[Placenta accreta: epidemiology, molecular mechanism (hypothesis) and some clinical remarks].

OBJECTIVE

To develop the hypothesis on biochemical mechanism of the placenta accreta and to review the epidemiological information on that complication.

STUDY

DESIGN

Data collected in 1995-2002 in the Medline System were the main source of analyzed literature.

RESULTS

Placenta accreta occurs in approximately 1 of 2500 deliveries, however among women with placenta praevia, the incidence is nearly 10%. Independent risk factors for placenta accreta are previous cesarean delivery and maternal age > or =35 years. Postpartum hemorrhage is the main cause of maternal mortality. Hysterectomy is often performed to save the life of the mother. Ligation of internal pelvic arteries is considered to be ineffective procedure in about 50%. An another option in management of hemorrhage is embolisation of pelvic arteries. Recombinant factor VIIa is recommended is a new agent in pharmacological therapy. Our hypothesis is as follows: The complex of uPA/uPAR (urokinase plasminogen activator/receptor of urokinase plasminogen activator complex) plays crucial role in the generation of plasmin-dependent proteolysis, which takes place in the surface of trophoblast. Penetration of the villi into the tissues is controlled by plasminogen activator inhibitors--plasminogen activator inhibitor 1 (PAI-1) and plasminogen activator inhibitor 2 (PAI-2), mainly by PAI-2. PAI-2 inactivates uPA/uPAR complexes forming triplicate complexes. If the PAI-2 concentration in placenta and myometrium is low, the invasion of placenta villi is excessive.

CONCLUSION

Disturbance of balance between plasminogen activator and their inhibitors (PAI-1 and PAI-2) in placenta and myometrium can lead to the formation of placenta accreta.