Changes in hepatic vitamin K1 levels after prophylactic administration to the newborn.

We undertook a study of hepatic concentrations of vitamin K (vitamin K1 or phylloquinone, vitamin K1-epoxide, and menaquinones) in 18 infants, ages 1-8 days, with or without vitamin K1 supplementation. The infants who had no supplementation had a total hepatic storage ranging between 0.1 and 0.9 micrograms. Also, hepatic storage of phylloquinone was poor (< 1 microgram) when compared with daily requirements. Moreover, we did not detect any menaquinone in the livers of these infants in our study. The prophylaxis applied to the other infants was very efficient. Hepatic vitamin K1 concentrations, obtained < 24 h after administration, were very high (62.8-93.5 micrograms/g). Vitamin K1-epoxide concentrations were high, which proved the efficiency of the vitamin K cycle. In contrast, the decrease in vitamin K1 concentrations was also very rapid, since the median value after 48 h was 8.4 micrograms/g and only 2.9 micrograms/g 5 days after administration. However, hepatic total storage after 5 days in one infant with vitamin K1 supplementation was much higher (112 micrograms) than in infants who had not received supplementation. In conclusion, hepatic phylloquinone storage at birth was poor (< 1 microgram). The newborn infant might be in a situation of potential deficiency. After prophylactic oral administration of phylloquinone, uptake by the liver was quite satisfactory, but concentrations dropped quickly. However, phylloquinone hepatic storage remained elevated (112 micrograms) after 5 days.

Neonatal hypercalcemia in preterm infants fed with human milk.

Hypercalcemia (serum Ca greater than or equal to 2.83 mmol/l) was detected in 10 premature infants (gestational age: 31-37 weeks and birthweight: 1100-1950 g). All were fed with pooled human breast milk. Urinary Ca excretion was high (greater than 0.200 mmol/kg/24 h) in all but one infant while serum phosphorus (P) concentration and urinary P excretion were low. Serum immunoreactive parathyroid hormone and plasma 25-hydroxyvitamin-D concentrations were normal. A significant positive correlation was found between serum Ca concentration and urinary Ca excretion, and a negative correlation between serum Ca concentration and serum P concentration or urinary P excretion. Hypercalcemia disappeared spontaneously in two patients, was corrected by a humanized milk in three patients and by P supplementation in five patients. These data suggest that neonatal hypercalcemia is related to P depletion induced by human breast milk in premature infants.

[Plasma 25-OH D deficiency in Maghrebian children more than 10 years of age immigrated to France]. / Déficit plasmatique en 25 OH D chez les enfants maghrébins de plus de 10 ans immigrés en France.

From 1984 Feb 1st to April 30, 63 blood samples were collected from children more than 10 years old in the pediatric unit of CHR de St-Etienne, and analysed for 25 OH D, calcium, phosphate, magnesium and alkaline phosphatase serum concentrations. Mean 25 OH D is lower (22,6 nmol/1) in 26 migrant children (24 from Maghreb and 2 from Turkey) than in 37 European children (mean = 48,6 nmol/1; p less than 0,001). Serum concentration is under 10 nmol/1 in 3 of the 37 Europeans (8%), versus 13 of the 26 Maghrebians (50%). Mean alkaline phosphatase and phosphate are significantly higher in the 36 boys than in the 27 girls. A significative positive correlation is found between alkaline phosphatase and phosphate (r = 0,535; p less than 0,01). There is no relation between age, month of assessment, sex, height, weight, place of late holidays and any of the measured serum values.

Late evolution of serum immunoreactive parathyroid hormones, calcitonin and plasma 25-hydroxy cholecalciferol concentrations in very low birthweight infants.

The plasma concentrations of 25-hydroxycholecalciferol (25-OH-CC), immunoreactive parathyroid hormone (iPTH) and calcitonin (iCT) were measured at the age of 30 and 66 days in thirteen preterm neonates (birthweight: 970 to 1300 g). At the age of 30 days when all infants were fed only with breast milk (BM) serum iCT and iPTH levels were normal. During the second month 7 infants were fed with BM only (control group) and 6 infants were supplemented with formula (supplemented group). At the age of 66 days, mean +/- S.D. serum iPTH concentration was higher in the supplemented group than in the control group: 169 +/- 79 vs. 60 +/- 33 microliterEq/ml (p less than 0.01). Serum iCT levels remained undetectable (less than 150 pg/ml) in both groups. Plasma 25-OH-CC concentrations were normal and similar in both groups. Serum iPTH concentrations were positively correlated with phosphorus intake and negatively correlated with calcium intake from BM only. The results suggest that secondary hyperparathyroidism can be detected in very low birthweight infants supplemented with a formula, probably because of a phosphorus load or decreased intestinal absorption of calcium.

Congenital hyperparathyroidism and vitamin D deficiency secondary to maternal hypoparathyroidism.

A new case of congenital hyperparathyroidism secondary to maternal hypoparathyroidism is described. Neonatal roentgenograms of the skeleton showed severe bone demineralisation and the distal metaphyses of the long bones were spread, frayed and cupped. Elevated levels of serum immunoreactive parathormone (iPTH) were found at the age of 41 days=270 mulEq/ml (Normal: less than 50 mulEq/ml). A very low plasma 25-OH-D concentration (less than 4 ng/ml) was found at the same time in spite of previous administration of 600 units of vitamin D every day for 18 days and in spite of healing of the bone lesions. At the age of 3 months, 15 mg of vitamin D was given orally: iPTH levels which remained high 3 weeks before (210 mulEq/ml) were found to be normal one week after this vitamin D load (37 mulEq/ml). It is suggested that in congenital hyperparathyroidism secondary to maternal hypoparathyroidism, hyperparathyroidism increases the infants needs for vitamin D. This could result in a state of vitamin D deficiency which in turn would maintain the parathyroid hyperactivity.