Intake and fecal excretion of PCDDs, PCDFs, HCB and PCBs (IUPAC Nos. 138, 153, 180) were measured in a breast-fed and a formula-fed infant at the age of 1 and 5 months. As expected, the intake of these compounds was clearly higher in the breast-fed infant. In this baby an almost complete absorption was observed for lower chlorinated PCDDs and PCDFs and also for HCB and PCBs, whereas for hepta- and octachlorinated PCDDs and PCDFs fecal excretion was considerably higher (from 20% up to nearly 100% of the intake). Due to low concentrations in diet and feces of the formula-fed infant an evaluation was possible only for a few compounds at the age of 5 months. These values were in the same range when compared with those of the breast-fed infant. For collection of feces new cotton diapers were used which were pre-extracted in order to reduce the levels of polychlorinated compounds. Unexpectedly, after washing the tissue a much higher contamination was observed which made a calculation of fecal excretion rates in the formula-fed infant at the age of 1 month impossible.

Breast Feeding↗

PubMedDate not supplied

Time course of PCDD/PCDF/PCB concentrations in breast-feeding mothers and their infants.

PCDD/PCDF/PCB concentrations were measured in samples from four mothers (at delivery and during lactation) and their infants (at birth and the end of first year of life). For two of these mothers it was the second delivery and breast-feeding period, and additional data were available from first lactation period and the first-born infant at the age of 11 to 12 months. Five of the six infants were fully breast-fed for at least 17 weeks. In four of them a distinct PCDD/PCDF/PCB accumulation was observed at the end of the first year of life: concentrations in blood fat were 1.5 to 3.6 times higher than maternal levels measured at the same time. Due to decreasing maternal body burdens during lactation, PCDD/PCDF concentrations at 11 to 12 months of life were only about half as high in the second infant as in the first one at the same age. During second pregnancy, no important change of the concentrations was observed in maternal blood.

Adult↗

PubMedDate not supplied

Impaired fat utilization in parenterally fed low-birth-weight infants suffering from sepsis.

Lipid infusion in low-birth-weight infants suffering from sepsis is still controversial. Consequently, we investigated the fat tolerance in six low-birth-weight infants with sepsis and 15 low-birth-weight infants without sepsis. For measurement of fat clearance, we assayed the serum concentrations of triglycerides enzymatically, and of the free fatty acids by colorimetric micromethod. The fatty acid oxidation was analyzed with the [13C]triolein breath test by means of ratio-mass spectrometry. The infants were maintained on continuous parenteral nutrition with various amounts of soybean oil emulsion (1 g, 2 g, and 3 g fat/kg body weight per day). Comparing the lipid infusion of 1 and 2 g fat/kg body weight per day between the two groups, we found triglyceride and free fatty acid values in both groups to be in the normal range. At a dose of 3 g of fat/kg body weight per day, septic low-birth-weight infants showed a significantly higher concentration of triglycerides (2.02 +/- 0.46 mmol/liter) and of free fatty acids (2.06 +/- 0.45 mmol/liter) than the nonseptic low-birth-weight infants (triglycerides: 1.09 +/- 0.43 mmol/liter; free fatty acids: 1.05 +/- 0.41 mmol/liter). The low-birth-weight infants with sepsis showed a reduced fat oxidation rate of 16.0 +/- 1.5% in contrast to that of the low-birth-weight infants without sepsis, whose rate was 38.4 +/- 1.8%. Accordingly, we apply dosages not exceeding 2 g of fat/kg body weight per day to septic low-birth-weight infants.

Fat Emulsions, Intravenous↗

PubMedDate not supplied

Anticonvulsants during pregnancy and lactation. Transplacental, maternal and neonatal pharmacokinetics.

Few data are available on placental transfer of anticonvulsants during early pregnancy. Nevertheless, it has been demonstrated that at this early stage of gestation, considerable amounts of phenytoin, primidone/phenobarbitone and carbamazepine as well as some of their metabolites are already present in fetal tissues. Potentially reactive metabolites of anticonvulsants can be formed by the fetal liver and accumulate in some organs. At term, most anticonvulsants are present in neonatal plasma in concentrations similar to those in maternal plasma. Valproic acid, on the other hand, can accumulate in fetal blood, for still unknown reasons. Elimination by the neonate is variable and is dependent on several factors, such as clinical state, pre- or perinatal enzyme induction, absorption of the drugs and their plasma protein binding. Neonatal acquisition of anticonvulsants via breast-feeding does not seem to be harmful for the neonate. In the case of phenobarbitone, however, the drug may accumulate in nursing neonates to levels approaching or even exceeding those of their mothers. Significant drug levels can also build up in neonates and infants nursed by carbamazepine- and ethosuximide-treated mothers. This review contains relevant pharmacokinetic data on anticonvulsant drugs widely used during pregnancy and the neonatal period. The differences between pregnant and non-pregnant adults as well as between neonates and older age groups are emphasized. Some pharmacokinetic data are correlated with clinical manifestations, such as seizure frequency, neonatal depression and withdrawal symptoms.

Anticonvulsants↗

PubMedDate not supplied

Effect of tolbutamide on blood glucose, plasma free fatty acids and insulin in normal and obese children.

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Adolescent↗