PubMed · 5787354
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G K Steigleder. 1969-06-27. [Periocically occurring aphthae].. https://pubmed.ncbi.nlm.nih.gov/5787354/
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OBJECTIVE: The objective of the study was to determine the efficacy and side effects of corticosteroid therapy for pregnant women with severe preeclampsia in the prevention of respiratory distress syndrome in their premature neonates. STUDY DESIGN: A prospective double-blind randomized trial enrolled 218 pregnant women with severe preeclampsia and gestational age between 26 and 34 weeks. One hundred ten received betamethasone (12 mg administered intramuscularly, repeated after 24 hours and then once a week) and 108 received placebo. Relative risks and 95% confidence intervals of respiratory distress syndrome and other neonatal and maternal complications were calculated for corticosteroid use. RESULTS: Frequency of respiratory distress syndrome was significantly reduced in the corticosteroid group (23%) with respect to the placebo group (43%), with a relative risk of 0.53 (95% confidence interval 0.35-0. 82). Relative risks of intraventricular hemorrhage, patent ductus arteriosus, and perinatal infection were significantly decreased in the corticosteroid group: 0.35 (95% confidence interval 0.15-0.86), 0.27 (95% confidence interval 0.08-0.95), and 0.39 (95% confidence interval 0.39-0.97), respectively. There was no significant difference in the frequency of stillbirth, but the neonatal mortality rate was lower in the corticosteroid group (14%) than in the placebo group (28%), with a relative risk of 0.5 (95% confidence interval 0.28-0.89). There was increased risk of gestational diabetes but of no other maternal complication after corticosteroid therapy, and mean blood pressures were similar in the 2 groups. CONCLUSIONS: Antenatal corticosteroid therapy with betamethasone for acceleration of fetal lung maturity is a safe and efficient treatment in patients with severe preeclampsia at between 26 and 34 weeks' gestation.
OBJECTIVE: Maternal salivary estriol levels are an indirect measure of fetal adrenal activity, which may be affected by administration of betamethasone. The objective was to compare sequential salivary estriol levels in patients receiving serial betamethasone therapy with those of healthy pregnant patients. STUDY DESIGN: Ten patients at high risk for preterm delivery were asked to obtain salivary specimens before and 1 to 2 days after each administration of weekly betamethasone treatments between 24 and 32 weeks' gestation. These values were compared with those of specimens obtained throughout gestation in healthy women who were not delivered preterm. Unconjugated salivary estriol was measured with a sensitive and specific enzyme-linked immunoassay (Biex, Inc, Dublin, Calif). RESULTS: The effect of betamethasone on salivary estriol levels did not change with time, showing an average of 23.1% drop from pretreatment to posttreatment levels but rebounding to the same starting level before the next dose. When weekly pretreatment values were looked at across time, the geometric mean of the individual patients' slopes did not differ significantly from no change. The same was true of the posttreatment values. The rate of change with advancing gestation was compared between 182 control subjects and the 10 study subjects. The average change was +8.8% per week in the control subjects and -1.3% per week in the study patients (P =.003). CONCLUSIONS: Maternal administration of betamethasone significantly suppressed salivary estriol levels. These levels returned to pretreatment values each week before the next dose; however, the rise normally associated with advancing gestational age was not observed.
During the course of human pregnancy, glucocorticoid (GC) treatment is given when preterm delivery is expected. This treatment is successful in stimulating the development of the fetal lung. However, in animal studies, a number of side effects of perinatal GC treatment have been described. The aim of the present study was to evaluate in humans the effects of antenatal GC treatment on development of the immune system. In addition, we examined the development of immune reactivity in infants born preterm and at term who did not receive GC treatment antenatally. We tested mitogen-induced T cell proliferation, natural killer cell activity, and lipopolysaccharide-induced IL-6 production in cord blood samples. We found that there is a significant effect of gestational age on the capacity of T cells to proliferate and of natural killer cells to kill K562 tumor cells. The capacity to produce IL-6 does not change between gestational age 26 and 41 wk. Moreover, our results show that antenatal treatment with GC does have immunomodulatory effects: T cell proliferation is decreased in infants born very preterm (gestational age 26-31 wk) as well as in infants born between 32 and 36 wk of gestation. In contrast, the activity of natural killer cells is only increased in GC-treated infants born between 26 and 31 wk. We did not observe a significant effect of antenatal GC treatment on the capacity to produce IL-6.