Maternal diabetes and neonatal respiratory distress. I. Maturation of fetal surfactant

Abstract

summary The phospholipid composition of amniotic fluid samples from 30 normal patients and 44 diabetic patients over the last 10 weeks of pregnancy was studied. Higher levels of phosphatidylcholine (PC) and phosphatidylinositol (PI) were found in diabetic pregnancies where there was excellent glucose control. These differences were statistically significant at 34–36 weeks. Phosphatidylglycerol (PG) aeared significantly earlier in the well controlled diabetic pregnancies. but even in the poorly controlled diabetics the levels of PC, PI and PG were comparable to those in normal pregnancies. There was no evidence of delayed aearance of fetal surfactant phospholipids in either the well or poorly controlled diabetic pregnancies. The absolute lecithin (PC)/sphingomyelin (SM) ratio in diabetic pregnancies was generally greater for any given gestational age than those in normal pregnancies. Whilst in most cases this was due to a higher PC concentration, in a few poorly controlled diabetics it was the result of a lower concentration of SM.

Macrosomia in Pregnancy Complicated by Insulin-Dependent Diabetes Mellitus

“…Despite attention to all these measures, macrosomia will still occur but should not be associated with significant perinatal complications if the patient has achieved good glycemic control in the latter half of pregnancy and if neonatal hypoglycemia is rapidly detected and corrected. Even if good glycemic control in pregnancy will not guarantee the birth of a nonmacrosomic infant, there is such compelling evidence that meticulous diabetic control reduces perinatal morbidity and mortality that euglycemia remains the therapeutic aim for every diabetic patient during pregnancy (8,19,(27)(28)(29)(30)(31).…”

Surfactant Maturation and Preterm Premature Membrane Rupture: A Case Study

“…It may be that it is a manifestation of the normal surfactant maturation process, which normally commences, on average, at 34 weeks [1], and which has been unaffected by the membrane rupture. Studies on plate let-activating factor (PAF) in amniotic fluid have suggested that the two processes might be commonly related [10].…”

“…Onemillilitre aliquots of each sample were subjected to a standard lipid extraction technique [8]. The phospho lipid content of the lipid extract was then assayed using a method previously described [1]. The concen trations of three surfactant phospholipids were mea sured: phosphatidylcholine (PC), phosphatidylinosi tol (PI) and phosphatidylglycerol (PG) together with the concentration of sphingomyelin (SM).…”

“…A number of factors are known to in fluence fetal surfactant production, includ ing maternal diabetes [1], rhesus disease [2], maternal treatment with steroids [3] and ma ternal heroin addiction [4], Preterm premature membrane rupture (PPROM) has also been shown to accelerate fetal lung surfactant maturation. Evidence for this principally comes from the observa tion of a lower incidence of respiratory dis tress syndrome in babies delivered preterm, where the preceding duration of membrane rupture exceeded 48 h [5,6], The mecha nism whereby lung maturation is accelerated in PPROM is unclear.…”

Dexamethasone Enhances Surfactant Protein Gene Expression in Streptozotocin-Induced Immature Rat Lungs

“…In humans, the lecithin: sphingomyelin ratio of 2 2 and the presence of phosphatidylglycerol in amniotic fluid (1 1, 12) suggests fetal lung maturity. However, the infants in full term diabetic pregnancies are at increased risk of developing RDS, despite normal lecithin: sphingomyelin ratio of 2 2 (13)(14)(15). Some reports have shown that the level of SP-A is reduced in amniotic fluid of pregnant diabetic women (16,17), suggesting that decreased SP-A contributes to the increased incidence of RDS in infants of diabetic mothers.…”