Effect of fetal hyperinsulinism on oral glucose tolerance test results in patients with gestational diabetes mellitus

OBJECTIVE: This study was undertaken to evaluate the impact of the fetoplacental glucose steal phenomenon on the results of oral glucose tolerance testing in pregnancies complicated by gestational diabetes mellitus with fetal hyperinsulinism. STUDY DESIGN: This was an analysis of the cases of 34 patients with two consecutive abnormal oral glucose tolerance test results and amniotic fluid insulin measurement before institution of insulin therapy. Patients were divided into groups on the basis of normal versus elevated amniotic fluid insulin concentrations. RESULTS: Oral glucose tolerance tests were done at a mean (+/-SD) of 24.9 +/- 5.7 and 30.7 +/- 3.2 weeks' gestation, and amniotic fluid insulin measurements were done at 31.1 +/- 3.2 weeks' gestation. In 13 women with gestational diabetes mellitus with normal amniotic fluid insulin concentration, maternal postload blood glucose levels at 1 hour increased by 12 mg/dL (168 vs 180 mg/dL; 9.3 vs 10.0 mmol/L; P = .0006) during the course of 6 weeks. In contrast, in 21 women with gestational diabetes mellitus with elevated amniotic fluid insulin levels (>7 microU/mL; >42 pmol/L), 1-hour postload blood glucose levels decreased by 22 mg/dL (201 vs 179 mg/dL; 11.2 vs 9.9 mmol/L; P = .002) during the same period. The higher the amniotic fluid insulin level, the larger the decrease (R = 0.504; P =.02). Although low amniotic fluid insulin levels were correlated significantly with 1-hour glucose levels of the first and second oral glucose tolerance tests, high insulin levels were no longer correlated with the second oral glucose tolerance test. CONCLUSION: Exaggerated fetal glucose siphoning may provide misleading oral glucose tolerance test results in pregnancies complicated by fetal hyperinsulinism by blunting maternal postload glucose peaks. Consequently, oral glucose tolerance test results in a pregnancy complicated by gestational diabetes mellitus with a fetus that already has hyperinsulinemia may erroneously be considered normal.     

Increasing amniotic fluid magnesium concentrations with stable maternal serum levels: a prospective clinical trial

OBJECTIVE: To compare the effect of prolonged maternal intravenous MgSO4 administration on amniotic fluid and serum concentrations of magnesium over time in preterm labor patients. STUDY DESIGN: Patients at 24-34 weeks of singleton gestation who presented with contractions (> 8 in 60 minutes) underwent amniocentesis to rule out intrauterine infection after signing an informed consent form. Some of these women who were clinically judged to have preterm labor received intravenous MgSO4: a 4-g loading dose followed by a 2 g/h maintenance dose. For technical reasons some patients had amniocentesis performed before initiation of MgSO4 (controls), while others had the procedure during tocolytic therapy (study subjects). Duration of treatment until amniocentesis was recorded, and blood samples were drawn at the time of amniocentesis. Maternal serum and amniotic fluid magnesium levels were measured using a colorimetric end point method. Data were evaluated using the Student t test and linear regression analysis. RESULTS: Mean magnesium levels in maternal serum rose from 1.74 +/- 0.2 mg/dL in controls to 4.01 +/- 0.4 mg/dL in the study group. Mean magnesium levels in Mean magnesium levels in amniotic fluid were 1.41 +/- 0.18 mg/dL in the controls versus 2.28 +/- 0.53 mg/dL in the treatment group. Duration of MgSO4 treatment ranged from 3 to 22 hours. Amniotic fluid magnesium concentrations increased significantly during therapy (correlation coefficient = 0.89; p < 0.001), while maternal serum levels remained stable over time (correlation coefficient between maternal serum levels and time = -0.39; p=0.34). CONCLUSION: Although maternal serum magnesium levels remained stable with intravenous MgSO4 therapy, concentrations continued to rise in amniotic fluid over time. However, amniotic fluid magnesium levels never exceeded maternal serum concentrations during the study period.     

Does fetal acidosis develop with maternal glucose infusion during normal labor?

The actual effects of glucose infusion on fetal acid-base status were studied during 125 normal deliveries in which plasma glucose and acid-base parameters were determined after maternal infusion of either 10% glucose or Ringer's solution. After 80 minutes, mean (+/- SD) plasma glucose levels were significantly higher in the glucose group (N = 59) than in the Ringer's group (N = 66), both for the mother (183.6 +/- 46.8 versus 95.3 +/- 18.0 mg/dL) and the fetus (108.4 +/- 41.4 versus 64.8 +/- 16.2 mg/dL). Fetal plasma lactate concentrations did not differ between the glucose and the Ringer's groups, but were significantly lower in the fetuses delivered by elective cesarean section in both groups. With glucose administration, fetal pCO2 was higher and pH values were lower than in the Ringer's group. However, the magnitude of acid-base status changes, indicated by both pH and pCO2 shifts (ie, the difference between umbilical artery and scalp values), failed to differ between the two groups. In fetuses with progressing hypoxia, no differences in any of the acid-base parameters were observed between glucose and Ringer's administration. These data indicate that at a glucose infusion rate of 30 g/hour, fetal acidosis, when it occurs, results from hypoxia rather than from maternal glucose administration.     

Does amniotic fluid analysis reflect acid-base balance in fetal blood?

OBJECTIVE: The purpose of the study was to examine whether the acid-base balance in amniotic fluid reflects the acid-base state in fetal blood. STUDY DESIGN: The pH, PCO2, PO2, bicarbonate, and base excess concentrations were measured in umbilical venous, umbilical arterial, and maternal venous blood and in amniotic fluid samples obtained at fetoscopy. This was performed before intraamniotic termination of 16 normal pregnancies (mean gestation 19.4 weeks), as well as in 14 red blood cell isoimmunized pregnancies (mean gestation 28.4 weeks) undergoing fetoscopy for the diagnosis and treatment of fetal anemia. RESULTS: In normal pregnancies, amniotic fluid pH and bicarbonate were significantly lower than umbilical venous and umbilical arterial blood concentrations, and this was due to the high concentration of base deficit in amniotic fluid. Whereas amniotic fluid PCO2 did correlate significantly with fetal umbilical venous PCO2 values, there was no correlation between other acid-base characteristics. CONCLUSION: Simultaneous sampling of human fetal umbilical blood and amniotic fluid under the acute conditions of this study did not show significant correlations in acid-base values.     

Longitudinal changes in plasma glucose values of the 75-g glucose tolerance test in triplet pregnancies

We evaluated longitudinal changing patterns of 75 g glucose tolerance test (GTT) in triplet pregnancies. Eight triplet pregnancies were prospectively studied. All triplet pregnancies were fertilized with artificial reproductive techniques; patients showed no glucosuria or fasting hyperglycemia > 100 mg/dL before pregnancy. The 75-g GTT was performed at first, second, and third trimester, as well as at postpartum. Longitudinal changes in glucose levels at fasting, 1 hour, and 2 hours were compared by one-way repeated-measure analysis of variance (ANOVA) and Bonferroni/Dunn test ( p < 0.05). Values were expressed as mean +/- standard deviation. Each of the 3-point values of 75-g GTT decreased after 28 weeks of gestation in triplet pregnancies. During the third trimester, fasting values were significantly decreased compared with postpartum values (65.5 +/- 13.4 versus 74.6 +/- 4.0 mg/dL), and 2-hour values were significantly decreased from those of second-trimester 75-g GTT (116.3 +/- 19.5 versus 99.6 +/- 17.1 mg/dL). Longitudinal glucose values of 75-g GTT improve during third trimester in triplet pregnancies, suggesting that fetoplacental fuel drain may counterbalance maternal insulin resistance.     

The effects of oral carbohydrate administration on fetal acid base balance

AIMS: Little evidence-based data are available on the effects of eating and drinking during labor. Intravenous glucose administration has been related to fetal metabolic acidosis. The question is, whether oral intake of carbohydrates effects the fetal acid-base balance. METHODS: In a double blind, prospective placebo controlled study 100 nulliparous women were randomized at 8-10 cm of cervical dilatation. All women were asked to drink 200 cc of either a carbohydrate solution (containing 25 grams carbohydrates) or placebo. In all women, both arterial and venous umbilical cord pH, pCO2, pO2, HCO3- and base excess/deficit were assessed. In a subgroup of women, whose deliveries were complicated by mild signs of fetal distress, clinical outcome and acid-base status was described separately. RESULTS: Fetal arterial umbilical cord pH were identical: 7.20 +/- 0.07 in the placebo group and 7.20 +/- 0.08 in the carbohydrate group and the base excess -6.6 +/- 2.8 versus 6.6 +/- 3.7. In the women with mild signs of fetal distress, no differences were observed as well. CONCLUSIONS: Oral carbohydrate intake during labor seems to be safe regarding the fetal acid-base balance. Further study on the maternal and fetal metabolic parameters is essential to give a more complete picture.     

Can glucose tolerance test predict fetal hyperinsulinism?

Objective To establish cut off levels for oral glucose tolerance test in pregnancy using fetal hyperinsulinism as a clinical endpoint.
Design Capillary blood glucose levels at 0, 1, and 2 hours after the ingestion of either 1 g/kg or 75 g glucose, at 28 (SD 5) weeks of gestation were analysed in 220 women with elevated amniotic fluid insulin levels [≥ 42 pmol/L (≥ 7 μU/mL)] after a mean (SD) of 31 weeks (3) and in 220 nondiabetic controls.
Results In women with elevated amniotic fluid insulin levels the mean (SD) capillary blood glucose values at 0, 1, and 2 hours were 5.2 mmol/L (1.0) [94 mg/dL (18)], 10.5 mmol/L (1.4) [189 mg/dL (25)] and 8.2 mmol/L (2.0) [147 mg/dL (36)], respectively. The one-hour value had the highest sensitivity to predict elevated amniotic fluid insulin levels. The 5th centile of the one-hour blood glucose levels representing a detection rate of 95% was 8.9 mmol/L (160 mg/dL).
Conclusion Glucose cut off levels in most established oral glucose tolerance test criteria are too high, to accurately predict amniotic fluid hyperinsulinism. A one-hour test may be sufficient for detecting amniotic fluid hyperinsulinism. Since different loads (1 g/kg, 75 g or 100 g) and blood fractions (venous plasma or capillary blood) have minimal impact on oral glucose tolerance test results, a single one-hour cut off of 8.9 mmol/L (160 mg/dL), independent of the sampling method, may be appropriate for the diagnosis of gestational diabetes mellitus severe enough to cause amniotic fluid hyperinsulinism.     

Correlation between amniotic fluid glucose concentration and amniotic fluid volume in pregnancy complicated by diabetes

OBJECTIVE: Pregnancies complicated by diabetes are frequently characterized by an increased volume of amniotic fluid, and the pathophysiologic mechanism of this increase is not known. Our goal was to evaluate the relationship between amniotic fluid glucose concentration and the amniotic fluid index in pregnancies complicated by insulin-treated diabetes and to compare it with that seen in normal pregnancies. STUDY DESIGN: Amniotic fluid index and amniotic fluid glucose levels were measured before elective repeated cesarean delivery in 41 women with insulin-treated diabetes and in 35 women without diabetes. Only singleton gestations without anomalous fetuses were included. Women with diabetes were hospitalized for approximately 4 weeks before delivery, during which time glycemic control was optimized. Amniotic fluid index and amniotic fluid glucose concentration were correlated with each other and were compared between the groups with and without diabetes. RESULTS: The mean amniotic fluid index was significantly increased in the diabetes group (16.6 +/- 5.0 cm in the diabetes group vs 13.4 +/- 3.5 cm in the control group; P =.002). The amniotic fluid glucose concentration was also significantly greater in the diabetes group than in the control group (39 +/- 17 mg/dL in the diabetes group vs 24 +/- 11 mg/dL in the control group; P <.001). Among women with diabetes the amniotic fluid glucose concentration was significantly correlated with the amniotic fluid index (r = 0.32; P =.04), a correlation not found among the control women. The mean fasting blood glucose concentration among the women with diabetes for the week before amniocentesis was 82 +/- 11 mg/dL. CONCLUSION: The amniotic fluid index parallels the amniotic fluid glucose level among women with diabetes. This finding raises the possibility that the hydramnios associated with diabetes is a result of increased amniotic fluid glucose concentration.     

Gestational diabetes and screening during pregnancy

The oral glucose tolerance test is an unreliable test in screening for diabetogenic fetal disease. In diabetogenic fetopathy due to gestational diabetes (White class A diabetes), the insulin content in the umbilical cord blood as well as in the fetal urine is considerably raised. As increased amounts of insulin pass into the amniotic fluid via the fetal urine, the fetal disease can be diagnosed from the amniotic fluid insulin content. In 75 pregnant women with potential diabetes, the blood sugar value was below 160 mg/dL at maximum under glucose loading in 28 patients; it was over 200 mg/dL in 25 patients. However, diabetogenic fetopathy was present in only 14 patients. The endangered and the healthy fetus could be distinguished in each case by amniotic fluid insulin content. The mean amniotic fluid insulin values in diabetogenic fetopathy were about seven times the normal.     

Are amniotic fluid C-reactive protein and glucose levels, and white blood cell counts at the time of genetic amniocentesis related with preterm delivery?

OBJECTIVE: To compare women with spontaneous preterm delivery before 37 weeks and women who delivered at term with respect to amniotic fluid C-reactive protein (CRP), glucose levels, and white blood cell counts at the time of genetic amniocentesis. STUDY DESIGN: The study was conducted on 216 pregnant women who underwent genetic amniocentesis between the 15th and 18th weeks of gestation at Baskent University Obstetrics and Gynecology Department. All patients were followed until delivery for the occurrence of pregnancy complication. Indications for amniocentesis included abnormal triple test results showing increased risk for Down's syndrome, advanced maternal age and sonographic findings indicative for chromosomal abnormalities. The samples were carried immediately to the laboratory for cytogenetic and biochemical examination. Women with spontaneous preterm delivery before 37 weeks (n = 20) and those who delivered at term (n = 196) were compared with respect to some maternal and infant characteristics, amniotic fluid C-reactive protein, glucose levels, and amniotic fluid white blood cell counts. RESULTS: During the study period 244 patients underwent amniocentesis. A chromosomal abnormality was present in 11 patients. 1 patient had a spontaneous pregnancy loss within 3 weeks after the procedure and 16 patients were delivered for fetal or maternal indications (preeclampsia, fetal growth restriction, placenta previa). The remaining 216 women were included in the study and investigated for the risk of preterm delivery. The prevalence of spontaneous preterm delivery before 37 weeks was 9.3% (20/216). There were no significant differences between the preterm delivery and the term delivery groups with respect to C-reactive protein levels and white blood cell counts. Mean amniotic glucose levels were significantly lower in the preterm delivery group (P<0.05). Amniotic fluid glucose levels of < or = 46 mg/dL had a sensitivity of 100% and NPV of 100%. CONCLUSION: Amniotic fluid glucose levels at the time of genetic amniocentesis are lower in women with spontaneous preterm delivery before 37 weeks compared to those who delivered at term. Amniotic fluid glucose levels of < or = 46 mg/dL at the time of genetic amniocentesis may be more sensitive, cheaper and have higher negative predictive value than C-reactive protein levels and white blood cell counts for the prediction of patients in spontaneous preterm labor. The greatest benefit of amniotic fluid glucose testing might be when the physician judges the patient to be at low risk for preterm delivery.     

The effect of nuchal cord on amniotic fluid and cord blood erythropoietin at delivery

OBJECTIVE: We investigated the effect of a nuchal cord on fetal hypoxia by using amniotic fluid and cord blood erythropoietin as markers of chronic and acute hypoxia, respectively. METHODS: A total of 167 full-term pregnancies without maternal complications or fetal prelabor complications except fetal growth restriction of unknown cause were studied prospectively. Of these, 47 had a nuchal cord at delivery, and 62 had one or more complications during labor and delivery (nonreassuring fetal heart rate pattern, birth weight less than 2500 g, Apgar score at 1 minute less than 7, presence of meconium-stained amniotic fluid, oligohydramnios), and 26 had both nuchal cord and at least one of the intrapartum complications. RESULTS: Erythropoietin levels (mean +/- standard error of the mean) were not significantly different between the nuchal cord group (n = 47) and the no nuchal cord group (n = 120) in either amniotic fluid (19.3 +/- 4.1 mU/mL versus 13.7 +/- 1.1 mU/mL) or cord blood (57.9 +/- 10.3 mU/mL versus 52.1 +/- 4.9 mU/mL). Similarly, in the 62 fetuses with intrapartum complications, there were no significant differences in amniotic fluid (14.3 +/- 2.0 mU/mL versus 18.8 +/- 2.9 mU/mL) or cord blood erythropoietin (66.9 +/- 16.8 mU/mL versus 72.6 +/- 12.6 mU/mL) levels between those with (n = 26) or without a nuchal cord (n = 36). Among the 107 uncomplicated cases, however, amniotic fluid erythropoietin was significantly elevated in the nuchal cord group (25.5 +/- 8.7 mU/mL, n = 21) compared with that in the no nuchal cord group (11.5 +/- 0.9 mU/mL, n = 84) (P <.05), whereas there was no significant between-group difference in cord blood erythropoietin levels between nuchal cord and no nuchal cord groups (46.8 +/- 10.0 mU/mL versus 43.3 +/- 4.1 mU/mL). Tightness of the nuchal cord did not affect amniotic fluid or cord blood erythropoietin concentrations. CONCLUSION: Although nuchal cord may not significantly increase the risk of acute or labor-associated fetal hypoxia, it appears to be an independent risk factor of mild, chronic, prelabor fetal hypoxia.     

Doppler assessment of the fetal cerebral hemodynamic response to moderate or severe maternal anemia

OBJECTIVE: The purpose of this study was to evaluate the fetal vascular adaptation to moderate and severe maternal anemia. STUDY DESIGN: Biometry; amniotic fluid index; uterine, cerebral, and umbilical Doppler; and maternal hemoglobin level were measured at admission and 8 days after treatment. RESULTS: Group 1 consisted of 16 pregnancies (maternal hemoglobin level, 6.9 +/- 0.6 g/100 mL); group 2 consisted of 23 pregnancies (maternal hemoglobin level, 5 +/- 0.6 g/100 mL). At admission the cerebral and cerebral/umbilical Doppler indexes, amniotic index, and biometry were lower in group 2. The uterine index was normal in both groups. An abnormal fetal heart rate was found in group 2 only (48%). At day 8, maternal hemoglobin level and amniotic index increased more in group 2 than in group 1. The cerebral index and the cerebral-to-umbilical resistance ratio increased only in group 2. The abnormal fetal heart rate disappeared in group 2. CONCLUSION: Only severe maternal anemia (maternal hemoglobin level, <6 mg/L) triggered fetal cerebral vasodilation and reduced amniotic volume.     

Detection of glucose intolerance in pregnancy

Between 6 and 28 weeks of gestation, 2-hour postprandial blood glucose determinations were performed on 66 pregnant patients who had no history of diabetes. Each patient received two methods of carbohydrate loading on separate occasions in a random, crossover fashion. One group received a 100-g carbohydrate meal and then a 50-g glucose load (Glucola). The order of the test regimens was reversed for the second group. The average 2-hour postprandial glucose value following a meal was 103.1 +/- 3.7 mg/dL, and the mean value for the 2-hour postprandial glucose following Glucola was 102.5 +/- 3.8 mg/dL. The difference in glucose values obtained with the two methods was not statistically significant. A 12% incidence of emesis was encountered after Glucola but none was encountered after the meal. The 100-g carbohydrate meal is recommended as the method of testing for glucose intolerance.     

Concentrations of growth hormone, prolactin and thyroid-stimulating hormone in the maternal, fetal and amniotic compartments

GH, PRL and TSH in the maternal, fetal and amniotic compartments were measured by radioimmunoassay in normal pregnant women (group I, n = 16) and patients with anencephalic fetuses (group II, n = 10). The concentrations of GH (20.6 +/- 8.5 ng/ml, mean +/- SD) in cord blood of normal fetuses were significantly higher (p less than 0.001) than those (5.1 +/- 3.5 ng/ml) in anencephalic fetuses. Both maternal PRL levels in group I and group II were lower than their respective cord bloods. The concentrations of PRL (283.1 +/- 127.5 ng/ml) in normal fetuses were higher, but not significantly, than those (199.4 +/- 111.8 ng/ml) in anencephalic fetuses. Also, compared with PRL levels in the maternal and cord blood, those in amniotic fluid were significantly higher (p less than 0.001) in both groups. On the contrary, GH and TSH levels in amniotic fluid were much lower than those in the maternal and fetal blood. The concentration of TSH (10.2 +/- 4.6 microU/ml) in normal fetuses was significantly higher (p less than 0.05) than those (7.1 +/- 3.1 microU/ml) in maternal blood, but not significantly different from those (11.3 +/- 3.6 microU/ml) in anencephalic fetuses. These results suggest that GH, PRL and TSH do not cross human placenta and biosyntheses of these hormones in the maternal and fetal pituitaries are independent.     

Diagnosis and treatment of gestational diabetes according to amniotic fluid insulin levels

In spite of dietary treatment, the infants of pregnant patients with abnormal glucose tolerance have hyperinsulinism and diabetogenic fetopathy in 10 to 36% of cases. Those patients, who require insulin to prevent from fetopathy cannot be reliably selected by maternal parameters such as blood glucose and glycosylated hemoglobin values. We recommend the measurement of amniotic fluid insulin between the 28 and 32 weeks of pregnancy to differentiate whether the fetus is compromised or not. Subjects with values above the 97th centile require insulin therapy. Inadequate insulin dosage or delayed fetal hyperinsulinism can be discovered by checking the amniotic fluid insulin level at 33 to 36 weeks. In a total of 88 gestational diabetic patients 19 had raised amniotic fluid insulin levels indicating the onset of diabetic fetopathy at an early stage. Diabetic patients with raised amniotic fluid insulin levels needed large doses of insulin, namely 64.6 +/- 29.5 (Mean +/- SD) U/24 h. This treatment reduced mean blood glucose levels from 98 +/- 9 (Mean +/- SD) mg/dl to 82 +/- 10 mg/dl and was sufficient to prevent from diabetic fetopathy.     

Comparison of fetal and maternal hind limb metabolic quotients in sheep

This study compared substrate utilization by the fetal hind limb and the maternal hind limb in 26 sheep at 120 to 135 days of gestation. Catheters were placed in the mother and the fetus to sample femoral arterial and venous blood by use of a nonocclusive technique. Arterial and venous concentrations of oxygen content, glucose, lactate, acetate, and ketoacids were measured simultaneously and were used to calculate metabolic quotients. The fetal hind limb was perfused with arterial blood having a lower oxygen content than the maternal hind limb (3.03 +/- 0.17 versus 4.94 +/- 0.24 mmol/L, p less than 0.001) and had a smaller arteriovenous difference of oxygen content (0.97 +/- 0.05 versus 2.68 +/- 0.104 mmol/L, p less than 0.001). Despite a lower fetal arterial glucose concentration (0.81 +/- 0.05 versus 2.58 +/- 0.13 mmol/L, p less than 0.001), the glucose/oxygen quotient (0.82 +/- 0.05 versus 0.20 +/- 0.02, p less than 0.001) and the arteriovenous difference of glucose (0.13 +/- 0.01 versus 0.08 +/- 0.01 mmol/L, p less than 0.001) were higher in the fetal hind limb than in the maternal hind limb. Both limbs were net producers of lactate. The (glucose + lactate)/oxygen quotient was also higher in the fetal hind limb than in the maternal hind limb (0.68 +/- 0.05 versus 0.12 +/- 0.04, p less than 0.001). In the maternal hind limb, acetate and ketoacids uptake could account for 48% +/- 6% of total oxygen consumption whereas in the fetal hind limb it accounted for only 12% +/- 4% (p less than 0.001). The data demonstrate that, in relation to oxygen uptake, fetal hind limbs have approximately a 2.8% higher rate of perfusion and take up approximately four times as much glucose as the hind limbs of the mother in the resting state.     

Impaired glucose tolerance associated with adverse pregnancy outcome: a population-based study in southern Sweden

OBJECTIVE: We conducted a population-based study of maternal and neonatal characteristics and delivery complications in relation to the outcome of a 75-g, 2-hour oral glucose tolerance test at 25 to 30 weeks' gestation. STUDY DESIGN: An oral glucose tolerance test was offered to pregnant women in a geographically defined population. Pregnancy outcome was analyzed according to the test result. RESULTS: Among women delivered at Lund Hospital, we identified 4526 women with an oral glucose tolerance value of <7.8 mmol/L (<140 mg/dL), 131 women with a value of 7.8 to 8.9 mmol/L (140-162 mg/dL), and 116 women with gestational diabetes (> or =9.0 mmol/L [> or =162 mg/dL]). A further 28 cases of gestational diabetes were identified, giving a prevalence of 1.2%. An increased rate of cesarean delivery and infant macrosomia was observed in the group with a glucose tolerance value of 7.8 to 8.9 mmol/L (140-162 mg/dL) and in the gestational diabetes group. Advanced maternal age and high body mass index were risk factors for increased oral glucose tolerance values in 12,657 screened women in the area. CONCLUSION: The study stresses the significance of moderately increased oral glucose tolerance values.     

Fetal hyperinsulinism and maternal one-hour postload plasma glucose level

OBJECTIVE: Fetal insulin concentrations reflect the intrauterine glucose load given the fetus by the mother. In this study, we assessed the association between maternal glucose levels during oral glucose tolerance testing and fetal cord insulin. METHODS: Pregnant women with an oral glucose tolerance test (OGTT) result were included in this prospective study. The patients were divided into 3 groups according to their 1-hour OGTT glucose concentration: up to 160 mg/dL (control, group I), 160-179 mg/dL (intermediate, group II), and gestational diabetes mellitus (GDM, group III). Patients with GDM were assigned to insulin therapy if blood glucose levels were not in the preferable range. RESULTS: Of the 930 patients who entered the study, 570 (61.3%) were assigned to group I, 76 (8.2%) to group II, and 284 (30.5%) to group III. The cord blood insulin value was significantly (P < .001, Mann-Whitney test) higher in group II (median, 12.8 microU/mL; range, 3-130 microU/mL) than in group I (median, 7.25 microU/mL; range, < 3-98 microU/mL). Cord blood insulin values were higher, albeit not significantly (P = .100, Mann-Whitney test), in group II than in group III (median, 9.9 microU/mL; range, < 3-61 microU/mL). CONCLUSION: Children whose mothers had a 1-hour value between 160 and 179 mg/dL had significantly higher cord blood insulin values than offspring of women with a 1-hour value below 160 mg/dL.     

Effect of esophageal ligation on amniotic fluid volume and urinary flow rate in fetal sheep

OBJECTIVE: Although the fetus normally swallows large volumes of amniotic fluid each day, it is unclear whether amniotic fluid volume increases after fetal esophageal obstruction or whether fetal urine production changes. Our objective was to determine the effects of fetal esophageal ligation on amniotic fluid volume and urinary flow rate over time. STUDY DESIGN: Seven late-gestation fetal sheep underwent esophageal ligation, and 7 served as time control animals. The urachus was ligated to eliminate urine flow to the allantoic cavity. On days 1, 3, 5, 7, and 9 after surgery, we measured the composition of amniotic fluid, fetal urine, and fetal and maternal blood, as well as amniotic fluid volume and fetal urinary flow rate. A 3-factor analysis of variance was used for statistical analysis. RESULTS: Amniotic fluid volume did not change with time in the control group, averaging 876 +/- 142 mL (mean +/- SEM), and it decreased in the esophageal ligation group (P =.020), averaging 309 +/- 75 mL on day 9. Fetal urinary flow rate was lower (P =.0063) in the esophageal ligation group (431 +/- 27 mL/d) than in the control group (631 +/- 54 mL/d). There were no differences in fetal or maternal blood compositions between the two groups. Amniotic fluid sodium and chloride increased in the ligated animals. CONCLUSION: Polyhydramnios did not occur after esophageal ligation, even though the fetuses excreted approximately 4000 mL of urine over the 9-day study period. This suggests that intramembranous absorption is substantially increased. With only small changes in amniotic solute concentrations, intramembranous solute absorption must occur simultaneously with water, suggesting a near-zero reflection coefficient for solutes. We speculate that fetal urine, lung secretions, or both contain a factor that increases intramembranous permeability.     

Fluoride concentration in amniotic fluid and fetal cord and maternal plasma

Fluoride concentrations were determined in plasma of 50 pregnant women, 44 samples of amniotic fluid and fetal cord blood of 29 fetuses at various stages of normal pregnancies, from an area with a relatively low water fluoride (less than 0.5 ppm) content. The mean concentrations of fluoride from maternal plasma, cord plasma and amniotic fluid (+/- S.D.) were 0.033 +/- 0.003, 0.028 +/- 0.005 and 0.017 +/- 0.003 ppm, respectively. Maternal and fetal plasma fluoride concentrations did not differ significantly. In the older age group fetal cord plasma fluoride concentration was significantly lower than maternal plasma levels (0.012 +/- 0.08 ppm vs. 0.023 +/- 0.001, respectively; p less than 0.05). Amniotic fluid fluoride levels were significantly higher at term than in midtrimester pregnancy, 0.017 +/- 0.0018 vs. 0.010 +/- 0.009 ppm (P less than 0.05), respectively. This higher concentration may imply higher fetal urinary excretion of fluoride at term due to the lower sequestration of fluoride as the process of bone calcification is more complete.