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Objective: To describe the outcome of pregnancy in women with inherited antithrombin (AT) deficiency., Study Design: A descriptive retrospective study was performed. Medical records were reviewed in order to collect data about maternal thrombotic complications and pregnancy outcomes. All women with known inherited AT deficiency and at least one pregnancy looked after at the Vall d'Hebron University Hospital were included. Relatives with known AT deficiency but no pregnancies looked after in our institution were excluded. Eighteen pregnancies were registered among nine AT-deficient women during 1991-2005. This cohort included women without antithrombotic treatment because AT deficiency was not known at the time of their pregnancies., Results: In 12 pregnancies (66.7%) anticoagulant therapy with low-molecular weight heparin was given, while not in the other six (33.3%) because AT deficiency was not known at this time. Three episodes of venous thromboembolism were recorded (16.7%). Among all pregnancies 10 suffered an adverse outcome (55.6%), including miscarriage (11.1%), stillbirth (11.1%), intrauterine growth restriction (33.3%), placental abruption (6.7%), preeclampsia (6.7%) and intrapartum fetal distress (23.1%). No relation between AT activity and pregnancy complications was found. A lower incidence of pregnancy complications was observed among women with antithrombotic treatment., Conclusions: Inherited antithrombin deficiency is associated with a high risk of venous thromboembolism during pregnancy and the puerperium. We also observed a high incidence of poor pregnancy outcome among AT-deficient women., (Copyright 2009 Elsevier Ireland Ltd. All rights reserved.)

Objective: To evaluate the brain venous circulation in fetuses with severe intrauterine growth restriction (IUGR) before 32 weeks of gestation., Study Design: Fifty fetuses with severe IUGR diagnosed between 27 and 32 weeks of gestation and 50 appropriate-for-gestational age (AGA) fetuses matched by gestational age were evaluated. IUGR fetuses were classified according to their hemodynamic deterioration pattern in relation to the Doppler examination of the umbilical artery (UA), middle cerebral artery (MCA) and ductus venosus (DV). The fetal venous brain blood flow was evaluated in the vein of Galen (VG), superior sagittal (SS), straight and transverse venous sinuses., Results: Only the transverse sinus (TS) showed a significant reduction in the pulsatility index (PI) values in IUGR fetuses. All other veins showed similar PI values between IUGR and AGA fetuses. All cerebral veins of IUGR fetuses showed significantly increased maximum and mean velocities. All these findings did not change in relation to the hemodynamic IUGR deterioration. In nearly all normal and all IUGR fetuses, a pulsatile blood flow pattern was observed in the straight and transverse sinuses, whereas an increased pulsatile pattern in the VG and in the SS was noted in IUGR fetuses., Conclusion: Brain venous blood flow in IUGR fetuses shows an increment in the maximum and mean velocities of all veins and a reduction in the PI in the transverse sinus.

We present here the first described case of Nail-patella syndrome (NPS) and pregnancy. Complications occurred during the pregnancy with the onset of preeclampsia at 22 weeks, leading to intrauterine fetal death at 24 weeks. The nephropathy of the NPS began clinically during the course of gestation. Postpartum, it persisted as isolated proteinuria, which became a nephrotic syndrome 18 months later.

Serum fructosamine was measured in 569 samples of pregnant women without gestational diabetes. We defined abnormal fructosamine as mean + 2SD, and analysed its potential value to detect patients with gestational diabetes diagnosed with current screening criteria. We found serum fructosamine to be an insensitive parameter: Measured at the time of a positive 50 g glucose screening, SF would have detected 4/48 gestational diabetes.

Defective plasmatic stimulation of prostacyclin (PGI2) production by vascular cells has been described in patients with lupus anticoagulant (LAC). A young woman with recurrent abortions, LAC and evidence for deficient PGI2 production was studied. Serial measurements of a plasma PGI2 inhibitor, LAC and anticardiolipin antibodies (ACA) have been performed before and throughout her fourth pregnancy. Antenatal care and treatment with prednisone and heparin started at 10 weeks gestation. The plasma of our patient continued to inhibit PGI2 production by vascular cells despite treatment. The presence of inhibitor(s) of PGI2 release was confirmed by mixing the patient's plasma with normal plasma. In addition, an IgM lupus anticoagulant fraction (but not the IgG fraction) interfered with the release of arachidonic acid in human endothelial cells induced by thrombin. Despite prednisone and heparin treatment we did not find a complete correction of the LAC activity and the ACA (IgM type) still remained positive before the detection of a fetal death at 26 weeks. The placenta showed abundant infarcts and areas of ischaemic necrosis. We suggest that the defect in vascular PGI2 release could compromise fetal outcome.

553 cases of intrapartum fetal acidosis (pH less than 7.25) were treated with a betamimetic agent (ritodrine 250-300 micrograms/min). In 403 cases (72.8%), an improvement of fetal pH greater than 0.05 pH U was observed. Improvement was comparable in cases where the cause of fetal distress was abnormal uterine activity and in those where this was not the cause. Indeed, the recovery rate was the same, independent of the percentage of uterine activity inhibition. The neonatal condition was better in the pH recovered versus not recovered group. We suggest that conservative treatment of fetal distress with betamimetic drugs is a reasonable measure for improvement of fetal and neonatal condition.

The palmitic and stearic acids and the palmitic/stearic ratio in fetal rabbit lungs were studied after orciprenaline administration to the mother from the 26th to the 31st day of gestation. The results were significantly higher in the treated groups than in the control group for the palmitic acid and palmitic/stearic ratio.

In a double-blind and randomized study the administration of a betamimetic drug to the mother from week 33 to 35 produces a significant increase in amniotic fluid palmitic acid levels. We suggest that the administration of a betamimetic drug during pregnancy to the mother can be useful in producing an acceleration of the fetal lung maturation.

In 87 premature labors, 31 were treated with betamimetic drugs. The incidence of RDS in the treated group has been lower than in the non-treated group, especially when gestational age was shorter than 35 wk and when newborn's weight was lower than 2000 g.