Diffuse intravascular coagulation in liver disease?
The evidence for intravascular coagulation in liver diseases is critically reviewed. Alternative mechanisms for hypofibrinogenemia and the accelerated disappearance of fibrinogen from blood are proposed, such as loss into extravascular compartments (e.g., ascites, areas of liver necrosis, etc.). Possible mechanisms other than DIC for the elevation of serum FDP are also considered, such as extravascular fibrinogen proteolysis with subsequent transfer of FDP to blood. Therapy is discussed with reference to the current knowledge on pathophysiology of the coagulation defect in liver diseases.
D000347:Afibrinogenemia / Q000150:complications; D001772:Blood Cell Count; D001792:Blood Platelets; D004211:Disseminated Intravascular Coagulation / Q000150:complications* / Q000188:drug therapy; D005166:Factor V Deficiency / Q000150:complications; D005337:Fibrin / Q000378:metabolism; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006207:Half-Life; D006467:Hemophilia A / Q000150:complications; D006493:Heparin / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008107:Liver Diseases / Q000150:complications*; D010447:Peptide Hydrolases / Q000494:pharmacology; D013921:Thrombocytopenia / Q000150:complications; D013927:Thrombosis / Q000150:complications
D005338:Fibrin Fibrinogen Degradation Products; D005337:Fibrin; D005340:Fibrinogen; D006493:Heparin; D010447:Peptide Hydrolases