Index Of Fetal Lung Maturity Research Articles

Contemporary practice patterns in the use of amniocentesis for fetal lung maturity

Purpose: Fetal lung maturity (FLM) testing has been performed to help direct delivery timing in complex obstetrical conditions. We explored current practice patterns of FLM testing attempting to identify factors affecting its use.Materials and methods: We distributed a 31-question survey to obstetricians and perinatologists that examined practice characteristics potentially affecting FLM usage. Logistic regression measured associations between these factors and test utilization. Weighted averages were calculated for conditions in which respondents considered FLM testing helpful.Results: Three hundred four surveys were completed. The response rate for respondents actively practicing obstetrics was 52%. The majority of respondents utilize FLM testing; however, 80% reported a decline in use over the past five years with 64% citing “published guidelines” as the reason. Respondents found FLM testing most applicable for poorly dated pregnancies. After an immature FLM test, 44% of respondents administer antenatal corticosteroids in the late-preterm period. None of the factors surveyed were significantly associated with FLM testing use.Conclusion: The majority of respondents use FLM testing although significant factors contributing to its use were not identified. We discover a high frequency of antenatal corticosteroid administration beyond 34 weeks gestational age in response to immature FLM indices that may be an area for future study.

Comparative analysis of amniotic fluid lamellar body count and foam stability test as indices of fetal lung maturity

Respiratory distress syndrome of the newborn caused by the fetal lung immaturity is a very serious clinical problem. Different tests of prenatal analysis of amniotic fluid, such as lamellar body count and Clements' test, are available for predicting the fetal lung maturity. A prospective clinical study was conducted on amniotic fluid samples from 2005 to 2006. The amniotic fluid samples were obtained at the gestational age of 30 to 42 weeks and collected by vaginal amniotomy, amniotomy during Caesarean section and 72 hours before the delivery by amniocentesis. A haematology analyzer (Nikon - Kohden) was used to determine the lamellar body counts. Clements' test involved adding an equal volume of 96% ethanol to the multiple amniotic fluid volume (1:2, 1:4, 1:16. 1:32), followed by shaking and noting the presence of ring of bubbles. After the delivery, we compared the lamellar body count results and Clements' test and the outcome of pregnancies, primarily the development of respiratory distress syndrome. The most specific lamellar body cutoffs for maturity and immaturity were determined according to receiver operating characteristic curves. Out of 232 amniotic fluid samples which were tested, 112 samples were collected after vaginal amniotomy, 88 during the Caesarean delivery and 32 samples by amniocentesis. The overall incidence of respiratory distress syndrome was 14.6%. Receiver operating characteristic curves were used to identify cutoff points for the test. We found that both tests are good screening tests for predicting the fetal lung maturity with the area under the curve of 0.782 in Clements' test and 0.751 in the lamellar body count. Clements' cutoff 2 with sensitivity of 67.6% and specificity of 72.2%, proved best in the prediction of the fetal lung maturity. The lamellar body count cutoff of 42 x 10(3)/microl had the sensitivity of 82.4% and specificity of 64.6% in predicting the fetal lung maturity. Although both tests are good in predicting the fetal lung maturity, the lamellar body count has more advantages, because it is not only more objective, but also inexpensive, easy and fast to do, requires a small sample volume and is universally available.

Association between maternal-fetal Doppler velocimetry and fetal lung maturity.

To correlate maternal-fetal Doppler velocimetry parameters to indices of fetal lung maturity (FLM). Fifty-five consecutive third trimester pregnancies in which a pulsed-wave Doppler study, including uterine resistance index (Ut RI), umbilical artery pulsatility index (UA PI), middle cerebral artery pulsatility index (MCA PI) and the UA/MCA ratio was performed within 24 hours before amniocentesis and within a week from birth. FLM was determined by amniotic fluid lamellar bodies count (LBs). A positive correlation between MCA PI and LBs (p < 0.007, r = 0.44) was found. MCA PI showed a trend to lower values in fetuses that developed RDS at birth (1.3 +/- 0.5 vs. 1.7 +/- 0.4, NS). LBs significantly decreased as Ut RI increased (O.R.: 0.98, C.I. 0.97-0.99, p < 0.05). A mean Ut RI > 0.64 was correlated to delayed FLM (LBs < 20,000/microl; sensitivity: 90.9%, specificity: 90.3%; positive predictive value: 76.9%, negative predictive value: 96.6%). In third trimester pregnancies abnormal uterine artery waveforms may be associated to a delayed FLM, as expressed by decreased amniotic fluid LBs.

Fetal lung maturity indices—a plea for gestational age–specific interpretation: A case report and discussion

A fetus with mature amniotic fluid lung indices was delivered with subsequent respiratory distress syndrome, demonstrating that fetal pulmonary maturity needs to be viewed as a probability. We calculated the probability of respiratory distress as a function of gestational age and fetal lung maturity. The percent risks are displayed in an easily readable table format. (Am J Obstet Gynecol 2002;187:1721-2.)

Time-dependent effects of maternal continuous propranolol on fetal lung development in rats.

Previous studies have demonstrated a role for the beta-adrenergic system in the maturation of the fetal alveolar epithelium. Chronic blockade of beta-adrenergic binding sites has been shown to adversely effect physiologic and biochemical indices of fetal lung maturation. In the present study timed-pregnant female Sprague-Dawley rats were treated with a continuous 0.5 mg/hr dose of propranolol HCl, or saline, via an osmotic pump. The treatment periods were days 18-21, or 20-23 of gestation. Fetal body weights were obtained, and the morphology of the fetal lungs studied by light and electron microscopy. Cytoplasmic volume densities of lamellar inclusion bodies and glycogen within developing type II alveolar epithelial cells were also determined. In addition, total phospholipids (as phosphorus) and glycogen content were determined biochemically. The fetuses from females treated from day 20-23 demonstrated no differences between saline-treated and propranolol-treated groups, in either fetal weight or the morphologic appearance of the developing lung. In contrast, the fetuses from mothers treated from day 18-21 with propranolol were significantly smaller, and their lungs appeared less mature than saline-treated counterparts. The glycogen content of developing type II alveolar epithelial cells was significantly more abundant (as judged by stereologic and biochemical analyses) in the propranolol-treated fetuses. In addition, total phospholipids were decreased in the propranolol-treated 21-day fetuses. The results of the present study suggest that the development of the alveolar epithelium is sensitive to continuous beta-adrenergic blockade by propranolol during a critical time late in gestation.

When betamethasone and dexamethasone are unavailable: hydrocortisone.

To review the literature on alternatives to betamethasone and dexamethasone for enhancement of fetal lung maturity. A medline search was conducted from 1966 to the present. Trials dealing with enhancement of fetal lung maturity using modalities other than betamethasone or dexamethasone were reviewed. Eight studies met inclusion criteria. Excluding betamethasone and dexamethasone, the most frequently studied glucocorticoids, for fetal lung maturation, are methylprednisolone and hydrocortisone. Methylprednisolone does not cross the placenta. Two grams of hydrocortisone has been shown to improve indices of fetal lung maturity (i.e., L/S ratio) and to improve fetal outcomes compared to no treatment. There is limited information about alternatives to betamethasone and dexamethasone for the enhancement of fetal lung maturity in women at risk of preterm delivery. In the absence of these two preferred drugs, hydrocortisone can be given at a dose of 500 mg intravenously every 12 hours for four doses for this indication.

Fetal lung maturity in pregnancies complicated by insulin-dependent and gestational diabetes: a matched cohort study

Objective. To study fetal lung maturity (FLM) as determined by amniotic fluid (AF) tests in diabetic pregnancies (DP) under euglycemic metabolic control, in comparison with matched controls (C). Patients and methods. From 514 consecutive pregnancies where amniocentesis was performed for FLM assessment, we selected 45 glycemic controlled DP. Nineteen DP were Type I (IDDM) and 26 pregnancies were diagnosed Type III (GDM). Cases were matched to C by therapy with corticosteroids, gestational age at amniocentesis, pregnancy complications other than diabetes and gender. FLM was determined by the shake test and lamellar bodies (LB) count, lecithin/sphingomyelin (L/S) ratio (planimetric and stechiometric) and phosphatidylglycerol presence (PG). DP were further sub-divided according to gestational age period at amniocentesis, type of diabetes, associated therapy and fetal malformations. Results. RDS ( n=2) and neonatal wet lung ( n=5) were diagnosed in neonates from diabetic mothers. We found no statistical difference when comparing FLM indices between DP and C groups: shake test 3.1:1±1.2 vs. 2.7:1±1.2, P<0.40; planimetric L/S 3.4±1.4 vs. 3.1±2.0, P<0.27; stechiometric L/S 8.2±7.4 vs. 7.1±6.1, P<0.54; percentage of PG positivity 57% vs. 46%, P<0.13; lamellar bodies count (×10 3/μl) 42.8±36.9 vs. 41.5±30.4, P<0.72. No differences were found between DP and controls for subgroups according to gestational age, type of Diabetes (IDDM or GDM), congenital lesions and associated therapy. Conclusions. In euglycemic, metabolically controlled diabetic patients FLM is not delayed, however an increased risk for neonatal wet lung should be considered.

The effect of primary cytomegalovirus infection on fetal lung maturity indices.

The aim of this study was to evaluate the impact of primary cytomegalovirus (CMV) infection on fetal pulmonary surfactant production as assessed by different tests for the diagnosis of fetal lung maturity (FLM) on amniotic fluid (AF). A cross-sectional cohort study. AF samples from 11 pregnant women with primary CMV infection were examined for FLM between the 26th and 37th week of gestation. Normal pregnancies (n = 11) were matched for gestational age at amniocentesis and at delivery, birth weight, Apgar score and gender sex. FLM was assessed by planimetric and stoichiometric lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG) presence and lamellar bodies count (LB). Maternal immunological parameters (T-cells, natural killer [NK] activity) were also considered. Mean planimetric L/S ratio (4.2+/-2.1 vs 2.3+/-0.7, P < 0.01) and LB count (42.6 x 10(3)+/-19.0 x 10(3) vs 16.8 x 10(3)+/-11.5 x 10(3), P < 0.004) were higher in controls when compared to CMV infected patients. Moreover, planimetric L/S ratio was higher in five CMV non-infected babies compared to six CMV-infected babies (3.1+/-1.3 vs 1.9+/-0.8, P < 0.05). When FLM was related to maternal immunological results, planimetric and stoichiometric L/S and LBs count were negatively correlated with CD8+ T-cells (r = -0.8, P < 0.05; r = -0.9, P < 0.05; r = -0.9, P < 0.01, respectively); LBs was also negatively correlated with CD14+ T-cells (r = -0.8, P < 0.03). In contrast, a positive correlation was found between stoichiometric L/S and NK activity (r = 0.9, P > 0.01). Maternal primary CMV infection impairs FLM indices as a possible result of reduced surfactant release and/or production. Significant correlations were found between immunity status of CMV-infected mothers and FLM tests.

The Effect of Glucocorticoid Therapy on Fetal Lung Maturity Indices in Hypertensive Pregnancies

The Effect of Glucocorticoid Therapy on Fetal Lung Maturity Indices in Hypertensive Pregnancies

The effect of glucocorticoid therapy on fetal lung maturity indices in hypertensive pregnancies

Objective: To assess fetal lung maturity tests in hypertensive pregnancies and to examine the effect of glucocorticoid therapy. Methods: In a cohort study involving 68 pregnant women with hypertension, 34 received antenatal betamethasone before amniocentesis and 34 did not. Controls were 68 women with uncomplicated pregnancies, matched for gestational age at amniocentesis and fetal gender. Amniotic fluid (AF) samples were analyzed by lamellar body count, planimetric and stechiometric lecithin-sphingomyelin ratio (L/S), and presence of phosphatidylglycerol. Results: Fetal lung maturity, as determined by lamellar body counts and by planimetric L/S, was lower in hypertensive pregnancies not treated with steroids than in controls (19,600 ± 14,500 versus 39,800 ± 22,700, P < .009, and 1.9 ± 0.6 versus 3.9 ± 1.8, P < .01, respectively). In the period of 24 to 33 weeks’ gestation, the percentage of untreated pregnancies with mature lamellar body counts and mature L/S was significantly lower than that of controls (13% versus 33%, P < .001; 6% versus 40%, P < .002 and P < .003, respectively). In contrast, in patients treated with betamethasone, the percentage of cases with mature indices for both tests was not significantly different from that of controls, but was higher than that of untreated hypertensive patients (40% versus 13%, P < .001; 33% versus 6%, P < .001). Phosphatidylglycerol did not differ among groups. From 34 to 38 weeks, no difference was found in the percentage of mature cases for lamellar bodies in pregnant women with hypertension not treated with steroids in comparison with controls (68% versus 84%), nor between cases treated and controls (74% versus 84%). In the same period, no difference in L/S values was found among groups, and the percentage of cases positive for phosphatidylglycerol was lower in hypertensive pregnancies than in controls (47% versus 95%, P < .001) and was not affected by steroid treatment (37% versus 95%, P < .001). Conclusion: Fetal lung maturity, as reflected in AF tests, is delayed in hypertensive pregnant patients, and steroids increase all lung maturity indices except phosphatidylglycerol between 24 and 33 weeks’ gestation.

Intraamniotic surfactant for prevention of neonatal respiratory distress syndrome (IRDS): rationale and personal experience

Objective: To evaluate the efficacy of intramniotic instillation of supplementary surfactant for the prophylaxis of neonatal IRDS in an emergency obstetric setting. Study design: Supplementary natural surfactant (SS) was administered intra-amniotically (80 mg in 1 ml) under ultrasound guidance in the proximity of the fetal nostrils and mouth in six pregnant women at 24–32 weeks gestation, with immature amniotic fluid indices of fetal lung maturity, and whose delivery was imminent because of severe fetal distress, deteriorating maternal conditions, or refractory vaginal bleeding. The administration of SS was preceded by IV aminophylline to the mother (a bolus of 240 mg over 10 min, and a maintenance dose of 0.02 – 0.1 mg kg −1 min −1) in order to elicit sustained fetal breathing movements. Results: The clinical conditions of the six newborn infants were good with no respiratory problems in four cases, and with mild IRDS in the remaining two, which, however, resolved uneventfully. Conclusions: It is suggested that this prophylactic approach has a great potential for becoming a reliable option for the antenatal prevention of IRDS.

AMNIOTIC FLUID CLARA CELL PROTEIN CONCENTRATION IN NORMAL PREGNANCY, A MARKER OF FETAL AIRWAY GROWTH OR FETAL LUNG MATURATION? † 1355

Clara cells protein (CCP) is a lung secretory protein of 16 KD molecular mass that is synthesized by nonciliated bronchial and bronchiolar cells including Clara cells. This protein is produced in the developing fetal airways and can be quantified in amniotic fluid (AF) as early as 15-16 weeks of gestation. The concentration of CCP in AF increases progressively with advancing gestation and has been suggested as a marker of growth of the fetal airways (Pediatr Res 36:771, 1994). However, whether the changes of CCP in AF are also related to the process of fetal lung maturation is unclear. We measured CCP by RIA in 98 AF samples obtained by amniocentesis between 25 and 41 weeks of gestation, from pregnancies without conditions that accelerate or delay fetal lung maturation, and determined its relationship with other known markers of this process. These were the lecithin/sphingomyelin (L/S) ratio determined by thin layer chromatography (TLC), and the concentrations of saturated phosphatidylcholine (Sat PC) measured by TLC after exposure to osmium tetroxide and surfactant protein A (SP-A) quantified by ELISA. With advancing gestational age (GA) the AF concentration of CCP increased slightly(R=0.27, p = 0.006), but more pronounced increases of the L/S ratio (R=0.58, p<0.00001), Sat PC (R=0.45, p <0.0001) and SP-A (R=0.60, p<0.00001) were found. There were extremely weak correlations of CCP with the L/S ratio(R2=0.09, p=0.008) and the AF concentration of Sat PC (R2=0.08, p=0.004), but not with the AF concentration of SP-A (R2=0.02, p=0.10). Using multiple linear regression, the ability to predict changes in the AF concentration of CCP using GA, L/S, Sat PC and SP-A as independent variables was poor (F=3.82, R2=0.19, p=0.007). Conversely, SP-A, Sat PC and GA accounted for most of the variation of the L/S ratio (F=34.71, R2=0.61, p<0.000001). These data suggest that the concentration of CCP in AF has a poor correlation with known indices of fetal lung maturation and probably reflects primarily the development of the fetal airways. (Supported in part by FONDECYT-1930854).

Analysis of saturated phosphatidylcholine in amniotic fluid by 31P NMR.

A technique using solubilization with sodium cholate to resolve 31P NMR resonances of phospholipid molecular species was applied to amniotic fluid samples from 16 subjects. Gestational ages from 25 to 40 weeks were represented, and two subjects were sampled sequentially. Fitting of the partially resolved 31P NMR signal of phosphatidylcholine (PC) generated an estimate of percent disaturated acyl PC (%dsPC) which correlated more highly with gestational age than did several other potential indices of fetal lung maturation, such as the ratio of PC to inorganic phosphate from the solubilized spectra, or PC to sphingomyelin from extract spectra. In a few cases, enzyme-catalyzed PC hydrolysis limited the precision, but did not appear to affect the accuracy, of the %dsPC estimates. Resolution of palmitoyl and oleoyl lyso-PC species was observed for both the 1- and 2-acyl isomers. Upfield shifts due to the presence of cis double bonds in the lone acyl chain of the lyso-PCs were analogous to those observed for the diacyl PCs.

Fluorescence anisotropy as an index of fetal lung maturation in vitro.

Fluorescence techniques have been used to assess the viscosity of surfactant-containing fluids in vivo and have been successfully employed clinically as indices of lung maturity. However, fluorescence measurements have not been previously used as indicators of fetal lung maturation in an in vitro system. Lung explants derived from 19-, 20-, and 21-day fetal rats were cultured in F-12 medium for 24-72 h. Tissue homogenates and culture medium were eluted on Sephacryl S-300 columns, a diphenylhexatriene (DPH) probe was added to each fraction, and fluorescence anisotropy and intensity were measured after excitation at 357 nm and emission at 435 nm. Elution fractions containing the major fluorescence peak were demonstrated to correspond to the phosphatidylcholine-containing fraction and were shown to contain lamellar bodies. Fluorescence anisotropy of tissue homogenates obtained from 19-day lung explants decreased after 72 h in culture, suggesting lower microviscosity of the surfactant-containing fractions. Assessment of culture media collected at 24-h intervals revealed significant decreases in anisotropy by 48 h for the 19-day explants, and by 24 h for the 20- and 21-day explants. Anisotropy of the final (48-72 h) culture media aliquots was significantly lower for 21-day explants (0.144 +/- 0.004, SE), than for 20-day (0.172 +/- 0.013) or 19-day explants (0.197 +/- 0.008), p < .005. Anisotropy of culture medium tended to be lower than anisotropy of corresponding tissue homogenates, suggesting that viscosity of recently secreted surfactant may be different from viscosity of surfactant within lamellar bodies in type II cells. Relative fluorescence intensity of tissue homogenates also increased with time in culture. These results indicate that fluorescence anisotropy can be used to assess the viscosity of surfactant in vitro and serve as another index of fetal lung maturation in in vitro systems. Estimation of the microviscosity of the surfactant phospholipid bilayer using anisotropy measurements may provide additional insight into such roles of surfactant function as adsorption and spreading.

Ontogeny of Surfactant Proteins A and B in Human Amniotic Fluid as Indices of Fetal Lung Maturity

Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome. Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation. SP-A was detected at 19 wk gestation and increased dramatically in the 3rd trimester of pregnancy. SP-B was first detectable at 31 wk gestation and increased significantly to term. SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively). In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS. The greatest sensitivity and specificity were achieved with the measurement of L/S less than 2.0 and negative PG, which correctly predicted 100% of the infants with RDS and 94% of those who did not develop the disorder. Measurement of SP-A or SP-B did not improve the prediction of RDS. SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications. SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers. SP-A was significantly elevated in amniotic fluid from mothers who smoked during pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of ammiotic fluid viscosity measurements to establish fetal lung maturity

A Haake viscosimeter was used to determine the viscosity of amniotic fluid and this value correlated with fetal lung maturity. The results were evaluated along the weeks of pregnancy and compared to those obtained using Gluck's method (lecithin/sphingomyelin ratio ( L S )). Using 91 separate amniotic fluid samples, free of meconium and blood contamination, we found that the new method was quick and easy to perform. Thirty-one neonates were delivered within 48 h of the amniotic fluid sampling and the percentage of correct prediction of respiratory distress syndrome (RDS) was 71% with a mature L S ratio and 83% with viscosity < 1.17 cP. In cases with an immature L S ratio (value below 2) the correct prediction of RDS was 64%; with the fluorescence polarization (FP) technique it was 91%. We conclude that the amniotic fluid FP value is a reliable index of fetal lung maturity and risk for developing RDS and has also specific technical and diagnostic advantages over the L S ratio.

Fetal lung maturity in diabetic pregnancies: Relation among amniotic fluid insulin, prolactin, and lecithin

Insulin, prolactin, and lecithin phosphorus levels were measured in 97, 62, and 44 amniotic fluid samples from third trimester normal, gestational diabetic, and insulin-dependent diabetic patients, respectively. There was no difference in lecithin phosphorus concentration (index of fetal lung maturity) among the three groups. The amniotic fluid insulin level was significantly higher in insulin-dependent diabetic patients, whereas there was no difference in amniotic fluid prolactin levels among the groups. Correlations of amniotic fluid prolactin levels with both lecithin phosphorus and insulin levels were not statistically significant in any of the groups. This is probably because amniotic fluid prolactin is decidual, rather than fetal, in origin. Even though amniotic fluid insulin levels, which reflect fetal levels, were significantly higher in insulin-dependent diabetic patients, there was no difference in the amniotic fluid lecithin phosphorus concentration in diabetic pregnancies compared with that in normal pregnancies. Moreover, there was a positive, and not a negative, correlation between amniotic fluid insulin and amniotic fluid lecithin phosphorus levels in diabetic pregnancies. These results do not support the theory that fetal hyperinsulinemia results in delayed pulmonic maturation in diabetic pregnancies.

Fluorescence polarization of amniotic fluid as an index of fetal lung maturity.

Fluorescence polarization of amniotic fluid as an index of fetal lung maturity.

Synergistic effect of triiodothyronine and dexamethasone on male and female fetal rat lung surfactant synthesis.

It has previously been reported that morphologic and functional indices of fetal lung maturation are delayed in male rabbit fetuses, and these differences cannot be overcome by glucocorticoid treatment. Since thyroid hormone also stimulates surfactant production we have studied the effects of triiodothyronine (T3) and dexamethasone on saturated phosphatidylcholine (SPC) synthesis by day 20 male and female rat lung. Control male lung slices incorporated significantly less 3H-choline into SPC than females; surgery on day 17 markedly stimulated 3H-choline incorporation into SPC by both sexes, but the sex difference persisted. The optimal dose of T3 inhibited SPC synthesis by both sexes while dexamethasone was stimulatory. When T3 and dexamethasone were given together they had a greater effect than that of dexamethasone or T3 alone. Based on these results we conclude that the male deficit in pulmonary surfactant production may be overcome by the synergistic effects of T3 and dexamethasone.

Amniotic fluid C-peptide and phosphatidyl glycerol in diabetic pregnancy.

The concentrations of C-peptide and phosphatidylglycerol in the amniotic fluid were determined in 36 pregnant diabetic women. Twenty-one patients who were being treated with insulin for gestational diabetes as well as 15 patients who were insulin dependent were studied. All patients were subjected to a program of strict metabolic control, and amniocentesis was performed at gestational week 36-37. Phosphatidyl glycerol was present in the amniotic fluid in 15 cases and absent in 21. The mean concentration of C-peptide did not differ whether phosphatidyl glycerol was present or absent. (C-peptide: 0.56 +/- 0.06 and 0.43 +/- 0.05 nmol/l respectively). Although the mean value for amniotic fluid C-peptide in both groups was close to that in diabetic pregnancies with an uneventful neonatal outcome, it was significantly higher than that in non-diabetic pregnancies, indicating minor fetal hyperinsulinemia. The level of C-peptide in the amniotic fluid showed a correlation to the subsequent birthweight of the infant (r = 0.50; p less than 0.01). It is concluded that with rigorous metabolic control of the pregnant diabetic patient, the presence or absence of phosphatidyl glycerol, as an index of fetal lung maturity, is apparently not related to the level of C-peptide in the amniotic fluid.