Search

Serum copper (Cu) and zinc (Zn) concentrations were measured in neonates with an appropriate birth weight for gestational age (AGA) and in small-for-gestational age infants. At 7 days of age, there was a positive correlation between serum Cu concentration and gestational age (GA) (r = 0.63; P < 0.001) and a negative correlation between Zn concentration and GA (r = 0.62; P < 0.01). At 7 days of age, the mean (± S.E.) concentrations in AGA full-term infants (Cu, 79 ± 8/μg/dl; Zn, 84 ± 4) were similar to those in small-for-gestational age. full-term infants (Cu, 78 ± 6 μg/dl; Zn, 85 ± 12). In preterm infants, there was also no difference between AGA and small-for-gestational age infants. In 23 AGA infants with a birth weight of less than 1500 g, serum Cu concentration increased from 51 ± 7μg/dl at the age of 7 days to 86 ± 7μg/dl at the age of 60 days (paired t-test: P < 0.05) whereas serum Zn concentration decreased from 149 ± 9 to 91 ± 5μg/dl (P < 0.01). A positive correlation was found between serum Zn concentration and daily intake of Zn (n = 39; r = 0.3458; P < 0.05), but no correlation was found for serum Cu concentration. The evolution of serum Cu and Zn concentration with total age (GA + postnatal age) in the infants with a low birth weight (i.e., < 1500 g) was similar to the evolution with GA.

Summary: Serum copper (Cu) and zinc (Zn) concentrations were measured in neonates with an appropriate birth weight for gestational age (AGA) and in small-for-gestational age infants. At 7 days of age, there was a positive correlation between serum Cu concentration and gestational age (GA) (r = 0.63; P < 0.001) and a negative correlation between Zn concentration and GA (r = 0.62; P < 0.01). At 7 days of age, the mean (± S.E.) concentrations in AGA full-term infants (Cu, 79 ± 8/µg/dl; Zn, 84 ± 4) were similar to those in small-for-gestational age. full-term infants (Cu, 78 ± 6 µg/dl; Zn, 85 ± 12). In preterm infants, there was also no difference between AGA and small-for-gestational age infants. In 23 AGA infants with a birth weight of less than 1500 g, serum Cu concentration increased from 51 ± 7µg/dl at the age of 7 days to 86 ± 7µg/dl at the age of 60 days (paired t-test: P < 0.05) whereas serum Zn concentration decreased from 149 ± 9 to 91 ± 5µg/dl (P < 0.01). A positive correlation was found between serum Zn concentration and daily intake of Zn (n = 39; r = 0.3458; P < 0.05), but no correlation was found for serum Cu concentration. The evolution of serum Cu and Zn concentration with total age (GA + postnatal age) in the infants with a low birth weight (i.e., < 1500 g) was similar to the evolution with GA.Speculation: In very-low-birth-weight infants, serum levels of Cu are influenced by the maturation whereas serum Zn concentrations depends also upon the dietary intake of Zn.

Extract: Five patients with Bartter's syndrome were investigated. Sodium restriction (<10 mEq/day for at least 5 days) showed a renal sodium wastage in only two patients (I and II) in spite of increased aldosterone secretion rate (from 151–427 to 680–842 µg/day). The effect of angiotensin II (A II) 80 ng/kg/min for 30–180 min, on plasma renin activity (PRA), plasma aldosterone, and urinary sodium excretion was compared with the effect of a previous infusion of 5% dextrose given at the same rate, 0.5 ml/min for 1 hr. A II infusion resulted in increased plasma aldosterone levels: from 236–330 pg/ml to 800–881 pg/ml in 30 min. This increase was also observed in patient II (from 139 to 600 pg/ml). PRA was decreased by A II infusion (from 1,142–2,462 to 121–1,625 ng/liter/min). In patient IV, this decrease in PRA was also observed when he was on a salt-restricted diet (from 1,934 to 370 ng/liter/min); but the minimal PRA was still higher (370 ng/liter/min) than with a normal diet (121 ng/liter/min). In no case could normal PRA level be obtained. A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80–90 to 265–230 µEq/min in 30 min). Urinary sodium excretion decreased in the other patients from (37.5–213 to 4.30–46 µEq/min) and fractional sodium excretion was reduced in patient V (from 0.56% to 0.45% at 30 min and to 0.29% at 120 min). No significant change with A II infusion was observed in patient IV when he was on a sodium-restricted diet (from 1 to 2.5 µEq/min in 30 min). Urinary potassium excretion was similar to sodium excretion. No change was observed in plasma potassium and sodium.Speculation: Hypersecretion of renin is not autonomous in Bartter's syndrome. It is not explained by an insensitive feedback effect of A II on renin secretion. Hypokalemia contributes to this high level of PRA. Salt craving, which is found in 50% of the cases (ZS), is increased by A II. Nevertheless, the presence of renal sodium wastage cannot be explained only by the high A II levels which are constant in this syndrome. A deficient Na-K-ATPase activity is postulated in such cases.

Since hypoglycemic neonates do not exhibit compensative ketosis, we investigated the possible involvement of carnitine deficiency or Ω-oxidation in neonatal hypoglycemia. In a first group of 49 neonates, serum free fatty acid, acetoacetate and β-hydroxybutyrate concentrations were similar in hypoglycemic and normoglycemic neonates. Serum free carnitine concentrations did not show any difference in the hypoglycemic small-for-date infants (median 40 μmol/l, range 16–92 μmol/l) compared to the normoglycemic small-for-date infants (median 30 μmol/l, range 8–64 μmol/l). In a second group of 45 neonates, urinary excretion of dicarboxylic acids (adipic, suberic, sebaric and succinic acids) was similar in hypoglycemic infants compared to normoglycemic neonates. Despite the limitations of interpretaion of free carnitine determination, these data do not suggest an impaired β-oxidation by carnitine depletion or an enzymatic defect in hypoglycemic neonates.

Plasma glucose, blood urea nitrogen, and ammonia were measured simultaneously in 44 newborns a few hours after birth. When the concentration of plasma glucose was below 30 mg/dl, plasma ammonia concentration was significantly higher (129 ± 67 μmol/l) than in normoglycemic infants (74 ± 33 μmol/l; p < 0.01). Blood urea nitrogen was slightly lower in hypoglycemic infants (3.65 ± 0.7 mmol/l) than in the control group (4.5 ± 1 mmol/l) but the difference was not significant. These data show that hyperammonemia can be associated to hypoglycemia in low birth weight infants. Therefore, further investigations are required to determine the link between urea and glucose production rates in hypoglycemic newborns and whether hyperammonemia participates in the deleterious effects of hypoglycemia on the neonatal brain.

Neonatal hypoglycemia is particularly dangerous for the brain when it is symptomatic or/and recurrent. In order to avoid symptomatic hypoglycemia a compensatory production of ketone bodies is required since they are actively taken up by the neonatal brain. Recurrent hypoglycemia can be avoided by stimulation of neonatal gluconeogenesis which is limited by glucose infusion and/or insulin secretion. Lipid administration induces a hyperglycemic response which is explained by a stimulation of gluconeogenesis. It also results in ketogenesis which provides the compensatory factors of hypoglycemia and which seems to be linked to gluconeogenesis. We therefore suggest that the best way to prevent neonatal hypoglycemia is achieved by supplementing the neonate with lipids and especially medium chain triglycerides.