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(Defibrotide) is an adenosine receptor agonist with multiple effects, and the mechanism of action of Sodium defibrotide (Defibrotide) has not been fully elucidated. Defibrinoside enhances the enzymatic activity of plasmin that hydrolyzes fibrin clots. Studies evaluating the pharmacological effects of defibrotide on endothelial cells (ECs) were primarily conducted in human microvascular endothelial cell lines.

Defibrotide increases tissue plasminogen activator (t-PA) and thrombomodulin expression and decreases von Willebrand factor (vWF) and plasminogen activator inhibitor-1 (PAI-1) expression, thereby reducing EC activation and increasing EC-mediated fibrinolysis. Sodium defibrotide (defibrotide) protects ECs from damage caused by chemotherapy, tumor necrosis factor-alpha (TNF-alpha), serum starvation, and perfusion.

Indications of defibrotide sodium: It is suitable for the treatment of adult and pediatric patients with hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome (SOS), and renal or pulmonary dysfunction after hematopoietic stem cell transplantation (HSCT).

Defibrotide (defibrinoside) may enhance the pharmacodynamic activity of antithrombotic/fibrinolytic agents such as heparin or alteplase. Concomitant use of defibrotide sodium (defibrinoside) with antithrombotic or fibrinolytic agents is contraindicated due to an increased risk of bleeding.

The recommended dose of defibrotide sodium (Defibrotide) for adult and pediatric patients is 6.25 mg/kg given every 6 hours as a 2-hour intravenous infusion. The dose should be based on the patient's baseline weight, which is defined as the patient's weight before the HSCT preparation protocol. Give sodium defibrate (defibrotide) for a minimum of 21 days. If signs and symptoms of hepatic VOD have not resolved after 21 days, continue defibrination until resolution of VOD or up to a maximum of 60 days. Defibrotide must be diluted prior to infusion.

Other studies have found that defibrotide sodium (defibrinoside) can bind to plasmin, increase plasmin activity and promote fibrinolysis, but it cannot activate plasminogen to plasmin. Another study found that bacterial lipopolysaccharide (LPS) can induce the expression of TF in vascular endothelial cells, increase the level of plasminogen activation inhibitor-1 (PAI-1) and reduce the level of tissue plasminogen activator (t-PA), while DF can inhibit these effects of LPS, thereby promoting fibrinolysis. (Defibrinoside) can also increase the expression of t-PA in resting endothelial cells, enhance fibrinolysis, and avoid fibrin deposition and vascular occlusion.

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