Search

Aims: Amniotic infection (AI) and preeclampsia (PE), which are commonly the reason for prematurity, inflict stress of different duration on immature fetuses. Whether chronic stress, as reflected by intrauterine growth retardation, influences the level of 17-OH progesterone (17-OHP), was not previously examined. Methods: We analyzed 17-OHP and TSH levels during neonatal screenings in the first hours of life of 90 premature infants born between 25 and 33weeks of gestation in infants with AI (n=37) or with PE (n=53). Control of acute stress parameters was derived from umbilical arterial cord blood pH and base excess (BE). Results: Mean 17-OHP levels of infants born to mothers with PE were 85.7nmol/L compared to 54.6nmol/L (P<0.001) in AI infants. 17-OHP was even higher when intrauterine growth restriction was present (99.8nmol/L). Antenatal steroids and mode of delivery did not significantly affect 17-OHP levels. Conclusions: Stress of relatively long duration, as in cases of PE, leads to a significant increase of 17-OHP level in preterm infants. The postnatal 17-OHP level may be considered as a measure for severity of intrauterine stress and might be used as an individualized indicator for earlier intensive care

Aim: To compare oxidative stress in patients with preeclampsia (PE) or intrauterine growth restriction (IUGR) vs. normal pregnancy (controls) during 48h after delivery. Study design: Women with singleton pregnancies were recruited immediately after delivery (gestational age >26.0weeks). Women with PE or IUGR were matched with healthy controls by age, BMI, gestational age and delivery mode. Venous blood samples and urine samples were tested for oxidative stress products 24h and 48h after delivery. Results: Plasma malondialdehyde (MDA) concentration 24h after delivery was significantly higher in subjects with PE or IUGR (3.41±1.14μmol/L, n=20) than in controls (2.91±0.82μmol/L, n=38) (P=0.04). Urine iPF2α-VI declined from 24 to 48h after delivery significantly in controls (P=0.006) and not in subjects with PE or IUGR (P=0.71). Conclusion: Of the markers tested only MDA is indicating higher oxidative stress in women with PE/IUGR than in normal pregnancy and only at 24h after delivery. No consistent pattern of change in the oxidative stress markers exists between 24-48h after delivery

Aims: Amniotic infection (AI) and preeclampsia (PE), which are commonly the reason for prematurity, inflict stress of different duration on immature fetuses. Whether chronic stress, as reflected by intrauterine growth retardation, influences the level of 17-OH progesterone (17-OHP), was not previously examined. Methods: We analyzed 17-OHP and TSH levels during neonatal screenings in the first hours of life of 90 premature infants born between 25 and 33weeks of gestation in infants with AI (n=37) or with PE (n=53). Control of acute stress parameters was derived from umbilical arterial cord blood pH and base excess (BE). Results: Mean 17-OHP levels of infants born to mothers with PE were 85.7nmol/L compared to 54.6nmol/L (P<0.001) in AI infants. 17-OHP was even higher when intrauterine growth restriction was present (99.8nmol/L). Antenatal steroids and mode of delivery did not significantly affect 17-OHP levels. Conclusions: Stress of relatively long duration, as in cases of PE, leads to a significant increase of 17-OHP level in preterm infants. The postnatal 17-OHP level may be considered as a measure for severity of intrauterine stress and might be used as an individualized indicator for earlier intensive care