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We sought to determine if there is a relationship between prepregnancy underweight status and placental abruption. We utilized the Missouri maternally linked cohort data files covering the period 1989 through 1997. We estimated the association between prepregnancy underweight subtypes and placental abruption using adjusted odds ratios. Subanalyses were performed to determine whether the amount of weight gained during pregnancy could modify the association. A total of 439,235 singleton pregnancies with 3696 abruptions were analyzed. Underweight mothers had a 40% greater likelihood for placental abruption (odds ratio 1.4; 95% confidence interval 1.3 to 1.5). The risk increased with ascending severity of underweight status ( P for trend <0.01). There was a trend toward decreased risk for placental abruption among underweight women with adequate weight gain in pregnancy. Prepregnancy maternal underweight status is associated with placental abruption. This risk may be reduced with adequate weight gain during pregnancy., (Thieme Medical Publishers.)

To determine if diabetes and preeclampsia are independent stimulators of erythropoietin, distinct from hypoxia, we measured umbilical cord plasma erythropoietin in 239 deliveries from 24 to 40 weeks of gestation. Mean plasma erythropoietin levels were not different between normal, diabetic, and preeclamptic women when all deliveries were analyzed. When infants with suspected intrauterine hypoxia were excluded, the mean erythropoietin level was considerably lower within all three groups but there was no difference among the groups. In suspected hypoxia, the mean fetal erythropoietin was elevated, but there was no difference between control, diabetic, or preeclamptic pregnancies. These results provide further support that hypoxia remains the only known stimulator of erythropoietin production in the fetus.

Biochemical and biophysical properties of umbilical arteries from normotensive and preeclamptic pregnancies were examined. The production of prostaglandins E and F, 6-keto-PGF1 alpha, and thromboxane B2 by umbilical arteries from normotensive, mildly preeclamptic, and severely preeclamptic pregnancies were measured in incubation media at baseline and after addition of arachidonic acid. The initial baseline values of 6-keto-PGF1 alpha were decreased in the severely preeclamptic patients with intrauterine growth retardation (IUGR) but not in any of the other groups. Addition of arachidonic acid resulted in a significant increase in 6-keto-PGF1 alpha production over initial baseline in all groups except in the severely preeclamptic pregnancies without IUGR. These results suggest a differential defect in the 6-keto-PGF1 alpha metabolic pathway in severely preeclamptic patients with IUGR compared with those without IUGR. The stretch response curve to serotonin was decreased in the severely preeclamptic group with IUGR compared with the control group. The contractile response to individual vasoactive agents (serotonin, prostaglandin F2, norepinephrine, angiotensin II, and arachidonic acid) showed no significant difference between the normotensive and preeclamptic groups.

A review of 46 perinatal deaths was conducted using a 1982 to 1985 regional perinatal network database of 6701 delivered postdate (greater than or equal to 42 weeks gestation) infants. Perinatal mortality (6.9 per 1000 births) increased as gestational age advanced beyond 42 weeks, and was higher in young teenagers or mothers with some additional antenatal complications, such as hypertension. Meconium staining of the amniotic fluid, low Apgar scores, low birthweight, congenital malformations, and neonatal complications, including pneumothorax, meconium aspiration, and seizures, were associated with perinatal death.