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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.
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PMID:Short- and long-range complications in offspring of diabetic mothers. 888 19

In summary, fetal macrosomia occurs in almost one third of diabetic pregnancies regardless of class. Abnormal fetal fat stores lead to difficult labor, dystocia, and birth injury as well as postnatal metabolic transition. The abnormal body fat distribution at birth may destine some of these infants to lifelong obesity. Abnormal fetal growth in diabetic pregnancy appears to occur with any elevations in maternal glucose levels, however modest. Detection of macrosomia is therefore a major goal of diabetic pregnancy management.
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PMID:Fetal growth in diabetic pregnancy. 942 92

Several groups have reported a risk of fetal macrosomia in pregnancies with maternal glucose intolerance which is intermediate between gestational diabetes (GDM) and normal glucose tolerance. The present study was designed to determine whether these pregnancies are also at risk for fetal obesity, hyperinsulinism and placental villous immaturity. 325 women with risk factors for GDM underwent a 75 g OGTT interpreted according to the O'Sullivan criteria. All women who met the criteria for GDM were managed with diet therapy. Insulin therapy was added for women with a mean serum glucose value > 100 mg/dl on a 24 hour glucose profile. Patients not meeting the GDM criteria were managed without special intervention. Primary outcome variables were measures of neonatal weight and skinfold thickness, fetal and neonatal insulin and glucose concentration, and placental villous maturation. Outcome parameters were compared among three groups: pregnancies with normal OGTT (control, n = 95), 1 abnormal value in the OGTT (1 abnl, n = 76) and GDM (n = 154). The outcome of pregnancies with 1 abnormal value in the OGTT was different from those with normal OGTT. Regarding fetal growth, rates of LGA were approximately twice as high in groups with one abnormal value and GDM (21% and 24%) compared to women with normal OGTTs (11%: p < 0.05 vs GDM and p = 0.07 vs 1 abnormal value). The percent of infants with skinfold thickness > 90th percentile was also greater in the 1 abnormal value and GDM groups (31.1 and 31.6% respectively) compared to controls (19.2%; p < 0.05 for GDM vs control only). Regarding fetal hyperinsulinism, AFI concentrations were similar in control and GDM groups (3.1 +/- 0.4 and 3.4 +/- 0.8 microU/ml, respectively), but were higher in the group with one abnormal OGTT value (4.3 +/- 1.2 microU/ml, p < 0.05 vs controls). Cord blood insulin: glucose ratios were elevated in both the 1 abnormal value and GDM groups (0.22 +/- 0.05 and 0.20 +/- 0.02 microU/ml per mg/dl), compared to controls (0.12 +/- 0.01 microU/ml per mg/dl, p < 0.05 vs 1 abnormal value). Neonatal glycemia < 30 mg/dl was significantly more common in the one abnormal value than in the control group (49% vs 34% of infants) and intermediate in the GDM group (40%). Severe placental villous immaturity was more than twice as frequent in the 1 abnormal value group compared to controls (24% vs 9%, p < 0.05) and the most frequent in the GDM group (33%; p < 0.001 vs controls). Pregnancies with glucose intolerance below the thresholds for diagnosis of GDM have an increased risk for fetal obesity, hyperinsulinism, postpartum hypoglycemia and placental immaturity. These findings indicate the continuum of risk for fetal morbidity associated with increasing maternal glucose intolerance in pregnancy.
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PMID:Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value. 959 64

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.
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PMID:Neonatal morbidities in gestational diabetes mellitus. 970 32

The presence of insulin-dependent or non insulin-dependent diabetes mellitus in pregnant women has been associated with an adverse effect on the maternal an fetal outcomes of pregnancy. The incidence of obstetrical and diabetic complications is increased, and a continuum has been observed between maternal blood glucose levels and perinatal outcome. The incidence of congenital malformations, macrosomia and prematurity is increased in offspring of diabetic mothers. Programming and intensive collaborative follow-up improve the outcome of such pregnancies. Gestational diabetes mellitus is an heterogenous condition defined as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. Short term complications are mainly represented by fetal macrosomia and high cesarean section rate. Women with a history of gestational diabetes mellitus are at increased risk of future diabetes, predominantly type 2. Obesity and type 2 diabetes are increased among their children.
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PMID:[Diabetes and pregnancy]. 1054 52

The aim of this work was to determine lipoprotein metabolism alterations in macrosomic newborns and to see whether these lipoprotein abnormalities are parallel or not to those found in their obese or nonobese mothers. Serum lipids, apo A-I, apo B100, lipoproteins (VLDL, LDL, HDL2, and HDL3), and LCAT activity were investigated in obese and nonobese mothers and cord blood of their macrosomic or appropriate-for-gestational-age (AGA) newborns. Serum and VLDL triglyceride concentrations were higher in obese mothers of AGA newborns than in nonobese mothers. Serum triglyceride, VLDL, and apo B100 levels were higher, while serum apo A-I and HDL2 cholesterol concentrations were lower in obese mothers of macrosomic newborns than in the other groups. In their macrosomic newborns, serum lipid, lipoprotein, apo B100, and apo A-I levels were higher as compared with those of other newborns. Macrosomic newborns of nonobese mothers had lipoprotein profiles similar to those in AGA newborns. LCAT activity was similar in both mother groups and in both newborn groups. In conclusion, maternal obesity and fetal macrosomia were associated with lipoprotein abnormalities consistent with high atherogenic risk.
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PMID:Impaired serum lipids and lipoproteins in fetal macrosomia related to maternal obesity. 1065 26

Fetal macrosomia is an heterogeneous condition in terms of definition and etiologic factors. Recent findings suggest that macrosomia should not be classified on the basis of birth weight and gestational age alone. The ponderal index delineates a symmetric and an asymmetric subtype of macrosomia. The relationship between maternal diabetes and fetal macrosomia has been extensively investigated. However, eighty percent of macrosomic infants are born to mothers who are not hyperglycemic, and various factors have been associated. Maternal factors explain approximately 50% of the variance in birth weight, whereas paternal factors have no significant effect. The predisposition to excessive fetal growth may be shared within the intra uterine environment and the fetal genome. The respective roles of lipids, amino acids, hormones such as leptin, and growth factors need to be evaluated. Perinatal morbidity and long term consequences such as obesity and glucose intolerance might be associated with some of the factors leading to fetal overgrowth.
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PMID:[Etiopathogeny of fetal macrosomia]. 1067 72

Obesity-related metabolic and functional disorders may disturb adaptation process taking place in pregnant women body. Insufficient adaptation may lead to development of several medical complications during pregnancy, labor, delivery, and puerperium. Maternal obesity is associated with increased frequencies of hypertension, preeclampsia, gestational diabetes mellitus, fetal macrosomia, congenital malformations, labor abnormalities (including prolonged second stage of labor, meconium-stained amniotic fluid, FHR abnormalities and shoulder dystocia), postdatism, and cesarean delivery. Operative complications among obese women undergoing cesarean delivery include increased blood loss, prolonged operative time, and increased rates of postoperative infection, thrombophlebitis. Treatment of these complications increases hospital stays and costs. Obese women should be carefully examined by dietetician before conception and cared for dietetically and medically during gestation.
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PMID:[Obesity as an obstetric risk factor]. 1089 90

The acid phosphatase locus 1 (ACP1) codes for a low molecular weight phosphotyrosine protein phosphatase that has the important action of dephosphorylating tyrosine phosphorylated proteins and peptides and a second important role in modulating flavin cofactor levels and the activity of flavo-enzymes. These functions significantly influence cell division, differentiation, and growth. Two alleles (ACP1*A and ACP1*B) reach polymorphic frequencies at the ACP1 locus in all human populations, while the ACP1*C and ACP1*R alleles reach polymorphic frequencies in restricted geographical regions. The worldwide distribution of these alleles, and data from several clinical studies, strongly suggest that the ACP1 locus functions to modulate growth and that selection at this locus is a component of the selective processes influencing body mass and human population adaptation to thermal stress. The ACP1*A allele reaches highest frequencies at extreme latitudes and appears to be associated with maximizing body mass and adaptation to cold stress, whereas the ACP1*B allele reaches highest frequencies in tropical and subtropical environments and appears to be associated with minimizing body mass and adaptation to heat stress. The high frequency of the ACP1*C allele at northern latitudes, where ACP1*A allele frequencies are elevated, may be a mechanism for limiting fetal and maternal complications associated with fetal macrosomia and adult obesity in populations where protein and calorie intake are relatively high. Am. J. Hum. Biol. 12:688-701, 2000. Copyright 2000 Wiley-Liss, Inc.
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PMID:Acid phosphatase locus 1 (ACP1): Possible relationship of allelic variation to body size and human population adaptation to thermal stress-A theoretical perspective. 1153 62

The present study was aimed to investigate pregnancy outcome among obese women and specifically the correlation between maternal obesity and incidence of caesarean section (CS) while controlling for the potential confounding effects of other variables associated with obesity. A population-based study was performed comparing all pregnancies of obese (maternal pre-pregnancy body mass index (BMI) of 30 kg/m2 or more) and non-obese patients, between the years 1988 and 2002. Patients with hypertensive disorders and diabetes mellitus as well as patients lacking prenatal care were excluded from the analysis. Stratified analyses, using the Mantel-Haenszel technique, and a multiple logistic regression model were performed to control for confounders. During the study period there were 126,080 deliveries meeting the inclusion criteria, of which 1769 (1.4%) occurred in obese patients. Using a multivariable analysis, the following conditions were significantly associated with maternal obesity: failure to progress during the first stage (odds ratio (OR) = 3.1; 95% confidence interval [CI] 2.5, 3.8; P < 0.001), fertility treatments (OR = 2.0; [95% CI 1.6, 2.5]; P < 0.001), previous CS (OR = 1.7; [95% CI 1.5, 1.9]; P < 0.001), malpresentations (OR = 1.4; [95% CI 1.2, 1.6]; P < 0.001), recurrent miscarriages (OR = 1.4; [95% CI 1.2, 1.7]; P < 0.001) and fetal macrosomia (OR = 1.4; [95% CI 1.2, 1.7]; P < 0.001). Higher rates of caesarean deliveries were found among obese parturients (27.8% vs. 10.8%; OR = 3.2; [95% CI 2.9, 3.5]; P < 0.001). When controlling for possible confounders, using the Mantel-Haenszel technique, the association between maternal obesity and CS remained significant. No significant differences were noted between the groups regarding perinatal complications such as perinatal mortality, congenital malformations, shoulder dystocia and low Apgar scores. In conclusion, a significant association was found between obesity and CS even after the exclusion of hypertensive disorders and diabetes mellitus. Importantly, obesity alone was not associated with adverse perinatal outcome. Obstetricians should be encouraged to allow obese patients not suffering from diabetes or hypertensive disorders an adequate trial of labour.
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PMID:Maternal obesity as an independent risk factor for caesarean delivery. 1513 Jan 59


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