[Somatic and psychomotor development of children of diabetic mothers in the 4th year in relation to neonatal findings]. / Somatische und psychomotorische Entwicklung von Kindern diabetischer Mütter im vierten Lebensjahr in Beziehung zu Neonatalbefunden.

340 infants of mothers with type I diabetes (IDM) were examined during the neonatal period for gestational age, somatic data and clinical symptoms of diabetogenic foetopathy and assigned to one of three groups: group I--those whose weight development was delayed or appropriate for gestational age and without symptoms of foetopathy; group II--neonates who were overweight or of appropriate weight for their gestational age and who showed clear symptoms of foetopathy; group III--macrosomic infants (weight and length in advance of gestational age) without any major symptoms of foetopathy. In a pilot study preparing for more comprehensive follow up, 20 children from each group were examined in their fourth year to check their psychomotor and somatic development. To evaluate their growth additional data obtained on IDMs by correspondence were included. Although the group as whole showed a normal weight development for the fourth year with a low obesity rate (8.4%), the distribution among the three groups proved non-homogenous. 11.4% of the macrosomic children were overweight; this comprises 57% of all the obese children registered. There was a still clearer trend towards macrosomia among the children in groups II and III where the average age: length percentiles amounted to 57 and 67%. The psychological test showed an IQ of less than 95 in 16.7% of the cases distributed homogeneously among the different groups. With reference to their psychomotoric and language development the children examined were normal, some slight deviations in group II in walking and concentration ability need to be checked further. Our studies show that in children of diabetic mothers there are links between neonatal findings and later psychomotor and somatic development. A classification of newborns which goes beyond the usual establishment of percentiles for weight and gestational age seems appropriate in order to identify risk cases (macrosomia, obesity). A follow up study is required on a larger representative group and should be conducted at a more advanced age and not before the sixth year.

Neonatal jaundice in infants of diabetic mothers.

357 IDMs and 20 healthy newborns of non-diabetic mothers were examined at term for body measurements, red blood cell count, serum bilirubin, cord blood insulin and blood glucose during the first postnatal week. The stage of maternal diabetes did not influence the course of neonatal bilirubin levels, but the IDMs had prolonged and higher bilirubinaemia compared with the controls. Hyperbilirubinaemia was found to be most prominent in newborns with an increased birthweight/length ratio and was not simply related to macrosomia (LGA). These infants had significantly lower blood glucose concentrations immediately after birth, whereas cord blood insulin was found to be identical between the IDM sub-groups. Bilirubinaemia in heavy for length infants was slightly correlated to haematocrit. For the pathogenesis of hyperbilirubinaemia in IDMs induction of heme oxygenase (due to a lack of energy provision following a phosphorylation disorder) is discussed. Nutritional support (early feeding, glucose infusions) does not affect the course of bilirubinaemia.

Bilirubin binding and acid-base equilibrium in newborn infants with low birthweight.

Acidosis is known as a risk factor for the development of bilirubin encephalopathy in neonatal jaundice. However, few attempts have been made to evaluate the influence of acid-base state on bilirubin-albumin binding state in blood of newborn infants. Therefore, in 171 appropriate and 83 small for gestational age newborns (birthweight less than 2,500 g) the acid-base state in blood and bilirubin (BR) binding state in serum was measured at the ages of 3, 4, 5, and 8 days. There is a weak but significant correlation between standard base deficit and the ratio BR/reserve albumin as well as the toxic potential of serum BR. The results suggest that the higher risk in acidosis is not only caused by increased tissue binding of BR but also--at least partially--attributable to decreased BR binding in serum.