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The decision for premature termination of a pregnancy has to be weighed against the potential risk of the respiratory distress syndrome (RDS). This is particularly critical in pregnancies complicated by EPH gestosis, diabetes mellitus, rhincompatibility, placenta praevia, placental insufficiency, and in cases of premature labor. The difficulty of estimating fetal lung maturation seems to have been largely alleviated by introduction of the lecithin/sphingomyelin ratio (L/S ratio) measurement into perinatal medicine [1,5, 6, 10]. A further reduction in the risk of a premature born developing RDS is allegedly the administration prior to delivery of betamethasone to the mothers, a prophylactic regime first used by LIGGINS and HOWIE [8, 9]. These authors have reported a remarkably lower incidence of RDS in premature newborns whose mothers had received betamethasone. It is generally believed, that this effect is due to activation of alveolar enzymes inducing the formation of the surface active agents. By betamethasone, this process Starts from cholin phosphate and diglycerides and finally results in an increased synthesis pflecithin [3,4,11]. We report here on the influence of betamethasone on amniotic fluid phospholipids. In this context consideration is also given to the effects of betamethasone administration on estriol excretion and on cortisol content in amniotic fluid.

The effect of betamethasone therapy on the L/S-ratio in amniotic fluid