SUMMARY Twenty-two patients with acute hepatic failure were studied to determine the incidence and magnitude of intravascular coagulation and fibrinolysis and their relation to the severity of bleeding and prognosis. The mean platelet count, Thrombotest, plasminogen activator, and plasminogen were reduced; the reduction in fibrinogen was not statistically significant. Fibrin/ fibrinogen degradation products were only moderately increased. Hepatic fibrin deposition was not extensive, being present in 11 of 22 hepatic sections, more in areas of confluent necrosis than in the sinusoids. The combination of increased fibrin/fibrinogen degradation products with decreased plasminogen activator, plasminogen, and thrombocytopenia isconsistentwith a diagnosis ofintravascular coagulation and secondary local fibrinolysis. However, neither of these processes was severe. Severity of bleeding was related only to plasminogen levels and prognosis only to Thrombotest levels. There was no relation between hepatic histological and haematological findings. Heparin therapy is not indicated in the routine management of acute hepatic failure, as intravascular coagulation is not severe and heparin may itself cause massive bleeding.
SUMMARY Porcine calcitonin given to guinea pigs in doses causing hypocalcaemia and hypophosphataemia decreased the bilirubin concentration and increased the activity of gamma glutamyl transpeptidase (GGTP) in the hepatic bile. Calcitonin had no effect on bile flow, its pH, electrolyte composition including calcium, or on the concentration of protein, glucose, cholesterol, nonprotein nitrogen (NPN), and bile acids. It also did not affect the activities of alanine aminotransferase (AIAT) and alkaline phosphatase (AP) in the hepatic bile. Calcitonin increased the calcium content in the liver.Calcitonin exerts an inhibitory effect on various secretory systems of the gastrointestinal tract in man and in animals reducing basal and stimulating gastric acid
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