Abstract
Pregnancy and puerperium are considered to be hypercoagulable states with increased
incidence of thromboembolic events. During normal pregnancy, changes in the hemostatic
mechanism involve increased stasis and increased coagulation factors and/or decreased
levels of anticoagulant proteins such as protein C and protein S as well as enhanced
thrombin generation and decreased fibrinolytic activity. The physiological or pathophysiological
activation of hemostasis during pregnancy results in the generation of the so-called
activation markers which increase, reflecting hypercoagulability and therefore representing
an imbalance in the hemostatic system. The most interesting markers of hemostasis
activation and, thus, of thrombin generation are: thrombin-antithrombin III complex
(TAT), antithrombin III itself, prothrombin fragment 1+2 (F 1+2), fibrin monomer (soluble
fibrin) and D-Dimer (which indicates also an increased fibrinolytic activity). Together
with fibrinogen levels and platelet counts, the activation markers are useful tools
in different pathological situations in pregnancy to predict and monitor the severity
of the condition.
Recently, a higher incidence of factor V Leiden mutation has been demonstrated in
selected populations in whom thrombotic events developed during pregnancy and puerperium.
Therefore, the combination of APC resistance/FV Leiden mutation and pregnancy may
predict a high risk for thromboembolic phenomena.
In newborns, the activation markers are elevated immediately after birth and decline
to near adult levels during the first 24 h of life. During infections the activation
markers are increased showing the same behavior as in the mature adult system. In
neonates and children, the same etiologies can be responsible for acquired and inherited
pathological hypercoagulable states as in the adult.
Keywords:
Markers of hemostasis activation - hypercoagulability - thromboembolism - pregnancy
- pediatrics
