Background:Knowing 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 ...Background:Knowing 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.Methods:We modeled diclofenac-induced hepatitis and tetracycline-induced hepa-tosis.Hemostasis response was gauged by measuring fibrinogen,factor X,protein C(PC),and prothrombin in plasma.The decarboxylated form of prothrombin was de-tected by measuring prothrombin index and ecamulin index.Platelet reactivity was studied using aggregometry.Results:Both 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.Conclusions:Our 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.展开更多
基金National Academy of Sciences of Ukraine research,Grant/Award Number:0119U002512。
文摘Background:Knowing 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.Methods:We modeled diclofenac-induced hepatitis and tetracycline-induced hepa-tosis.Hemostasis response was gauged by measuring fibrinogen,factor X,protein C(PC),and prothrombin in plasma.The decarboxylated form of prothrombin was de-tected by measuring prothrombin index and ecamulin index.Platelet reactivity was studied using aggregometry.Results:Both 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.Conclusions:Our 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.
