Abstract
Betamethasone (BM) administration in pregnancy has been shown to reduce the incidence and severity of neonatal respiratory distress syndrome. Its known diabetogenic impact, combined with placental insulin resistance, leads to a transient increase in glycemia. However, its effect on glucose homeostasis in pregnancy has not been adequately investigated. We closely monitored and assessed the glycemic profile of 83 pregnant women, with normal glucose metabolism, who were given BM during their hospitalization due to threatened premature labor. A significant change in the glycemic profile in most patients was noted, lasting 1.34 ± 1.05 days. Sixty-six of eighty-three women were eventually treated with insulin to maintain glycemia within acceptable limits. The mean ± SD insulin dosage was 12.25 ± 11.28 units/day. The need for insulin therapy was associated with higher BM doses and the presence of marginal values in the 75-g oral glucose tolerance test (OGTT) at 60 min. Our study demonstrates, following BM administration, the need for increased awareness and individualized monitoring/treatment of pregnant women with normal—yet marginal—values in the 75-g OGTT.
Highlights
The administration of corticosteroids in pregnancy is common practice in obstetrics, with the aiming of reducing the incidence/severity of respiratory distress syndrome and of intraventricular hemorrhage in neonates
Great attention is paid to the group of pregnant women who have either pre-existing diabetes or gestational diabetes, and especially those under insulin therapy
The presence of a statistically significant association between the need for insulin administration following BM and the presence of marginal blood glucose levels at 60 min of oral glucose tolerance test (OGTT) is a possible indication of a mild glucose homeostasis disorder
Summary
The administration of corticosteroids (mainly betamethasone, BM) in pregnancy is common practice in obstetrics, with the aiming of reducing the incidence/severity of respiratory distress syndrome and of intraventricular hemorrhage in neonates. The diabetogenic potential of BM is known, and combined with placental insulin resistance in pregnancy, leads to a transient increase in the blood glucose levels of pregnant women [7,8]. Great attention is paid to the group of pregnant women who have either pre-existing diabetes or gestational diabetes, and especially those under insulin therapy. In this case, it is recommended, by limited bibliographic data, to up-titrate the insulin dose by 30%–40% in order to prevent very high blood glucose levels, which may exacerbate an already at-risk pregnancy (hydramnios) [7,8,9,10,11,12,13,14,15,16].
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