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Gestational diabetes (GDM) is defined as glucose intolerance first diagnosed with a 75 gram oral glucose tolerance test based on IADPSG criteria which had been recently adopted by WHO. In industrial countries GDM is one of the most frequent pregnancy complications. In 2012, in Germany GDM had been diagnosed in 4,3 % of all births, overall 27,700 cases. GDM has to be considered as a preliminary stage of type 2 diabetes with insulin resistance and inadequate ß-cell-compensation. Additionally, adverse metabolic profile, associations with inflammatory parameters, with D vitamin metabolism, and insufficient decline of renal threshold for glucose had been identified in women with GDM. Within 10 years after GDM roughly 50 % of the women convert to overt diabetes, mostly type 2. GDM and type 2 diabetes share potential candidate genes. In about 1 % of GDM in Caucasian women a mutation in glucokinase gene had been found (GCK-MODY). Predisposition to GDM is predominantly characterized by family history of diabetes, previous GDM in pregnancies, factors of metabolic syndrome, and unfavorable life style. The probability for GDM rises with increasing mother's age and preconceptional BMI. Via fetal programming GDM dispones to offspring obesity as early as school entry. Prevention of GDM focus on regular physical exercise, normalizing body weight before conception, reducing excess intake of animal protein and soft drinks, planning of pregnancy in younger ages, and avoiding pollutant exposition as well as smoking cessation.

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HISTORY AND FINDINGS: A 39 year-old pregnant woman (with one healthy 11 year-old daughter) presented at the antenatal care clinic for routine non-stress test (NST) at the due date. The NST demonstrated normal fetal heart pattern. No anamnestic or clinical risk factors for diabetes during the course of pregnancy were noted in the case file. Ultrasound examinations up to 30 weeks of gestation had shown fetal growth appropriate for gestational age. Two days later, the NST was non-reacting with almost no heart rate variability, indicating an acute fetal risk. While the condition of the fetus was being further assessed by Doppler sonography, a fall in fetal heart rate prompted an emergency section for fetal bradycardia. The male newborn had marked macrosomia (birth weight 5180 g). The pH in umbilical artery blood of 6,77 indicated severe intrauterine hypoxia. Apgar score was 0/1/5. Absence of heart beat and of spontaneous breathing required resuscitation. Echocardiography revealed a hypertrophic cardiomyopathy with dysfunction of the right ventricle and hepatomegaly indicating diabetic fetal pathology. The placenta displayed typical signs of carbohydrate disorder. The maternal 75 g oral glucose tolerance test confirmed the suspicion of maternal diabetes (glucose values 96/210/215 mg/dl). TREATMENT AND COURSE: During the next the day the infant developed multi-organ failure involving the liver and kidneys, myocardial infarction with pericardial effusion and myoclonic seizures. His condition improved slowly under measures to stabilize the circulation, substitution of clotting factors and anticonvulsive therapy. Mechanical ventilation had to be continued for 5 weeks. Examination at 4 months of age revealed marked neurological abnormalities. The mother was referred to a diabetes specialist for further management. CONCLUSION: Undiagnosed and therefore untreated severe gestational diabetes may have fatal consequences for the fetus. Expert committees of obstetricians and diabetes specialists have recommended blood glucose screening between 24 - 28 weeks of gestation of every pregnant woman as part of the routine prenatal care.

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Preexisting type-I-diabetes (incidence 0.8%) and gestational diabetes (3-5%) are the two manifestations of disturbed carbohydrate metabolism in pregnancy. Maternal hyperglycemia and the resulting excessive glucose supply for the fetus leads to fetal hyperinsulinism which is responsible for the complications in the offspring. The most important clinical manifestations are the excessive growth of the fetus (macrosomia), the risk of intrauterine death and the neonatal morbidity caused by hypoglycemia and the delay of maturation of lungs and liver. Women with type-I-diabetes require preconception counseling and optimizing of glucose control to reduce the rate of abortion and of congenital anomalies of the offspring. Furthermore kidney function and retinopathia should be evaluated preconceptionally. The management of diabetic pregnancies requires a tight cooperation of obstetricians and diabetologists. Blood glucose levels have to be lower than outside pregnancy. Gestational diabetes is diagnosed by a screening test with 50 g glucose for all women followed by a regular 75 g oGTT when the glucose value is > or = 140 mg%. In most of the women euglycemia can be achieved by diet and exercise. Women after pregnancies with gestational diabetes should be retested postnatally and counseled about their increased risk to develop diabetes in later life.

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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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