Gamma-carboxyglutamic acid in urine of newborn infants.

Gamma-Carboxyglutamic acid (GLA) was measured in the urines obtained from 11 full-term infants, 48 pre-term infants appropriate for gestational age (AGA), and 25 small-for-gestational age (SGA) infants. Separation was performed by high resolution anion exchange chromatography. The results were similar in both AGA and SGA infants. During the first 3 days of life, urinary GLA mean (and range) was 1.66 (0.34-4.60) in the low birth weight infants versus 0.88 (0.26-1.38) in the full-term infants and 0.76 (0.62-1.15) mumol . kg-1 X 24 h-1 in the control adults. In the low birth weight infants, urinary GLA fell from 2.79 (0.61-5.75) at age 1-3 days, to 1.55 (0.26-4.04) mumol/24 h at day 8 (p less than 0.01); it then rose again slowly to 2.12 (0.65-3.93) mumol/24 h at day 45. In these infants there was no correlation between urinary GLA excretion and birth weight or gestational age, or urinary hydroxyproline or serum alkaline phosphatase. Despite the well-known reduced blood levels of vitamin K dependent coagulation factors in neonates, these results show that urinary GLA excretion is at least similar to the excretion in adults. These data suggest that these neonates can carboxylate glutamic acid and that the newborn infant has a high bone turnover.

[Study of the pathogenic mechanism of hypocalcemia in primary hypomagnesemia. Demonstration of a blockage of the mechanism of release of parathyroid hormone]. / Etude du mecanisme pathogenique de l'hypomagnesemie primitive. Mise en evidence d'un blocage du mecanisme d'excretion de la parathormone

Parathyroid function and peripheral responsiveness to parathyroid hormone were studied during magnesium dependent hypocalcemia in a 5 years old boy with primary hypomagnesemia. The bone system and the kidneys were responsive to exogenous bovine parathyroid extracts as demonstrated by the normalisation of the calcemia and the increase of urinary cyclic AMP, phosphorus and hydroxyproline. Low levels of serum immunoreactive parathyroid hormone gave also clear indication of impaired parathyroid function. By contrast intravenous injection of magnesium sulfate induced an instantaneous and very sharp increase of serum immunoreactive parathyroid hormone as shown by levels well above the normal range one minute after the injection ; this was followed by a regular decrease of hormonal levels reaching the normal range one hour later. This finding clearly demonstrates that severe magnesium depletion induces impaired parathyroid hormone release in man.