ArticleBMC gastroenterology2020
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.
Article in BMC gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Uncovering immune dysfunction in ACLF: Cellular mechanisms, molecular pathways, and therapeutic frontiers.Journal of hepatology · 2026Review
- Effect of Nutritional Status on Coagulation and Inflammation in Patients With Cirrhosis and Variceal Bleeding.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- The C3/C3aR pathway exacerbates acetaminophen-induced mouse liver injury via upregulating podoplanin on the macrophage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Dissociation Phenomenon of Erythrocyte Agglutination and Its Application to Assay of Functional Activity of the Complement System in Clinical Laboratory.Journal of clinical laboratory analysis · 2024Article
- Clinical analysis of patients with systemic lupus erythematosus complicated with liver failure.Clinical rheumatology · 2023Article
- Complement C3 Facilitates Stratification of Stages of Chronic Hepatitis B and Signifies Development of Acute-on-Chronic Liver Failure in Acute Decompensated Cirrhosis.Advances in therapy · 2023Article
- Emerging roles of the complement system in host-pathogen interactions.Trends in microbiology · 2022Review
- New Insights into the Role of the Complement System in Human Viral Diseases.Biomolecules · 2022Review
- A Flow Cytometry-Based Assay for the Measurement of Total Complement Activity in the Serum and Clinical Practice.Disease markers · 2022Article
- Leveraging omics to understand the molecular basis of acute-on-chronic liver failure.Advances in laboratory medicine · 2021Review
- Serum C1q Levels Have Prognostic Value for Sepsis and are Related to the Severity of Sepsis and Organ Damage.Journal of inflammation research · 2021Article
- Complement factor C4a does not activate protease-activated receptor 1 (PAR1) or PAR4 on human platelets.Research and practice in thrombosis and haemostasis · 2021Article
- Leukocytes, Systemic Inflammation and Immunopathology in Acute-on-Chronic Liver Failure.Cells · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundThe 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).
methodsBlood 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.
resultsThe concentrations of C3 was 6568 μg/ml in the HBV-ACLF group, 8916 μg/ml in the CHB group and 15,653 μg/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).
conclusionsOur 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.
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