ArticleLiver international : official journal of the International Association for the Study of the Liver2017
Plasma biomarkers to study mechanisms of liver injury in patients with hypoxic hepatitis.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Perspectives and Tools in Liver Graft Assessment: A Transformative Era in Liver Transplantation.Biomedicines · 2025Review
- Supplementing Silicoglycidol for the reduction of aflatoxin MJDS communications · 2024Article
- SARS-CoV-2-mediated liver injury: pathophysiology and mechanisms of disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Acute liver injury in COVID-19 patients hospitalized in the intensive care unit: Narrative review.World journal of gastroenterology · 2022Review
- Generation of pro-and anti-inflammatory mediators after acetaminophen overdose in surviving and non-surviving patients.Toxicology letters · 2022Article
- Advantages of a Novel Model for Predicting Hepatic Fibrosis in Chronic Hepatitis B Virus Carriers Compared with APRI and FIB-4 Scores.Journal of clinical and translational hepatology · 2022Article
- Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury.International journal of molecular sciences · 2022Review
- Article
- Potential Effects of Coronaviruses on the Liver: An Update.Frontiers in medicine · 2021Review
- Serum ceruloplasmin can predict liver fibrosis in hepatitis B virus-infected patients.World journal of gastroenterology · 2020Article
- Development and Validation of CAGIB Score for Evaluating the Prognosis of Cirrhosis with Acute Gastrointestinal Bleeding: A Retrospective Multicenter Study.Advances in therapy · 2019Article
- The Relationship Between Circulating Acetaminophen-Protein Adduct Concentrations and Alanine Aminotransferase Activities in Patients With and Without Acetaminophen Overdose and Toxicity.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2019Article
- Mechanistic identification of biofluid metabolite changes as markers of acetaminophen-induced liver toxicity in rats.Toxicology and applied pharmacology · 2019Article
- Acetaminophen Hepatotoxicity.Seminars in liver disease · 2019Article
- Mito-tempo protects against acute liver injury but induces limited secondary apoptosis during the late phase of acetaminophen hepatotoxicity.Archives of toxicology · 2019Article
- Biomarkers of drug-induced liver injury.Advances in pharmacology (San Diego, Calif.) · 2019Review
- High-Mobility Group Box-1 and Liver Disease.Hepatology communications · 2018Review
- Biomarkers of drug-induced liver injury: progress and utility in research, medicine, and regulation.Expert review of molecular diagnostics · 2018Review
- Mitochondrial dysfunction as a mechanism of drug-induced hepatotoxicity: current understanding and future perspectives.Journal of clinical and translational research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsHypoxic hepatitis is a clinical condition precipitated by prolonged periods of oxygen deprivation to the liver. It can have several underlying causes. Despite its prevalence in critically ill patients, which can reach upwards of 10%, very little is known about the mechanisms of injury. Thus, we set out to measure previously identified circulating biomarkers in an attempt to describe mechanisms of injury following hypoxic hepatitis.
methodsPlasma from patients diagnosed with hypoxic hepatitis was collected for this study. Biomarkers of hepatocellular injury, mitochondrial damage and cell death were measured. These results were compared against results obtained from well-characterized acetaminophen overdose patients.
resultsAt peak injury, ALT measured 4082±606 U/L and gradually decreased over 5 days, corresponding to the clinically observed pattern of hypoxic hepatitis. Levels of GDH showed a similar pattern, but neither ALT nor GDH were significantly higher in these patients than in acetaminophen patients. Plasma levels of DNA fragments mimicked hepatocellular injury as measured by ALT and miRNA-122. Interestingly, we found a significant increase in caspase-cleaved cytokeratin-18; however, the full-length form greatly exceeded the cleaved form at the time of maximum injury (45837±12085 vs 2528±1074 U/L). We also found an increase in acHMGB1 at later time points indicating a possible role of inflammation, but cytokine levels at these times were actually decreased relative to early time points.
conclusionsThe mechanism of injury following hypoxic hepatitis involves mitochondrial damage and DNA fragmentation. Importantly, necrosis, rather than apoptosis, is the main mode of cell death.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.