Fetal plasma ACTG, cortisol and C-peptide levels and fetal lung maturity in insulin-dependent diabetic pregnancies

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Objective: Maternal diabetes has been associated with an increase risk of fetal pulmonary immaturity. The maternal hyperglycemia which result fetal hyperinsulinemia and other endocrinology changes in fetus in diabetic pregnancies may be responsible for the delayed lung maturation.

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Methods: Fetal blood (FB) and amniotic fluid (AF) samples were obtained by transabdominal cordocentesis and amniocentesis in 24 women with pregnancy, complicated by insulin-dependent diabetes, at 34-37 weeks gestation. Lecithin / sphingomyelin (L/S) ratio was determined by optical density AF at 650 nm, ACTG and C- peptide - by radioimmunoassay, cortisol by immunoenzimaticassay methods. Optical density AF at 650 nm 0,150 is associated with L/S ratio equivalents 2. The statistics was made using Student t-test and correlation analysis.

Results: All women were classified in two groups: I group (n=11) included cases of uncomplicated diabetes and diabetic angiopathy and II group (n=13) — diabetes with severe vascular lesions (retinopahty, nephropathy, hypertension). Optical density AF was lower in the II group (M=0,120±0,05), than in the I (0,172±0,04). Low ACTG and cortisol levels were found out in FB in the II group (M=29,2±7,4 pg/ml and M=69,01 nmol/l), in compare with ACTG concentration M=64,3±34,3 pg/ml and cortisol - M=128,7±52,8 nmol/l in the I group. At the same time fetal hyperinsulinemia in the II group was more significant. The C-peptide mean levels were: in the I group - 0,69±0,27 pmol/l and in the II group - 1,22±0,45 pmol/l. Optical density AF was significantly associated with fetal ACTG and cortisol levels (r=0,537 and r=0,490, p<0,05). There was inverse correlation between AF optical density and C-peptide levels in FB (r=-0,532, p<0, 05). Five newborns from the II group had pulmonary disorders after delivery.

Conclusions: This study found out that fetal pulmonary maturation is different in different classes of diabetes. Severe vascular lesions of maternal insulin-dependent diabetes have been associated with delayed fetal lung maturity. High fetal insulin levels play negative role in pulmonary phospholipid metabolism. ACTG and cortisol accelerate functional lung maturation and alveolar stability and stimulate surfactant synthesis. Insulin showed antagonism in ACTG and cortisol action on fetal lung maturation.