group and 177,001 ng/ml in the control group, respectively (P < 0.05). The concentrations of C1q, C3, C3a, C4, C4a and sC5b-9 were significantly higher in the control group than those in the HBV-ACLF group (3.5, 2.4, 2.1, 1.4, 1.3 and 6.0 fold, respectively). However, there was no statistical significance of the differences in the plasma concentrations of mannose binding lectin and factor B between the HBV-ACLF group and control group. The levels of C3 and C3a were inversely correlated with MELDs or CLIF-C OFs (P < 0.05). Conclusions Our analysis demonstrated that the activation of the classical pathway mediated by C1q may play an important role in the pathogenesis of HBV-ACLF. Furthermore, the plasma levels of C3 and C3a may be potential novel biomarkers in predicting the outcome of HBV-ACLF.