The Fibrinolytic System in the Newborn: Role of Histidine-Rich Glycoprotein

Abstract

The fibrinolytic system controls fibrin deposition and its clearance. The efficacy of this system can be evaluated by plasminogen concentration determinations and by the behavior of factors such as histidine-rich glycoprotein (HRG) which controls plasminogen activation and α₂-antiplasmin which controls plasmin activity. Circulating plasminogen levels are decreased in the neonatal period. We studied factors affecting fibrinolysis in neonates and observed that an important reduction in HRG accompanied the reduced circulating plasminogen levels, with the result that 85% of circulating plasminogen was not bound to HRG and was thus free for binding to fibrin and for activation to plasmin. This condition is consistent with the increased fibrinolytic activity secondary to the ‘clotting activation’ observed in the neonatal period particularly on the 1st day of life.

Association of Prothrombin Gene Mutation with Sepsis in a Preterm with Multiple Intracardiac Thrombi

“…The neonatal hemostatic system is characterized by a physiological clotting activation caused by enhanced concentration and activity of several procoagulant factors, increased thrombin formation, and enhanced endothelial activation. In addition, all situations that are common in pathological neonates, such as sepsis, acidosis, hypoxia, polycythemia, and hypoperfusion, are able to enhance endothelial activation with subsequent production of coagulation and fibrin deposition 13,14 . In our patient, multiple risk factors, such as perinatal asphyxia, respiratory distress syndrome, 15 sepsis, and prothrombin gene mutation, could have been responsible for thrombosis development.…”

“…In addition, all situations that are common in pathological neonates, such as sepsis, acidosis, hypoxia, polycythemia, and hypoperfusion, are able to enhance endothelial activation with subsequent production of coagulation and fibrin deposition. 13,14 In our patient, multiple risk factors, such as perinatal asphyxia, respiratory distress syndrome, 15 sepsis, and prothrombin gene mutation, could have been responsible for thrombosis development. The risk of development of a thrombus increases with the increasing number of risk factors.…”

Successful use of tissue plasminogen activator (t-PA) in catheter-related intracardiac thrombi of two premature infants

“…Fibrin deposition control depends on fibrinolytic system. If the fibrinolytic system is impaired, as in case of enhanced request, thrombotic processes may occur (11,12).…”

Prevention of intraventricular haemorrhage: A role for recombinant activated factor VII?

“…However, this is partially offset by higher levels of α2‐macroglobulin 45,46 . The fibrinolytic system in neonates is also immature, with lower levels of circulating plasminogen, and ‘fetal’ forms of fibrinogen and plasminogen with reduced activity in comparison with the adult forms 46–51 . Despite these relative deficiencies the neonatal haemostatic system is effective, and normal infants do not experience spontaneous haemorrhage or thrombosis.…”