ArticleAnimal models and experimental medicine2023
Blood coagulation factors and platelet response to drug-induced hepatitis and hepatosis in rats.
Article in Animal models and experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 9 citations in OpenAlex.
- Development and validation of a nomogram for early prediction of sepsis-associated liver injury: a multicenter study.Frontiers in medicine · 2026Article
- Anti-Inflammatory and Antiplatelet Interactions on PAF and ADP Pathways of NSAIDs, Analgesic and Antihypertensive Drugs for Cardioprotection-In Vitro Assessment in Human Platelets.Medicina (Kaunas, Lithuania) · 2025Article
- Biomarkers of Hepatic Toxicity: An Overview.Current therapeutic research, clinical and experimental · 2024Review
- Blood coagulation factors and platelet response to drug-induced hepatitis and hepatosis in rats.Animal models and experimental medicine · 2023Article
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9 authors at 4 institutions in 1 country.
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Abstract
backgroundKnowing the variability of blood coagulation responses to liver damage of different origins can provide a key to curing liver tissues or to mitigating treatment side effects. The aim of the present work was to compare the changes in the main components of hemostasis under experimental drug-induced hepatosis and hepatitis in rats.
methodsWe modeled diclofenac-induced hepatitis and tetracycline-induced hepatosis. Hemostasis response was gauged by measuring fibrinogen, factor X, protein C (PC), and prothrombin in plasma. The decarboxylated form of prothrombin was detected by measuring prothrombin index and ecamulin index. Platelet reactivity was studied using aggregometry.
resultsBoth hepatitis and hepatosis decreased the synthesis of fibrinogen, factor X, and prothrombin. However, protein carboxylation was not disrupted in hepatosis but was much impaired in hepatitis. PC decreased in both models as a consequence of its consumption possibly during inflammatory response. Platelet aggregation rate was lower in hepatosis but higher in hepatitis.
conclusionsOur findings imply the need for a thorough monitoring of the hemostasis system in liver diseases to avoid possible thrombotic complications. Its state indicates the disorder's rate and character.
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