For five days, three groups of six premature infants each were fed human milk and given a daily dosage of one of the following: vitamin D3 (30 μg), 25-OH D3 (10 μg) and 1, 25-OH D3 (0.5 μg). The infants in the groups were matched for gestational age and birthweight. Administration of 25-OH D3 or 1, 25-(OH) 2 D3 did not significantly modify the course of early neonatal hypocalcemia as compared with infants receiving vitamin D3. Mean plasma Ca±SD (mg/100 ml) decreased to nadir values at 48 hr (D3: 5.7±1.2; 25 OH D3: 6.8±0.9; 1, 25-(OH) 2 D3: 6.7±1.1). A progressive increase toward normal values was seen at 120 and 168 hr in the three groups. Mean plasma immunoreactive parathyroid hormone±SD (μ Eq/ml) followed an opposite pattern with peak values at 48 hr (D3: 231±137; 25-OH D3: 281±138; 1, 25-(OH) 2 D3: 211±149). Mean plasma±SD 25-OH D values (ng/ml) were low at 1.2 hr (8.7±4.8) n: 16) and increased significantly after 7 days of D3 (18.2±4.2 P< 0.001) and 25-OH D3 administration (46±10.3 P< 0.001)/Mean plasma iCT±SD (pg/ml) reached peak values at 24 hr (D3: 457±186; 25-OH D3: 415±121; 1, 25-(OH) 2 D3: 443±183). These data suggest that the various forms of vitamin D are well absorbed in preterm infants and that administration of vitamin D metabolites during the first days of life is not warranted for the prophylaxis of early neonatal hypocalcemia.

Speculation: A defect in vitamin D metabolism is considered to be a possible pathogenetic factor in early hypocalcemia in premature infants. Since our data indicate adequate intestinal absorption and liver hydroxylation of vitamin D3 with no obvious effect on the D metabolites, it is speculated that the biotransformation pathway of vitamin D3 is operative in preterm infants after 32 wk of gestation.