Increased umbilical cellular fibronectin concentrations are associated with a decreased prevalence of growth restriction in preeclampsia.

OBJECTIVE: Cellular fibronectin (cFN), a marker of endothelial activation, is elevated in maternal and cord blood in preeclampsia. We tested whether maternal or fetal cFN is related to fetal growth restriction in preeclampsia, in the context of gestational age at delivery. METHODS: Cellular fibronectin was measured in maternal and cord blood of 29 preeclamptic women and their infants delivered at Magee-Womens Hospital at 25-41 weeks of gestation. Relationships among maternal and cord cFN, birth weight, birth weight percentile, and ponderal index were evaluated using Pearson correlation and regression analyses controlled for gestational age. RESULTS: Cord cFN was not significantly related to maternal cFN (r = -.34, P = .08) or gestational age (r = -.32, P = .09). The relationship of maternal cFN to each index of infant size was not significant. By contrast, higher cord cFN predicted higher birth weight, birth weight percentile, and ponderal index (P < .05). CONCLUSION: Elevated maternal and cord cFN concentrations have been reported in pregnancy complicated by preeclampsia. This study assessed the relationship among maternal cFN, cord cFN, and indices of fetal growth in preeclampsia. Elevated cord cFN was associated with measures of better fetal growth.

Evidence of endothelial activation and endothelial activators in cord blood of infants of preeclamptic women.

OBJECTIVE: In preeclampsia markers of endothelial activation (e.g., increased cellular fibronectin and activities that alter in vitro endothelial function (e.g., stimulation of nitric oxide and prostacyclin generation) are increased in the maternal circulation. We tested preeclamptic infant blood for these markers and activities and correlated these findings with fetal growth. STUDY DESIGN: Plasma was obtained from 17 term nulliparcus preeclamptic and normal pregnant women and their infants and from 8 additional preeclamptic mother-baby pairs from earlier gestations. Plasma cellular fibronectin and production of nitric oxide and prostacyclin by cultured endothelial cells exposed to 2% plasma were measured. RESULTS: Cellular fibronectin was higher in maternal plasma of preeclamptic than nonpregnant women (6.1 +/- 0.29 vs 4.2 +/- 0.27 microgram/ml, p < 0.01), as were stimulated endothelial nitric oxide and prostacyclin production (nitric oxide 42.5 +/- 3.9 vs 26.9 +/- 2.3 nmol nitrite/microgram protein/24 hours, p < 0.05; prostacyclin 261.7 +/- 31.2 vs 151.9 +/- 18.7 pg prostaglandin F1 alpha/microgram protein/24 hours, p < 0.05). In the preeclamptic infants cellular fibronectin was also greater (3.3 +/- 0.15 vs 2.6 +/- 0.14 microgram/ml, p < 0.01), as was endothelial nitric oxide production in response to the plasma (24.4 +/- 1.1 vs 21.4 +/- 0.09 mumol/L nmol nitrite/microgram protein/24 hours, p < 0.05). Prostacyclin production was not significantly different. In preeclamptic infants across a wide gestational age there was no correlation of endothelial activation and fetal growth. CONCLUSIONS: Infants of women with preeclampsia may be affected by endothelial dysfunction, as well as reduced uteroplacental perfusion.

Pulse dexamethasone does not impair growth and body composition of very low birth weight infants.

OBJECTIVE: Evaluation of repeated pulses of dexamethasone (PDEX), given to improve cardiopulmonary outcome, on growth of very low birth weight (VLBW, < 1500 g) infants. METHODS: In this prospective, double-blind, randomized clinical trial, VLBW infants mechanically ventilated at 1 week of age received intravenous PDEX or saline placebo (P) for 3 days, every 10 days, until no supplemental oxygen or ventilation was required or 36 weeks postmenstrual age (PMA). Weight gain, fluid intake, caloric intake, and serum glucose were monitored throughout the study. Nutritional assessment at 36 weeks PMA consisted of weight, length, head circumference, skinfold thickness measures, body composition by total body electrical conductance, and bone mineral content (BMC) by single beam photon absorptiometry. RESULTS: 37 PDEX and 31 P infants survived at least 36 days and completed the protocol. Average daily weight gain, fluid intake and caloric intake were not different between groups. The pattern of weight gain (g/kg/day, mean +/- SD) was different: PDEX infants showed significant growth delay during (3.0 +/- 11.4) and immediately after (7.8 +/- 8.7) each pulse, with subsequent growth acceleration (18.3 +/- 8.2) until the next steroid pulse. In contrast, growth rate of P infants was constant (12.6 +/- 3.7) (p = 0.04). Hyperglycemia requiring insulin therapy occurred only in the PDEX group (10/37). The catch-up growth noted between pulses in the PDEX group was explained only in part by insulin therapy. At 36 weeks PMA, there were no differences between groups in body size, composition, or BMC. CONCLUSION: PDEX negatively affected glucose metabolism and growth patterns during and immediately after drug exposure. However, assessment near term gestational age showed similar body composition and size in both groups.

Effect of pulse dexamethasone therapy on the incidence and severity of chronic lung disease in the very low birth weight infant.

We conducted a prospective, randomized, double-blind trial to assess the efficacy and safety of pulse doses of dexamethasone on survival without supplemental oxygen in very low birth weight infants at high risk of having chronic lung disease. Seventy-eight infants with birth weights < or = 1500 gm who were ventilator dependent at 7 days of postnatal age were randomly assigned to receive pulse doses of dexamethasone, 0.5 mg/kg per day, divided twice daily (n = 39), or an equivalent volume of saline solution placebo (n = 39), for 3 days at 10-day intervals until they no longer required supplemental oxygen or assisted ventilation, or reached 36 weeks of postmenstrual age. At study entry, the groups did not differ by birth weight, gestational age, or severity of lung disease. At 36 weeks of postmenstrual age, there was both a significant increase in survival rates without oxygen supplementation (p = 0.03) and a significant decrease in the incidence of chronic lung disease (p = 0.047) in the group that received pulse therapy. Supplemental oxygen requirements were less throughout the study period in the group that received repeated pulse doses of dexamethasone (p = 0.013). The total numbers of deaths and the durations of supplemental oxygen, ventilator support, and hospital stay did not differ between groups. Recorded side effects in the pulse therapy group were minimal and included an increase in the use of insulin therapy for hyperglycemia (p < 0.05). We conclude that in this population of very low birth weight infants, treatment with pulse doses of dexamethasone resulted in improvement in pulmonary outcome without clinically significant side effects.