thromboxane-b2 and Fetal-Death

Intra-uterine growth retardation, intra-uterine fetal death and pre-eclampsia have common abnormalities: A reduction of uteroplacental perfusion, lack of vasodilation of spiral arteries and subsequent thrombosis. These physiological processes have been explained by an imbalance between prostacyclin and thromboxane A2 production. Many studies have suggested that treatment with low-dose aspirin and steroids is effective in preventing pregnancy loss or pre-eclampsia, but the mechanism has not been established. We evaluated the effectiveness of these therapies in patients at risk for pregnancy loss with the aspect of intracellular ionized calcium mobilization. Low-dose aspirin directs the prostacyclin/thromboxane A2 balance to the dominance of prostacyclin and steroids suppress the activities of lupus anticoagulant or antiphospholipid antibodies. The intracellular ionized calcium concentration in platelets is decreased significantly after these therapies. Concerning the pathological examination of placenta, there were deposits of fibrin in only 2 out of 8 cases and there were no abnormal findings in the other 6 cases. These data show that the aggregation of platelets is suppressed in microvascular circulations. These therapies do not cause any adverse effect on the mother or fetus. It is concluded that low-dose aspirin therapy with steroids is useful for patients with a poor obstetrical history.

Topics: 6-Ketoprostaglandin F1 alpha; Aspirin; Calcium; Female; Fetal Death; Fetal Growth Retardation; Humans; Lupus Coagulation Inhibitor; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Thromboxane B2; Treatment Outcome

Abortion or delivery were induced by extra-amniotic instillation of Rivanol during the second trimester in twelve patients and during the third trimester in two patients with fetal death and one patient with fetal acrania. Serial sampling of amniotic fluid was performed through a transabdominal catheter and the levels of free arachidonic acid (AA), prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) were determined. The levels of AA, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and TXB2 in amniotic fluid increased significantly during induction with the exception of AA in fetal death which was high and remained constant during induction. Furthermore, PGF2 alpha, 6-keto-PGF1 alpha and TXB2 were all significantly correlated to AA. These observations suggested that free AA is released during Rivanol-induction of abortion and labour giving an increased synthesis of PGF2 alpha, PGE2 prostacyclin and thromboxane A2 in the fetal membranes and the decidua but not in the fetus. This increase might be relevant for the initiation and progress of abortion and labour in these patients.. Abortion or delivery were induced by extraamniotic instillation of Rivanol during the second trimester in 12 patients, during the third trimester in 2 patients with fetal death, and in 1 patient with fetal acrania. Serial sampling of amniotic fluid was performed through a transabdominal catheter and the levels of free (AA) arachidonic acid, (PGF2alpha) prostaglandin F2alpha, PGE2, 6-keto-PGF1alpha, and (TXB2) thromboxane B2 were determined. The levels of AA, PGF2alpha, PGE2, 6-keto-PGF1alpha, and TXB2 in amniotic fluid increased significantly duirng induction with the exception of AA in fetal death which was high and remained constant during induction. Furthermore, PGF2alpha, 6-keto-PGF1 alpha, and TXB2 were all significantly correlated to AA. These observations suggested that free AA is released during Rivanol induction of abortion and labor giving an increased synthesis of PGF2alpha, PGE2 prostacyclin, and TXA2 in the fetal membranes and the decidua but not in the fetus. This increase might be relevant for the intitiation and progress of abortion and labor in these patients.

Topics: Abortion, Induced; Acridines; Amniotic Fluid; Arachidonic Acids; Ethacridine; Female; Fetal Death; Humans; Labor, Induced; Pregnancy; Prostaglandins; Prostaglandins E; Prostaglandins F; Thromboxane B2; Thromboxanes; Time Factors