Excessive consumption of blood coagulation components as cause of hemorrhagic diathesis

Verstraete, Marc; Vermylen, C; Vermylen, J.; Vandenbroucke, J

doi:10.1016/0002-9343(65)90009-4

Cited by 134 publications

(34 citation statements)

References 41 publications

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“…Mild thrombocytopenia, even when platelet production is still active, was ob served in many patients with fulminant hepatic failure (28-31), severe liver cirrhosis (22)(23)(24)(32)(33)(34), and after homotransplantation of the liver (35). Fibrin degradation products were also often increased and the thrombin time prolonged even in the presence of normal fibrinogen levels.…”

Section: Similarity Of the Coagula Non Profile In Disseminated Intrmentioning

confidence: 99%

Intravascular Coagulation in Liver Disease

Verstraete¹,

Vermylen²,

Collen³

1974

Annu. Rev. Med.

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Section: Similarity Of the Coagula Non Profile In Disseminated Intrmentioning

confidence: 99%

Intravascular Coagulation in Liver Disease

Verstraete¹,

Vermylen²,

Collen³

1974

Annu. Rev. Med.

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“…There is a similarity between the complex coagulation and fibrinolytic disturbances in cirrhosis and those observed in clinical or experimental disseminated intravascular coagulation (8)(9)(10). To substantiate the hypothesis of chronic disseminated intravascular coagulation, potentially associated with secondary activation of the fibrinolytic system, the metabolism of labeled fibrinogen was analyzed in 50 patients with cirrhosis of the liver.…”

Section: Introductionmentioning

confidence: 99%

Metabolism of Fibrinogen in Cirrhosis of the Liver

Tytgat¹,

Collen²,

Verstraete³

1971

J. Clin. Invest.

128

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A B S T R A C T The metabolism of human fibrinogen labeled with radioactive iodine was studied in 50 patients with documented cirrhosis of the liver and in 35 healthy control subjects. Results in cirrhotic subjects were the following: plasma volume 47 ±+10 ml/kg; plasma fibrinogen concentration 250 ±102 mg/100 ml; total plasma fibrinogen pool 118 ±59 mg/kg, representing 0.73 +0.10 of the total body pool; fibrinogen half-life 2.99 +0.59 days; fractional catabolic rate 0.34 ±0.09 of the plasma pool per day; absolute catabolic rate 39 ±20 mg/kg per day; fractional transcapillary efflux rate 0.82 ±0.30 of the plasma pool per day. Results in the control subjects were the following: plasma volume 42 ±7 ml/kg; plasma fibrinogen concentration 284 ±71 mg/100 ml; total plasma fibrinogen pool 119 ±40 mg/kg, representing 0.72 +0.07 of the total body pool; fibrinogen half-life 4.14 ±0.56 days; fractional catabolic rate 0.24 ±0.04 of the plasma pool per day; absolute catabolic rate 28 ±9 mg/kg per day; fractional transcapillary efflux rate 0.60 ±0.26 of the plasma pool per day.A significant difference between cirrhotics and controls was observed for plasma volume, fibrinogen halflife, fractional and total catabolic rates, and transcapillary efflux rate. During heparinization of 10 cirrhotic patients the fibrinogen half-life was prolonged from 3.15 ±0.69 to 4.59 ±0.79 days. This was associated with a rise in plasma fibrinogen in six out of eight patients. Heparinization did not influence the fibrinogen half-life in five control subjects. Inhibition of the fibrinolytic system in 17 patients resulted in prolongation of the plasma radioactivity half-life of more than 1 day in only three patients, an incidence comparable with that in five control subjects.These results strongly support the concept of accelerated fibrinogen consumption by a process of disseminated intravascular coagulation in cirrhosis of the liver.

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“…Because of the occurrence of intravascular coagulation in the patients examined so far with hemolytic-uremic syndrome, heparin therapy is indicated [34], to prevent an increasing thrombosis and further renal damage. At the same time this would diminish the hemolysis, probably of mechanical origin [l], thus counteracting the hypercoagulability of the blood [26].…”

Section: Discussionmentioning

confidence: 99%