1970
DOI: 10.1055/s-0028-1108814
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Gerinnungsstörungen bei Lebererkrankungen

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1971
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Cited by 7 publications
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“…This subject matter was comprehensively reviewed by Bloom [12]. The spectrum of coagulation changes noted in patients with acute and chronic liver disease makes it conceivable that intravascular coagulation may contribute to the hemostatic defect [96,102,116,158]. Three possible mechanisms seem to account for this: (1) impairment of splanchnic circulation due to expansion and hemodynamic changes within the portal vasculature, (2) defective hepatic clearance of activated coagulation products, and (3) release of procoagulant material from hepatocytes during necrotic episodes.…”
Section: Anticoagulant Therapy With Heparinmentioning
confidence: 99%
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“…This subject matter was comprehensively reviewed by Bloom [12]. The spectrum of coagulation changes noted in patients with acute and chronic liver disease makes it conceivable that intravascular coagulation may contribute to the hemostatic defect [96,102,116,158]. Three possible mechanisms seem to account for this: (1) impairment of splanchnic circulation due to expansion and hemodynamic changes within the portal vasculature, (2) defective hepatic clearance of activated coagulation products, and (3) release of procoagulant material from hepatocytes during necrotic episodes.…”
Section: Anticoagulant Therapy With Heparinmentioning
confidence: 99%
“…The unresponsiveness of chronic liver disease, such as cirrhosis, to heparin therapy is of particular interest. The coagulation defect in these patients is usually characterized by defective factor synthesis and increased turnover of coagulation factors and platelets [70,96,102,157,158]. The latter can be demonstrated by a shortened fibrinogen half-life and platelet survival.…”
Section: Anticoagulant Therapy With Heparinmentioning
confidence: 99%