Hepatic veno-occlusive disease is a clinical syndrome characterized by hepatomegaly, ascites, weight gain and jaundice, due to sinusoidal congestion which can be caused by alkaloid ingestion, but the most frequent cau...Hepatic veno-occlusive disease is a clinical syndrome characterized by hepatomegaly, ascites, weight gain and jaundice, due to sinusoidal congestion which can be caused by alkaloid ingestion, but the most frequent cause is haematopoietic stem cell transplantation （STC） and is also seen after solid organ transplantation. The incidence of veno occlusive disease （VOD） after STC ranges from 0 to 70%, but is decreasing. Survival is good when VOD is a mild form, but when it is severe and associated with an increase of hepatic venous pressure gradient 〉 20 mmHg, and mortality is about 90%. Prevention remains the best therapeutic strategy, by using non-myeloablative conditioning regimens before STC. Prophylactic administration of ursodeoxycholic add, being an antioxidant and antiapoptotic agent, can have some benefit in reducing overall mortality. Defibrotide, which has pro-fibrinolytic and antithrombotic properties, is the most effective therapy; decompression of the sinusoids by a b-ansjugular intrahepatic portosystemic shunt （TIPS） can be tried, especially to treat VOD after liver transplantation and when multiorgan failure （HOF） is not present. Liver transplantation can be the last option, but can not be considered a standard rescue therapy, because usually the concomitant presence of multiorgan failure contraindicates this procedure.展开更多
Sustained accumulatin of 111 indium-labelled platelets is induced in the cerebral vascuiature or rabbits by bolus intracarotid (i. c. ) administration or thrombin (90 U/kg). Bolus i. c. injection of the fibrinolytic, ...Sustained accumulatin of 111 indium-labelled platelets is induced in the cerebral vascuiature or rabbits by bolus intracarotid (i. c. ) administration or thrombin (90 U/kg). Bolus i. c. injection of the fibrinolytic, recombiuant tissue plasminogen activator (rt-PA), 1 miu after thrombin,produced significant inbibition of the. platelet accumulation, albeit substantially less than that produced by 1 min Pretreatment. Hirulogm, PPACK and rt-PA alone had no direct effect on the hasalcirculating levels of 111 In-labedlled platelets in the pulmonary or cranial vasculature at the doses used.Hirulongm and PPACK did not enhance the ability or inrusion or a threshold dose of rt-PA to decrease an established cerebrovascular thromhosis, whereas Defibrotide plus rt-PA produced a significant reduction on accumulated plateiets. These results suggest that fiibrin deposition .plays the impor tant role in the induction and maintenance of the. sustained cerebral platelet accumulation induced bythrombin in this model and Defibrotide can .enhance the pro-fibrinolytic effect of rt-PA although thisProperty is not shared by direct thrombin inhibitors. The sustained platelet accumulation in the cranial vasculature in this model does not appear to be a result or continued generation or endogenousthrombin.展开更多
文摘Hepatic veno-occlusive disease is a clinical syndrome characterized by hepatomegaly, ascites, weight gain and jaundice, due to sinusoidal congestion which can be caused by alkaloid ingestion, but the most frequent cause is haematopoietic stem cell transplantation （STC） and is also seen after solid organ transplantation. The incidence of veno occlusive disease （VOD） after STC ranges from 0 to 70%, but is decreasing. Survival is good when VOD is a mild form, but when it is severe and associated with an increase of hepatic venous pressure gradient 〉 20 mmHg, and mortality is about 90%. Prevention remains the best therapeutic strategy, by using non-myeloablative conditioning regimens before STC. Prophylactic administration of ursodeoxycholic add, being an antioxidant and antiapoptotic agent, can have some benefit in reducing overall mortality. Defibrotide, which has pro-fibrinolytic and antithrombotic properties, is the most effective therapy; decompression of the sinusoids by a b-ansjugular intrahepatic portosystemic shunt （TIPS） can be tried, especially to treat VOD after liver transplantation and when multiorgan failure （HOF） is not present. Liver transplantation can be the last option, but can not be considered a standard rescue therapy, because usually the concomitant presence of multiorgan failure contraindicates this procedure.
文摘Sustained accumulatin of 111 indium-labelled platelets is induced in the cerebral vascuiature or rabbits by bolus intracarotid (i. c. ) administration or thrombin (90 U/kg). Bolus i. c. injection of the fibrinolytic, recombiuant tissue plasminogen activator (rt-PA), 1 miu after thrombin,produced significant inbibition of the. platelet accumulation, albeit substantially less than that produced by 1 min Pretreatment. Hirulogm, PPACK and rt-PA alone had no direct effect on the hasalcirculating levels of 111 In-labedlled platelets in the pulmonary or cranial vasculature at the doses used.Hirulongm and PPACK did not enhance the ability or inrusion or a threshold dose of rt-PA to decrease an established cerebrovascular thromhosis, whereas Defibrotide plus rt-PA produced a significant reduction on accumulated plateiets. These results suggest that fiibrin deposition .plays the impor tant role in the induction and maintenance of the. sustained cerebral platelet accumulation induced bythrombin in this model and Defibrotide can .enhance the pro-fibrinolytic effect of rt-PA although thisProperty is not shared by direct thrombin inhibitors. The sustained platelet accumulation in the cranial vasculature in this model does not appear to be a result or continued generation or endogenousthrombin.
