ABSTRACT
Two dangerous obstetric complications, amniotic fluid embolism and preterm prelabor
rupture of membranes (PROM), can be caused by amniotic fluid (AF) constituents. Disseminated
intravascular coagulation (DIC) is related to the former complication, whereas local
thrombin/plasmin-dependent collagenolysis in the decidua and fetal membranes is associated
with the latter. In AF, most proteins of the coagulation and fibrinolysis system,
known as plasma constituents, have been identified based on the activity and/or presence
of antigen. The AF levels of most of these proteins are low (< 2 to 5% of the respective
maternal plasma levels). However, there are some exceptions: tissue factor (TF), urokinase
plasminogen activator (uPA) and its receptor (uPAR), as well as plasminogen activator
inhibitors. The AF level of fetal fibrinogen is trace, which is a particular exception.
The key enzymes of coagulation and fibrinolysis, thrombin and plasmin, are generated
in AF. Thrombin generation is four- to fivefold higher than in maternal plasma as
measured by the concentration of the prothrombin fragments 1 + 2 (F 1 + 2) and thrombin-antithrombin
complexes, whereas plasmin generation is relatively low as measured by the plasmin–α-2-antiplasmin
complexes. Phosphatidylserine, a phospholipid, and thrombin-activatable fibrinolysis
inhibitor (TAFI) are novel components of AF. Phosphatidylserine contributes to DIC
in AF embolism; TAFI is considered a link between coagulation and fibrinolysis. uPA
and uPAR are the factors contributing to PROM via plasmin-dependent proteolysis. Intriguing
is the assumption that TF and its inhibitor can be risk factors for PROM through thrombin-dependent
activation of matrix prometalloproteinases in the decidua and fetal membranes. It
is unknown whether the amniotic pool of hemostatic components is involved in pre-eclampsia
pathogenesis.
KEYWORDS
Amniotic fluid - procoagulants - anticoagulants - fibrinolysis - PROM
REFERENCES
kizproped@amb.bydgoszcz.pl
