OBJECTIVE: The aim of the current study was to determine the effects of in vivo administration of prenatal betamethasone in patients at risk for preterm delivery on adrenomedullin (AM) concentrations in maternal and fetal plasma and on AM localization in placenta and fetal membranes. METHODS: A total of 62 pregnant women between 25 and 35 weeks' gestation were studied. Forty-seven pregnant women received betamethasone (2 x 12 mg intramuscularly given 24 hours apart) for stimulation of fetal lung maturity. Blood samples were collected before betamethasone administration and at different time points after the first and the second dose. Further samples were collected at delivery and, in women who did not deliver, after 1 week and 30 days from betamethasone administration. At delivery, placenta and membranes were collected. Fifteen patients who delivered at the same gestational age not receiving betamethasone represented the control group. AM concentration was determined by radioimmunoassay. Localization of AM in placental tissues was assessed by immunohistochemistry. RESULTS: Betamethasone caused approximately 50% increase in maternal plasma AM at 1 week after administration, whereas in fetal plasma AM levels increased by about 90% at 48 hours after betamethasone administration. There was increased immunohistochemical staining for AM in fetoplacental tissues collected after betamethasone administration. CONCLUSION: These results provide the first evidence for in vivo stimulation of AM, likely of placental origin, by glucocorticoids in the third trimester human pregnancy.
OBJECTIVE: The aim of the current study was to determine the effects of in vivo administration of prenatal betamethasone in patients at risk for preterm delivery on adrenomedullin (AM) concentrations in maternal and fetal plasma and on AM localization in placenta and fetal membranes. METHODS: A total of 62 pregnant women between 25 and 35 weeks' gestation were studied. Forty-seven pregnant women received betamethasone (2 x 12 mg intramuscularly given 24 hours apart) for stimulation of fetal lung maturity. Blood samples were collected before betamethasone administration and at different time points after the first and the second dose. Further samples were collected at delivery and, in women who did not deliver, after 1 week and 30 days from betamethasone administration. At delivery, placenta and membranes were collected. Fifteen patients who delivered at the same gestational age not receiving betamethasone represented the control group. AM concentration was determined by radioimmunoassay. Localization of AM in placental tissues was assessed by immunohistochemistry. RESULTS:Betamethasone caused approximately 50% increase in maternal plasma AM at 1 week after administration, whereas in fetal plasma AM levels increased by about 90% at 48 hours after betamethasone administration. There was increased immunohistochemical staining for AM in fetoplacental tissues collected after betamethasone administration. CONCLUSION: These results provide the first evidence for in vivo stimulation of AM, likely of placental origin, by glucocorticoids in the third trimester human pregnancy.