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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An analysis of 105 cases of prematures with respiratory distress syndrome, the idiopathic type were 9.5% (10/105). Fetal anoxia and ischemia, induced by pregnancy and during labour amounting to 87.6% (92/105), and of which 2.9% (3/105) was due to diabetes. It indicated that most cases of RDS are predominantly related with fetal anoxia and ischemia which results in pulmonary surfactant abnormality or impaired activity. It is important that in clinical diagnosis one should monitor cautiously the presence of premature birth with anoxia and ischemia, Thus, a preventive treatment must be given at least 24 hours prior to birth, and the earlier the least morbidity of RDS occurred.
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PMID:[Prevention and factors inducing respiratory distress syndrome in prematures]. 139 90

Respiratory distress syndrome (RDS) is primarily caused by an immaturity in the synthesis and secretion of surfactant by the fetal lung type II cell. Fetal hyperinsulinemia associated with maternal diabetes places the newborn at an increased risk of developing RDS, and therefore, it has been hypothesized that insulin inhibits type II cell differentiation. We have previously shown that insulin inhibits the accumulation of surfactant-associated protein A (SP-A), the major surfactant-associated protein, in human fetal lung explants maintained in vitro. In the present study, we used Northern blot analysis to evaluate the effects of insulin on the content of SP-A messenger RNA (mRNA) as well as on the content of mRNA for the hydrophobic surfactant-associated proteins SP-B and SP-C in human fetal lung explants maintained in vitro. Lung explants were maintained in serum-free medium with or without added insulin (0.25-2500 ng/ml) for up to 6 days. We observed that insulin, at concentrations of 25-2500 ng/ml, significantly inhibited the accumulation of SP-A mRNA when compared to controls (P less than 0.01). The inhibitory effect of insulin on SP-A mRNA accumulation was dose dependent with an approximately 75% inhibition observed at 2500 ng/ml. Insulin, at the concentration of 2500 ng/ml, significantly inhibited the accumulation of SP-B mRNA by approximately 30% when compared to control levels (P less than 0.01) but had no effect at lower concentrations. Insulin had no significant effect on SP-C mRNA levels at any concentration tested. Our findings provide evidence that insulin may delay fetal lung development by inhibiting SP-A and SP-B gene expression. A deficiency of these proteins in pulmonary surfactant may account for the increased incidence of RDS in infants of diabetic mothers.
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PMID:Insulin regulation of messenger ribonucleic acid for the surfactant-associated proteins in human fetal lung in vitro. 163 13

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)
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PMID:Ontogeny of surfactant proteins A and B in human amniotic fluid as indices of fetal lung maturity. 180 57

Preservation of own insulin production (residual pancreatic beta-cell function) has been shown to have a beneficial effect on glycemic control in insulin-dependent diabetic subjects, and its total lack has been suggested to be an independent risk factor during diabetic pregnancy. We studied the influence of residual beta-cell activity on the glucose control and the outcome of pregnancy in 29 diabetic women by sequentially measuring gestational postprandial plasma C-peptide (CPR) levels, diurnal blood glucose curves and blood glycosylated hemoglobin (Hb A1c) and by analyzing the morbidity and mortality of the offsprings. The 9 diabetics with moderate own insulin secretion (CPR levels over 1.0 microgram/l, White classes B and C, later referred to as group I) had significantly better glucose control than the remaining 20 subjects with lower CPR values (White classes C, D and NF, later referred to as group II) (figure 1, table I). There were two intrauterine deaths, both in group II. These deaths (one caused by multiple congenital contracture syndrome and the other by severe intrauterine growth retardation without any evident cause) could not be straightly connected with diabetes. Respiratory distress syndrome was seen in group II only. There was no other significant difference in the neonatal morbidity between the two groups (table II). All mothers of RDS infants were in White class NF where the birthweight was also smaller than in classes B and C. These were the only differences in neonatal morbidity between the White classes (table III). In conclusion, moderate residual beta-cell function seemed to be clinically important in maintaining strict glucose control during gestation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Maternal residual beta-cell function and the outcome of diabetic pregnancy. 329 78

Main indications for antenatal administration glucocorticoid to pregnant women are premature contractions, hemorrhage during pregnancy, conditions of fetal distress and maternal diseases. There are some absolute or relative contraindications as well: severe forms of preeclampsia, diabetes mellitus, premature rupture of membranes, maternal and/intrauterine infections. In a retrospective evaluation of the data obtained at our institution of 637 nonrandomized cases from the years 1980-1985, we could demonstrate the dependence of the therapeutic results on the sex of the newborn. The RDS incidence is significantly different after betamethasone prophylaxis. It was 1/25 (4%) in girls compared to 13/31 (42%) in boys. A marked reduction of the RDS incidence is only detectable after betamethasone therapy from the 32nd to the 34th week of gestation. Thus we recommend RDS prophylaxis for all patients with premature contraction, mainly between the 32nd and 34th week of pregnancy. In addition, it should be given in cases of confirmed lung immaturity. Special restrictions are necessary in cases of preeclampsia, eclampsia, diabetes and confirmed maternal infections. In the group of diabetes or preeclampsia patients an RDS prophylaxis should only be given, if at all, when it can be performed under intensive care conditions.
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PMID:Clinical aspects of antenatal glucocorticoid treatment for prevention of neonatal respiratory distress syndrome. 344 99

It seems quite likely that the normal process of fetal lung biochemical maturation is delayed by maternal diabetes and that abnormalities in the pulmonary surfactant system are involved. The appearance of PG in amniotic fluid and possibly in fetal lung is impaired or at least delayed. The same is possibly true for DSPC, the main constituent of surfactant, but recent discrepant data call for further clarification of this specific point. Careful determination of the fetal lung phospholipid profile by amniotic fluid analysis helps predict and prevent RDS in IDM, along with a careful control of the maternal diabetic condition. A study of alveolar surfactant at birth, if it could be performed in addition to amniotic fluid analysis, would help to better characterize surfactant deficiency in IDM. On the basis of both in vivo and in vitro experimental approaches, it seems clear that hyperglycemia and fetal reactional hyperinsulinism are both involved in the processes delaying fetal lung maturation. Further advances in the understanding of cellular and molecular mechanisms leading to this delay will be conditional on the availability of animal models reproducing the features of the metabolic and hormonal environment of human fetuses in diabetic pregnancies. The appropriateness of in vivo models needs to be defined by two kinds of criteria: 1) presence of simultaneous hyperglycemia and hyperinsulinemia in the fetus; 2) the presence of delayed fetal lung maturation as judged by morphology and morphometry of epithelial lung cells, by physiological assessment of surfactant, and by the phospholipid composition of the lung (and including lung tissue per se, bronchoalveolar lavage fluid, lamellar bodies, and/or isolated surfactant fractions). Therefore, future studies must necessarily be comprehensive in scope and include information indicating that fetal growth, blood glucose, and circulating insulin are all increased. Such models already exist in rats and rabbits. Rat models are possibly not the best because of the high basal level of fetal blood insulin in this species and the relatively rapid rate of lung maturation that is not analogous to the human. Monkey models are of interest, because of their close relationship with the human pregnancy, and need to be studied further. They are particularly attractive also because primary fetal hyperinsulinism can be studied (268), as well as the combination of hyperglycemia and hyperinsulinemia in pregnancies of STZ-treated monkeys (152). An appropriate model of the diabetic pregnancy could provide answers to the following questions. Are the biosynthetic pathways of surfactant phospholipids directly impaired?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Fetal lung development in the diabetic pregnancy. 388 50

In diabetic pregnancy, a high rate of postnatal development of RDS has been observed even with a mature lecithin/sphingomyelin (L/S) ratio, and the efficacy of phosphatidylglycerol (PG), a second major surfactant phospholipid, in predicting fetal lung maturity remains to be established. In this communication, we determined PG and phosphatidylcholine (PC) in 59 samples of amniotic fluid obtained from 46 pregnant diabetic patients, based on an enzymatic method reported previously. 35 infants who had more than critical PG concentrations (0.36 mumoles/dl) were all associated with normal postnatal respiratory function. 9 out of 10 infants with a PG value lower than this level developed RDS. PG values in patients with mild and severe type diabetes were compared with those of uneventful pregnant women. The appearance of PG was delayed in mild diabetes (Class A, B and C), while it appeared earlier in severe type diabetes (Class D, F and R). Determination of catecholamines together with PG in amniotic fluids of four pregnant women with diabetes indicated that PG values were closely associated with the activities of the fetal adrenergic system. Since an increase in adrenergic activity occurs as a response to fetal distress, amniotic fluid PG is important not only in assessing fetal lung maturity, but also in managing high-risk pregnancies such as diabetic patients.
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PMID:[Significance of amniotic fluid phosphatidylglycerol for the assessment of fetal lung maturity during diabetic pregnancy]. 405 34

Various synthetic dopamine (DA) analogues have been shown to produce glucose intolerance and inhibit the compensatory increase in serum insulin during an oral glucose tolerance test (OGTT). To investigate the possibility that there is a direct action of dopamine analogues to inhibit glucose-stimulated insulin release from the endocrine pancreas, the following compounds were compared with the effects of epinephrine (EPI) on isolated rat pancreatic islets: apomorphine (APO), pergolide, lergotrile, TL-99 (2-dimethylamino-6,7-dihydroxytetralin), and RDS-127 (2-di-n-propyl-amino-4,7-dimethoxyindane). EPI, TL-99, and pergolide inhibited insulin release in a concentration-dependent fashion (10(-7)-10(-5) M), whereas lergotrile inhibited at 10(-5) M but not at 10(-6) M. RDS-127 and APO were ineffective at 10(-5) M, but produced a greater than 50% inhibition at 2 X 10(-4) M. The potencies of the DA analogues fell into two groups: compounds that are approximately as active as EPI (e.g., TL-99 and pergolide) or compounds that are relatively inactive (e.g., APO, lergotrile, and RDS-127). The inhibitory actions of EPI, TL-99, and pergolide were blocked by the alpha 2-adrenergic receptor antagonist yohimbine, whereas the DA receptor antagonist, sulpiride, had no effect, suggesting an action initiated at alpha 2-adrenergic receptors. Drugs from both groups produced marked glucose intolerance and inhibited the compensatory increase in insulin during an OGTT. Adrenodemedullation blocked the glucose intolerance and inhibition of insulin release caused by RDS-127, whereas these effects of TL-99 were not attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1984 Sep
PMID:Inhibition of insulin release from rat pancreatic islets by drugs that are analogues of dopamine. 614 89

As shown in our previous report surfactant lipoprotein concentration (SLPC) in amniotic fluid measured by sucrose density gradient centrifugation predicts accurately the risk of RDS. In this study SLPC estimations were made on 91 amniotic fluid samples from abnormal pregnancies, spontaneous premature deliveries and anencephalies. The results were as follows. SLPCs increased in placental insufficiency and severe preeclampsia, especially associated with SFD infant, on the other hand, SLPCs decreased in maternal diabetes (Class B), Rh-isoimmunization and anencephaly as compared with normal pregnancy. In most of premature deliveries SLPCs were higher than those of normal pregnancies except for RDS cases. Present evidence suggests that the maturation of fetal lung is accelerated in severe preeclampsia and placental insufficiency and is delayed in maternal diabetes (Class B), Rh-isoimmunization and anencephaly, and it is considered that in spontaneous premature delivery surfactant production in fetal lung is not accelerated but surfactant excretion from fetal lung into amniotic fluid is enhanced by effect of uterine relaxant such as isoxsuprine or terbutaline.
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PMID:[Surfactant lipoprotein concentration in amniotic fluid of abnormal pregnancies and premature deliveries (author's transl)]. 689 7

This survey of 73 infants of insulin dependent (ID) diabetic mothers and 70 infants of gestational diabetics (GD) born at King George V Memorial Hospital between January, 1968 and December, 1975, showed that all 12 babies with RDS were from the ID group. RDS was the cause of all 6 neonatal deaths and together with the 5 stillbirths gave this high risk group a 15% mortality rate. Since no deaths occurred in the GD group, the overall mortality was 8%. In the 6 years, 1970-1975, RDS occurred 21 times more often in babies of ID mothers than in control babies born to non-diabetics. Babies born to ID mothers were of significantly lower mean gestational age than those born to the GD mothers. Within the ID group, those babies with RDS were of significantly lower gestation than those without and the mean gestation was similar to control babies with RDS. Provided the diabetes is controlled and fetal welfare ensured, later delivery, following documentation of lung maturity, may lower the incidence of RDS and therefore perinatal mortality and morbidity.
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PMID:Incidence of the respiratory distress syndrome in infants of diabetic mothers--perinatal influences. 693 12


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