Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of 30 women who had polyhydramnios in more than 1 pregnancy revealed that 8 of the 36 resultant pregnancies (22.2%) were associated with diabetes mellitus, 14 (37.8%) with fetal macrosomia, and the perinatal mortality was 16.2% (6 of 37). The incidence of major fetal malformations or abnormalities was 18.9% (7 of 37); 4 of the 6 deaths resulted from malformations (anencephalus (2), hydrocephalus (1), nonimmune hydrops (1)), and the other 2 deaths were from hyaline membrane disease associated with prematurity. Recurrent polyhydramnios occurred in 1 in 1,720 pregnancies. The onset was acute in 3, subacute in 2 and chronic in 31, the perinatal deaths in these categories being 2, 1 and 3 respectively. The risk of recurrent polyhydramnios is the risk of fetal malformation and premature delivery. The latter may be preventable by prompt therapy with indomethacin, and serial amniocentesis if this therapy fails.
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PMID:The significance of recurrent polyhydramnios. 849 34

The perinatal mortality rate of infants of diabetic mothers (IDMs) has declined dramatically from 250 per 1000 live births in the 1960s to a near-normal 20 per 1000 live births in the 1980s. Five to 8% of all IDMs suffer from major congenital malformations, and it is the latter that are responsible for 50% of these perinatal deaths. It has been shown that tight glycemic control prior to conception and during pregnancy can prevent an excess rate of congenital malformations, fetal macrosomia, birth trauma, and neonatal respiratory distress syndrome. We briefly review the short- and long-range complications that occur in offspring of diabetic mothers (ODMs) from gestation through young adulthood. Short-term neonatal complications, such as hypoglycemia, hypocalcemia, hypomagnesemia, hyperbilirubinemia, and polycythemia, are related mainly to fetal hyperinsulinemia, hypoxemia, and prematurity. They are readily controllable within the setup of modern neonatal intensive care units. Long-range complications include an increased rate of childhood and adolescent obesity, impaired glucose tolerance or diabetes mellitus, and subtle neuropsychological dysfunctions. These may be related to the severity of the maternal hyperglycemia during pregnancy, the consequent fetal hyperinsulinemia, and third trimester maternal lipid metabolism disturbances. Today we have at hand the knowledge and tools to properly treat both pregestational and gestational diabetes. Increased education of the general practitioner and the target population regarding early referral of pregestational diabetic mothers and the implementation of screening programs for gestational diabetes will further reduce diabetic pregnancy-related morbidity.
J Diabetes Complications
PMID:Short- and long-range complications in offspring of diabetic mothers. 888 19

The relationships between prior obstetrical complications and subsequent trial of labour and vaginal birth after Caesarean (VBAC) success likelihood were examined among a cohort of Washington State women with a first livebirth via Caesarean delivery and a second livebirth between 1987 and 1993 (n = 10110). Overall, 64% of the cohort undertook a labour trial, and 62% of those who attempted VBAC delivery were successful, for an overall VBAC rate of 40%. Women with fetal macrosomia, cephalopelvic disproportion, prolonged labour, diabetes, or placental problems in the first pregnancy were less likely to undergo a labour trial in the second pregnancy than those without these factors, while women with prior induced labour, genital herpes, fetal distress, or breech presentation were more likely to attempt vaginal birth. Approximately half of women with prior macrosomia, labour problems, or chronic medical conditions who attempted VBAC succeeded, as did three-quarters of women with prior breech presentation or placental conditions. Overall VBAC rates were around 33% for women with previous fetal macrosomia, labour problems, or chronic medical conditions, and 45-55% among those with herpes, fetal distress or breech presentation at the first birth. Trial of labour should especially be encouraged among women without prior labour problems.
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PMID:Attempt and success rates for vaginal birth after caesarean section in relation to complications of the previous pregnancy. 901 16

To date, measurements of GH-binding protein (GHBP) during human pregnancy have been carried out using assays susceptible to interference by the elevated levels of human placental GH typical of late gestation. We recruited a large cohort of pregnant women (n = 140) for serial measurements of GHBP and used the ligand immunofunctional assay for GHBP. For normal gravidas, GHBP levels fell throughout gestation. Mean levels were 1.07 nmol/L (SE = 0.18) in the first trimester, 0.90 nmol/L (SE = 0.08) at 18-20 weeks, 0.73 nmol/L (SE = 0.05) at 28-30 weeks, and 0.62 nmol/L (SE = 0.06) at 36-38 weeks. GHBP levels in the first trimester correlated significantly with maternal body mass index (r = 0.58; P < 0.01). GHBP levels in pregnancies complicated by noninsulin-dependent diabetes mellitus (NIDDM) were substantially elevated at all gestational ages. The mean value in the first quarter (2.29 nmol/L) was more than double the normal mean (P < 0.01). In contrast, patients with insulin-dependent diabetes mellitus (IDDM) showed reduced GHBP concentrations at 36-38 weeks. The correlation between body mass index and GHBP is consistent with a metabolic role for GHBP during pregnancy, as is the dramatic elevation in GHBP observed in cases of NIDDM. At 36 weeks gestation, GHBP was significantly elevated (P < 0.01) in those women whose neonates had low birth weight (< 10th percentile). In early gestation (< 14 weeks), GHBP tended to be higher in women whose fetuses were designated to be at risk of intrauterine growth retardation (1.39 nmol/L; n = 4; compared with 1.07 nmol/L in normals), but this did not reach statistical significance. Although both NIDDM and IDDM pregnancies are at risk of fetal macrosomia, their GHBP concentrations are markedly divergent. This paradox and the roles of glucose and insulin in the regulation of GHBP during gestation warrant further investigation.
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PMID:Growth hormone-binding protein in normal and pathologic gestation: correlations with maternal diabetes and fetal growth. 917

In this prospective study, we examined the effect of maternal glycemic control on fetal growth in pregnancies complicated by pregestational diabetes. One hundred and sixty-five pregestational diabetic pregnancies were studied with serial ultrasound scans and fetal growth was examined as a function of maternal glycemic control. There was a significant, although small, reduction in fetal biparietal diameter growth rate in the presence of poor maternal glycemic control during the first half of the pregnancy. In the second half of pregnancy, maternal hyperglycemia contributed to fetal macrosomia. We conclude that in pregnancies with pregestational diabetes, maternal hyperglycemia affects fetal growth in a biphasic manner. As a result of that, although babies born to diabetic mothers appear of relatively overall normal size and weight, they may have smaller heads than their potential and more fat.
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PMID:The effect of maternal glycemic control on fetal growth in diabetic pregnancies. 939 64

The purpose was to identify risk factors and document the incidence and prognosis for brachial plexus palsy (BPP) and clavicular fracture (CF) among consecutive hospital liveborn (LB) infants in the United Arab Emirates. During a 2-year period, all hospital-born infants were examined twice by paediatricians before discharge and those found to have BPP or CF were evaluated and followed up by an orthopaedic surgeon. Each clavicular fracture was confirmed radiologically. For the assessment of risk factors, three controls were selected for each case of BPP or CF. Of the 9231 LB, 27 (2.9/1000) had BPP while 24 (2.6/1000) sustained CF. After controlling for potential confounding variables, shoulder dystocia (SD), fetal macrosomia (birthweight > 4000 g), instrumental vaginal delivery and diabetes remained risk factors for BPP while only fetal macrosomia and instrumental delivery increased the risk of CF. The frequency of these risk factors was higher than that reported from the West. Infants with BPP had a higher incidence of SD (p = 0.0001) and tended to be heavier (p = 0.052) than those with CF. All infants with CF recovered while 20% of those with BPP had moderate to severe residual disabilities. This study highlights geographic differences in risk factors for BPP and CF and the possible contribution of BPP to morbidity in infancy. Early recognition of fetal macrosomia and improved management of SD and maternal diabetes are necessary to reduce the incidence of BPP and CF as well as morbidity from BPP in this community.
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PMID:Risk factors and prognosis for brachial plexus injury and clavicular fracture in neonates: a prospective analysis from the United Arab Emirates. 942 73

Extreme fetal macrosomia occurred in the first recorded case of diabetes in pregnancy in 1823. The belief that the diabetic condition was in some way a symptom of the pregnancy, which dates to that first report, has led to the more recent concept of gestational diabetes. Lesser degrees of maternal hyperglycemia were also recognized to be a risk to the baby, and early studies of carbohydrate intolerance in pregnancy in Boston and Los Angeles have set the stage for the worldwide interest in this maternal/fetal interaction.
Diabetes Care 1998 Aug
PMID:A historical perspective on gestational diabetes. 970 19

Metabolic perturbations associated with gestational diabetes mellitus (GDM) have been shown to result in significant clinical morbidity, both for the mother and the neonate. Although a number of studies have documented the changes in glucose metabolism in GDM, the data on nitrogen and protein metabolism remain scant. Recent data in GDM show that 1) the rate of irreversible nitrogen loss as measured by the rate of urea synthesis in GDM is similar to that in normal pregnancy and is less than that in nonpregnant women; and 2) possibly related to the magnitude of metabolic decompensation as assessed by the nature of therapeutic intervention (diet or diet plus insulin), the rate of protein turnover measured by leucine kinetics is increased in insulin-treated GDM. Whether the decompensation in protein turnover contributes to the persistent fetal macrosomia, even in rigorously managed GDM, remains speculative.
Diabetes Care 1998 Aug
PMID:Protein and nitrogen metabolism in gestational diabetes. 970 31

The currently accepted definition of gestational diabetes mellitus (GDM) is rather broad. One might expect that fetal and neonatal complications that may occur in GDM pregnancy would be similar to those in pregestational diabetic pregnancy. Comparative evaluation of reported data on morbidity in GDM are often hampered by confounding variables (maternal age, parity, obesity) as well as the influence of factors such as ethnic origin, diagnostic criteria, and intervention during pregnancy. Recent observations indicate that GDM may be associated with increased incidence of fetal malformation and perinatal mortality. Such poor outcome is likely confined to a subset of GDM patients in whom diabetes was present but unrecognized before pregnancy. The most frequent and significant morbidity is fetal macrosomia, which in turn is associated with increased risk of birth injuries and asphyxia. In a nationwide study in Sweden (1991-1993) of a large series (n = 3.322) of treated GDM pregnancies, perinatal mortality rate was not increased; but the rate of preeclampsia was doubled, and the rate of emergency cesarean section was 1.6 times higher than in the background population. The rates of fetal macrosomia (> or = 4,500 g), asphyxia, and transient tachypnea were two to three times higher than normal Erb's palsy was 0.7 and 5% in vaginally delivered infants weighing < 4,500 and > or = 4,500 g, respectively. There is a clear need to define the various levels of glucose intolerance in the mother that may have an adverse effect on the offspring. Of equal importance is to standardize and systematize the criteria used to assess the significance of any such impact.
Diabetes Care 1998 Aug
PMID:Neonatal morbidities in gestational diabetes mellitus. 970 32

This study was designed to investigate the effects of maternal diabetes on glucose transporter expression and glucose transport activity in the human placenta. Syncytiotrophoblast microvillous and basal membranes were prepared from placental tissue obtained at term from pregestational diabetics (White class B) and gestational diabetics controlled either by diet alone (class A1) or by diet and insulin (class A2). These membranes were used to measure GLUT1 glucose transporter expression and D-glucose transport activity. Diabetic groups showed no differences in placental weights or neonatal birth weights compared to controls, although 8 of 25 diabetic fetuses were macrosomic. Glycemic control in the diabetics at term, as assessed by maternal glycosylated hemoglobin, was within normal limits. Basal membrane GLUT1 density was about 2-fold higher in all diabetic groups compared to that in controls, as measured by immunoblotting, whereas no changes were found for the microvillous membranes. D-Glucose uptake across the basal membrane was increased by 40% in the diabetic groups; no changes were observed for the microvillous membrane. These results demonstrate that diabetes causes an increase in basal membrane GLUT1 expression and activity that persists despite a lack of evidence for current or recent maternal hyperglycemia. This suggests the potential for an extended increase in transplacental glucose flux in the absence of maternal hyperglycemia, which may contribute to fetal macrosomia and the other consequences of diabetic pregnancy.
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PMID:Diabetes alters the expression and activity of the human placental GLUT1 glucose transporter. 1002 40


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