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

In women with type-1 diabetes, the prevalence of maternal and fetal complications is high despite the overall adequate blood glucose control (HbA1c < 7%). Further improvements are hampered by the high incidence of maternal hypoglycaemia, including coma, especially during the first trimester of pregnancy. The reasons for this include the intensified insulin treatment, the decrease in hypoglycaemia awareness and the increase in glucose fluctuations. A further improvement of glucose control would provisionally seem possible only by using short-acting insulin analogues. These agents are currently under investigation. Continuous subcutaneous glucose measurements early in pregnancy show considerable glucose fluctuations despite almost normal HbA1c values. Moreover, they often reveal a hypoglycaemic event that the pregnant woman has not recognised. It is possible that these glucose fluctuations, rather than the too high average blood glucose levels, are responsible for congenital malformations and fetal macrosomia. Neonatal hypoglycaemia is associated with poor psychoneurological development. This relationship has not been established for maternal hypoglycaemia during pregnancy.
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PMID:[Diabetes and pregnancy; the prevention of hypoglycaemia]. 1570 35

More than three decades since the original published description of gestational diabetes mellitus (GDM), no consensus exists regarding its implications or management. Targeting fetal macrosomia as the greatest morbidity, treatment strategies for this pregnancy-induced disease of insulin resistance have largely been modeled from therapies proven successful in pregnant women with type 2 diabetes mellitus. Surrounded by a rapidly expanding array of treatment options for insulin-resistant diabetes, potentially legitimate concerns about teratogenicity and fetal metabolic effects have limited clinical trials of insulin analogs and oral antihyperglycemic agents during pregnancy. So far, only insulin lispro and glyburide (glibenclamide) have been tested prospectively in randomized trials of women with GDM. In limited studies, both of these agents have compared favorably with standard insulin regimens, and neither appear to cause any fetal or neonatal harm. Although acknowledged by the American Diabetes Association (ADA) and the American College of Obstetricians and Gynecologists (ACOG), these seminal studies have not yet prompted a recommendation from either organization on how to utilize insulin analogs or oral antihyperglycemic agents in the treatment of GDM. Although they lack an evidence base for many therapeutic strategies for GDM, the current ADA and ACOG guidelines still provide a reasonable set of treatment recommendations.
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PMID:Gestational diabetes: a review of the treatment options. 1598 52

Insulin-dependent diabetes mellitus (Type I) is associated with disregulation of the glucose and oxygen metabolic pathways during pregnancy, both of which affect placental villous development. Term complete placentas and placental bed biopsies, between 37 and 40 weeks, from 12 singleton pregnancies complicated by Type I diabetes were collected following delivery by elective Caesarean section. The controls consisted of 10 term placentas from uncomplicated pregnancies delivered by elective Caesarean section. Villous morphology was investigated using unbiased histomorphometric techniques, in relation to the degree of transformation of the spiral arteries and the presence of fetal macrosomia. A significant increase in fetal and placental weights, placental volume, volumes of the intervillous space and the trophoblast was found in the diabetic group compared to the controls. A significant reduction in the villous membrane specific diffusing capacity was observed between the diabetic and control groups (1.32 vs 1.72 cm3 min(-1)mmHg(-1)kg(-1), P=0.032). A significant increase in the volume of the intermediate and terminal villi, the surface area of the villi and of the fetal capillaries, and the harmonic thickness of the villous membrane was found in the macrosomic subgroup compared to the controls. There were no differences between the hypertensive subgroup with histological evidence of partial transformation of the spiral arteries and the controls. These data indicate that placental development in insulin-dependent diabetic pregnancies is affected differentially when pregnancies complicated by fetal macrosomia are separated from those complicated by maternal hypertensive disorders with partial transformation of the spiral arteries. The reduction in the specific diffusing capacity of the villous membrane may contribute to the fetal hypoxia and increased fetal and neonatal morbidity associated with diabetes.
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PMID:Villous histomorphometry and placental bed biopsy investigation in Type I diabetic pregnancies. 1600 23

Shoulder dystocia and brachial plexus injury occur in 0.5% to 1.5% of all births. Risk factors for both include maternal obesity, excessive prenatal weight gain, maternal diabetes, protracted labor, and fetal macrosomia. These factors are involved in only about 50% of births complicated by shoulder dystocia or brachial plexus injury. Shoulder dystocia has a low recurrence rate (9.8%-16.7%), although history of previous shoulder dystocia is the most reliable predictor of occurrence. Brachial plexus injury is the most common morbidity associated with shoulder dystocia, but 50% of newborns who present with this injury were not subject to shoulder dystocia at birth. Most brachial plexus injuries are transient, although 5% to 22% become permanent. Shoulder dystocia followed by permanent brachial plexus injury or mental impairment is one of the leading causes of malpractice allegations. Prompt assessment and management of shoulder dystocia and preparation to maximize the efficiency of shoulder dystocia maneuvers are critical. Documentation of the appropriate use of maneuvers to relieve shoulder dystocia demonstrates standard of care practice, thereby decreasing the potential for successful malpractice allegations.
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PMID:Shoulder dystocia: etiology, common risk factors, and management. 1626 Mar 63

Polycystic ovarian syndrome (PCOS) is a condition that is present in 5-6% of women of reproductive age. It has potentially profound implications for women with regard to anovulatory infertility and symptoms related to elevated androgen levels. In addition, in later life women are prone to significant health problems related to hyperinsulinaemia, with an excess risk for diabetes and cardiovascular risk factors. Evidence suggests that the adverse features of PCOS can be ameliorated with lifestyle intervention, such as diet and exercise, while further short-term benefits related to ovulation and cardiac risk factors may be derived from medication with metformin. Evidence for the long-term use of metformin to protect against adverse cardiovascular outcomes and for the use of metformin throughout pregnancy to reduce the risk of miscarriage, gestational diabetes, pre-eclampsia and fetal macrosomia is still lacking.
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PMID:Polycystic ovarian syndrome--prognosis and outcomes. 1676 28

Maternal diabetes can cause fetal macrosomia and increased risk of obesity, diabetes, and cardiovascular disease in adulthood of the offspring. Although increased transplacental lipid transport could be involved, the impact of maternal type 1 diabetes on molecular mechanisms for lipid transport in placenta is largely unknown. To examine whether maternal type 1 diabetes affects placental lipid metabolism, we measured lipids and mRNA expression of lipase-encoding genes in placentas from women with type 1 diabetes (n = 27) and a control group (n = 21). The placental triglyceride (TG) concentration and mRNA expression of endothelial lipase (EL) and hormone-sensitive lipase (HSL) were increased in placentas from women with diabetes. The differences were more pronounced in women with diabetes and suboptimal metabolic control than in women with diabetes and good metabolic control. Placental mRNA expression of lipoprotein lipase and lysosomal lipase were similar in women with diabetes and the control group. Immunohistochemistry showed EL protein in syncytiotrophoblasts facing the maternal blood and endothelial cells facing the fetal blood in placentas from both normal women and women with diabetes. These results suggest that maternal type 1 diabetes is associated with TG accumulation and increased EL and HSL gene expression in placenta and that optimal metabolic control reduces these effects.
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PMID:Placental triglyceride accumulation in maternal type 1 diabetes is associated with increased lipase gene expression. 1694 May 51

Maternal pregravid obesity is a significant risk factor for adverse outcomes during pregnancy. In early pregnancy there is an increased risk of spontaneous abortion and congenital anomalies. In later gestation maternal metabolic manifestations of the metabolic syndrome, such as gestational hypertensive disorders and diabetes, become clinically recognized because of the increased insulin resistance in obese compared with nonobese women. In women with pregestational glucose intolerance, hypertension, central obesity, and lipid disorders, the physiologic changes in pregnancy increase the risk of problems previously not routinely encountered during pregnancy. These include chronic cardiac dysfunction, proteinuria, sleep apnea, and nonalcoholic fatty liver disease. At parturition the obese patient is at an increased risk of cesarean delivery and associated complications of anesthesia, wound disruption, infection, and deep venous thrombophlebitis. For the fetus there are short-term risks of fetal macrosomia, more specifically obesity, and long-term risks of adolescent components of the metabolic syndrome. Although preliminary results of bariatric surgery are encouraging, the procedure is expensive and not for all obese women, and we recognize that long-term follow-up data on offspring of obese women who have undergone bariatric surgery before pregnancy are lacking. In the interim, we need to encourage obese women to lose weight before conception, using lifestyle changes if possible. During pregnancy, weight gain should be limited to Institute of Medicine guidelines (currently under review) and encouragement given for physical activity.
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PMID:Management of obesity in pregnancy. 1726 45

To assess whether HbA1c and plasma glucose predicts abnormal fetal growth, 758 pregnant women attending 5 Diabetic Centers were screened for gestational diabetes mellitus (GDM). On glucose challenge (GCT) at 24-27 weeks of gestation (g.w.), negative cases formed the normal control group (N1). Positive cases took an oral glucose tolerance test (OGTT): those found negative were classed as false positives screening test (N2); if they had an OGTT result at least as high as their normal glucose levels, they were classed as having one abnormal glucose value (OAV) at OGTT; two values as GDM. HbA1c was assayed on the day of GCT. We considered fetal macrosomia, large for gestational age (LGA), ponderal index and mean growth percentile. Mean age, pre-pregnancy BMI, fasting plasma glucose (FPG) and HbA1c were progressively higher from N1 to GDM patients. The newborn of N2 mothers were heavier than those with N1 or GDM. The mean growth percentile was significantly higher in N2 than in N1. More LGA babies were born to OAV than to N1 or N2 women. Macrosomia and ponderal index did not differ significantly in the four groups. At logistic regression only plasma glucose at GCT could predict LGA babies and a ponderal index above 2.85. At risk analysis, GDM and OAV significantly predicted LGA babies, and GDM a ponderal index >2.85. In conclusion, FPG at GCT could predict fetal overgrowth and plasma glucose >85mg/dl doubles the risk of LGA infants. HbA1c at 24-27g.w. does not predict fetal overgrowth. Mild alterations in glucose tolerance correlate with fetal overgrowth and needs monitoring and treatment.
Diabetes Res Clin Pract 2007 Sep
PMID:Can plasma glucose and HbA1c predict fetal growth in mothers with different glucose tolerance levels? 1735 Jan 35

Fetal macrosomia (birth weight >/=4,500 g) is known to increase a number of adverse maternal and perinatal outcomes. Although there is a clear association between maternal diabetes mellitus and fetal macrosomia, the majority of macrosomic infants are born to non-diabetic mothers. We wished to determine the recurrence rate of macrosomia in non-diabetic pregnancy and to see if a history of multiple prior macrosomic infants confers additional risk. A retrospective analysis of 14,461 term, singleton, infants born to non-diabetic mothers in 1997 and 1998 was performed, using a computerised hospital database. Among 14,461 term pregnancies, 529 infants (3.7%) were macrosomic, and the incidence was significantly higher in parous women (4.6%) compared with nulliparas (2.4%, p < 0.0001). Over the next 5 years, 164 of these women returned for another delivery. Women with a history of one macrosomic infant are at significantly increased risk of another macrosomic infant in a subsequent pregnancy (OR 15.8, 95% CI 11.45 - 21.91, p < 0.0001). For women with two or more macrosomic infants, the risk is even greater (OR 47.4, 95% CI 19.9 - 112.89, p < 0.0001). Macrosomia was associated with increased rates of instrumental delivery and anal sphincter injury regardless of parity, and additionally with increased rates of caesarean delivery and shoulder dystocia among nulliparas. Overall, 88% of women who laboured with a macrosomic infant achieved vaginal delivery.
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PMID:Recurrence of fetal macrosomia in non-diabetic pregnancies. 1765 89

Endogenous inhibitors of the Na/K-ATPase (NKA) and diabetes mellitus (DM) are both risk factors for preeclampsia and NaCl sensitive hypertension. Our goal was to test the hypothesis that NaCl supplementation, induces preeclampsia-like symptoms in pregnant rats with DM via stimulation of marinobufagenin (MBG), a natriuretic and vasoconstrictor inhibitor of the NKA. Type 2 DM in female Sprague-Dawley rats was induced by administration of 65mg/kg streptozotocin at day 4 post-partum. In intact rats, pregnancy was associated with a twofold increase in MBG levels and a mild impairment in glucose tolerance. Pregnant rats with DM exhibited fetal macrosomia, greater impairment of glucose tolerance, and higher levels of MBG as compared to that in normal pregnant rats. As compared to intact pregnant rats, NaCl supplementation of diabetic pregnant rats (drinking 1.8% NaCl during days 12-19 of pregnancy) was associated with an increase in systolic blood pressure, decreased fetal and placental weight, fivefold elevation of MBG excretion, and 42% inhibition of NKA in erythrocytes. In nonpregnant rats, in vivo pretreatment with anti-MBG antibody produced an exaggerated response of plasma levels of glucose and insulin in oral glucose tolerance test. These results suggest that MBG is a common factor in the pathogenesis of DM and preeclampsia, and that regulation of glucose tolerance may be one of the physiological functions of endogenous cardiotonic steroids.
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PMID:Endogenous sodium pump inhibitors, diabetes mellitus and preeclampsia Preliminary observations and a hypothesis. 1794 87


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