Stimulation of sucking and swallowing to promote oral feeding in premature infants.

AIM: To study the effect of stimulation of sucking and swallowing on weaning from nasogastric (NG) feeding and length of hospital stay in premature infants. METHOD: Randomized controlled trial with blinded evaluation. Premature infants on NG feeds and post-menstrual age (PMA) less than 36 weeks who had poor ability to suck were randomized to receive one daily session of stimulation according to Vojta or no intervention other than standard nursing care. RESULTS: Of 36 infants, 18 received stimulation and 18 were observed without intervention. Mean gestational age at birth was 32.2 weeks (SD 2.4) versus 31.4 (2.3) weeks, p = 0.27, and PMA at study entry 35.1 weeks (0.8) versus 34.4 (0.9) weeks, p = 0.01, respectively. NG feeding was discontinued at 36.8 weeks (0.9) versus 36.3 (0.9) weeks' PMA, p = 0.25, and they were discharged at 37.8 weeks (0.9) versus 37.7 (1.3) weeks, p = 0.81. CONCLUSION: The stimulation programme did not result in earlier weaning from NG feeding or earlier discharge. However, such studies may need to be large to limit the possibility of type II errors.

Therapeutic electrical stimulation in cerebral palsy: a randomized, controlled, crossover trial.

The aim of this study was to evaluate the effect of therapeutic electrical stimulation (TES) applied to antagonists of spastic leg muscles on gross motor function in children with spastic diplegic cerebral palsy. Twelve children between 5 and 12 years of age completed a 24-month crossover study in which six were randomly assigned to receive TES for the first 12 months and the remaining six for the last 12 months. Physiotherapy and a home training program were not altered. All were evaluated blindly in terms of tests of motor function and video recordings at the start and at 12 and 24 months. At the end of the study parents/carers gave a subjective assessment of the effect of TES. No significant effect of TES on motor or ambulatory function was found on the blinded evaluation, but parents of 11 of the 12 children stated that TES had a significant effect. We conclude that it is unlikely that TES has a significant effect on motor and ambulatory function in spastic diplegia.

Randomised controlled trial of infantile colic treated with chiropractic spinal manipulation.

AIMS: To investigate the efficacy of chiropractic spinal manipulation in the management of infantile colic. METHODS: One hundred infants with typical colicky pain were recruited to a randomised, blinded, placebo controlled clinical trial. RESULTS: Nine infants were excluded because inclusion criteria were not met, and five dropped out, leaving 86 who completed the study. There was no significant effect of chiropractic spinal manipulation. Thirty two of 46 infants in the treatment group (69.9%), and 24 of 40 in the control group (60.0%), showed some degree of improvement. CONCLUSION: Chiropractic spinal manipulation is no more effective than placebo in the treatment of infantile colic. This study emphasises the need for placebo controlled and blinded studies when investigating alternative methods to treat unpredictable conditions such as infantile colic.

[Intestinal invagination in children in the county of Hordaland 1983-92]. / Tarminvaginasjon hjå barn i Hordaland fylke 1983-92.

The incidence of intussusception was examined with respect to whether children lived in the city of Bergen, where pediatricians were the primary contacts in 45% of the cases, or in the remaining municipalities where pediatricians were the primary contacts in 18%. Diagnosis and course of illness were compared for children admitted by pediatricians and general practitioners. Information was retrieved from hospital medical records. During 1983-92, 142 children 0 to 14 years were given the diagnosis on basis of barium enema (139 children) or surgery (three children). The incidence was 1.8 per 1,000 children per year for Bergen vs. 1.4 in the rest of the county (p = 0.3). Children admitted by pediatricians more often had the correct referral diagnosis (70% vs. 42%, p = 0.003), but they did not differ with respect to median age (8 months for both), median duration of symptoms (12 vs. 24 hours), percent in need of surgery (58% vs. 59%) or in symptoms. The lack of difference in incidence between Bergen and the more distant municipalities suggests that spontanous resolution of intussusception is uncommon. Although pediatricians more often admitted the children with the correct diagnosis, duration of symptoms and outcome did not differ from those admitted by general practitioners. This suggests that the general practitioners also appreciated the urgency of the symptoms.

Nephrocalcinosis, hypercalciuria and elevated serum levels of 1,25-dihydroxyvitamin D in children. Possible link to vitamin D toxicity.

Ten children age 1 1/2 to 14 years, had bilateral nephrocalcinosis and hypercalciuria, but normal serum calcium (Ca) and phosphate (P) concentrations. Patients with hypercalciuria were divided into absorptive (n = 4) and renal (n = 6) subgroups, and in the latter four patients had a primary Ca-leak and two had a P-leak. All the children had received intermittent high dose vitamin D prophylaxis during infancy. At the time of investigation all had normal serum levels of 25-hydroxyvitamin D, yet all but one had elevated values of 1,25-(OH)2D. Although the hypercalciuria was indistinguishable from the various known forms of idiopathic hypercalciuria, the previous clinical course and the pattern of bone mineral homeostasis suggest that both clinical features, namely nephrocalcinosis and hypercalciuria were related to vitamin D toxicity through various pathogenetic pathways.

Intermittent high-dose vitamin D prophylaxis during infancy: effect on vitamin D metabolites, calcium, and phosphorus.

In infants receiving intermittent high dose vitamin D prophylaxis (600,000 IU ergocalciferol per dose orally) every 3-5 mo, the serum concentrations of vitamin D metabolites, calcium (Ca), and phosphorus (P) were determined before and 2 wk after each dose. The 25-hydroxyvitamin D (OHD) concentrations increased to well above normal but the values returned to the normal range before each subsequent dose. The 24,25- and 25,26-dihydroxyvitamin D ([OH]2D) levels followed a pattern similar to that of 25-OHD, and both were closely related to the latter (r = 0.85, p less than 0.005, and r = 0.84, p less than 0.005, respectively). The 1,25-(OH)2D concentrations did not vary in a consistent pattern and remained largely within the normal range. All infants had normal Ca levels before the first dose but 14 infants (34%) later had one or both Ca values above the upper normal limit of 2.80 mmol/L (2.81-3.32 mmol/L), indicating that the vitamin D doses were excessive despite the lack of accumulative increases in serum vitamin D concentrations.

Serum concentrations of vitamin D metabolites in vitamin D supplemented pregnant women. A longitudinal study.

The serum concentrations of the vitamin D metabolites 25-OHD, 1,25-(OH)2D, 24,25-(OH)2D and 25,26-(OH)2D, and of vitamin D binding protein (DBP), were determined longitudinally in 22 vitamin D supplemented pregnant women, and in 17 age-matched non-pregnant women studied during the summer. The pregnant women had higher 25-OHD and 1,25-(OH)2D, similar 24,25-(OH)2D, and lower 25,26-(OH)2D concentrations than the non-pregnant group. The relative concentrations of 24,25-(OH)2D and 25,26-(OH)2D (expressed as the molar ratio of these metabolites to 25-OHD) were lower during pregnancy. The DBP levels were increased in pregnancy, but the calculated free fraction (i.e. not bound to DBP) of the hormonal form of vitamin D, 1,25-(OH)2D, was still persistently higher in the pregnant than in the non-pregnant women. The study suggests that a daily vitamin D supplement of 400 IU satisfies the vitamin D requirement of pregnant women living in a cool climate with limited sun exposure. The increased absolute and relative concentration of 1,25-(OH)2D and decreased relative levels of 24,25-(OH)2D and 25,26-(OH)2D further suggest that the increased intestinal calcium and phosphate absorption, which is known to occur during pregnancy, is at least partially mediated by the vitamin D endocrine system.

Vitamin D deficiency rickets and vitamin B12 deficiency in vegetarian children.

During the years 1978-83 four vegetarian children have been admitted to the pediatric departments of Ullevaal and Aker Hospitals in Oslo and Haukeland Hospital, Bergen, with the diagnosis of vitamin D deficiency rickets. One had vitamin B12 deficiency as well. All had been fed a vegetarian diet with some cows' milk, but without vitamin supplementation. All had marked hypocalcemia, and three had tetany or convulsions. All responded well to conventional doses of vitamin D therapy. Two of the mothers had vitamin D deficiency, and one of them also had vitamin B12 deficiency. This report describes the case histories of these children, and also discusses predisposing factors of vegetarian diets for the development of nutritional rickets.

25-Hydroxyvitamin D and 1,25-dihydroxyvitamin D of D2 and D3 origin in maternal and umbilical cord serum after vitamin D2 supplementation in human pregnancy.

Serum concentrations of 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] of vitamin D2 and D3 origin were determined separately in 10 women before vitamin intake in early pregnancy, and repeated in maternal and cord serum obtained at delivery after 20 to 30 wk of vitamin D2 supplementation in a dose of 400 IU/day. Before supplementation 25-OHD2 and 1,25-(OH)D2D2 were present in just traceable or nondetectable concentrations, but the levels increased in all to a mean +/- 1 SD of 7.3 +/- 3.7 ng/ml and 37.2 +/- 18.1 pg/ml, respectively (p less than 0.0025), by the time of delivery. At delivery the total 25-OHD and 1,25-(OH)2D levels were always lower in the cord than in the maternal serum (30.7 +/- 14.2 versus 20.1 +/- 9.1 ng/ml, and 90.1 +/- 31.2 versus 37.3 +/- 11.6 pg/ml, p less than 0.0025). The paired concentrations of 25-OHD were closely related (r = 0.89, p less than 0.0005), while the association for 1,25-(OH)2D was not statistically significant (r = 0.53, p less than .01). The 25-OHD of D2 and D3 origin accounted for a similar proportion of the total 25-OHD in the maternal and cord serum (ratio of 25-OHD2 to 25-OHD3: 0.40 +/- 0.28 versus 0.45 +/- 0.29, p = NS), as did the respective 1,25-(OH)2D metabolites [ratio of 1,25-(OH)2D2 to 1,25-(OH)2D3: 0.73 +/- 0.35 versus 0.90 +/- 0.50, p = NS].(ABSTRACT TRUNCATED AT 250 WORDS)

Anticonvulsant drug therapy in human pregnancy: effects on serum concentrations of vitamin D metabolites in maternal and cord blood.

Serum concentrations of the main vitamin D metabolites and of calcium, phosphate, and alkaline phosphatase were determined in each of the three trimesters of pregnancy and in simultaneously obtained maternal and cord blood at delivery in 22 epileptic women treated with diphenylhydantoin or carbamazepine alone or with a combination with one other drug. The results were compared with similarly obtained data from 22 normal pregnancies. Women in both groups received supplements of 400 IU vitamin D3 per day. All the women had 25-hydroxyvitamin D levels within the normal range for healthy adults (greater than 12 ng/ml) throughout pregnancy. The epileptic women had, however, significantly (p less than 0.05) lower median 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels and higher median 25,26-dihydroxyvitamin D values than the reference group. The 24,25-dihydroxyvitamin D concentrations did not differ significantly, but the median ratio of 24,25-dihydroxyvitamin D to 25-hydroxyvitamin D was higher in the epileptic women at the end of pregnancy (p = 0.05). The respective differences in cord serum concentrations reflected those of the mothers at delivery. Serum calcium tended to be lower during epileptic pregnancy, but none were hypocalcemic. The alkaline phosphatase and phosphate values did not consistently differ from those of the reference women. The median alkaline phosphatase level of cord serum was slightly higher in the epileptic group, but the calcium and phosphate levels were similar to the reference values. The various biochemical parameters of the carbamazepine-treated women tended to be intermediate between those of the healthy and diphenylhydantoin-treated groups. Antiepileptic drug therapy appears to affect vitamin D metabolism and calcium homeostasis during pregnancy. The derangements may not be of major clinical significance, however, in vitamin D-supplemented and normally functioning women on long-term low-dose therapy.

Plasma concentrations of vitamin D metabolites in premature infants.

The plasma concentrations of 25-hydroxyvitamin D (OHD), 1,25-(OH)2D and 24,25-(OH)2D were determined in 28 healthy premature infants (median gestational age 33, range 28-36 wk; and median birth weight 1880, range 900-2350 g) during the first 5-10 wk of life, and in a reference group of 17 young adults. The infants received a vitamin D supplement of 500 IU/d and a diet low in calcium (Ca) and phosphorus (P) compared with that of corresponding intrauterine accretion rates. The median 25-OHD concentration increased from 11 (range 6-30) ng/ml at 1 d to 27 (range, 15-41) ng/ml by 5-10 wk of age (P less than 0.01). 1,25-(OH)2D concentrations at age 1 d were similar to the adult levels (median 37, range 8-64 versus 35, range 18-58 pg/ml), but increased significantly within 1 wk to 48 (26-156) pg/ml (P = 0.01), and between 1 and 3-4 wk of age to 104 (58-203) pg/ml (P less than 0.01). The levels at 5-10 wk were similar to the 3-4 wk value. 24,25-(OH)2D concentrations were persistently low compared with the adult levels (medians 0.4-0.5, range less than 0.3-2.1 versus 1.7, range 0.4-2.0 ng/ml, P less than 0.01). The relative concentrations, expressed as the ratio of 24,25-(OH)2D to 25-OHD, were comparable to those of the adults at birth, but decreased significantly within 2 wk. The data demonstrate that healthy premature infants can produce high plasma levels of 1,25-(OH)2D.

Plasma concentrations of vitamin D metabolites before and during treatment of vitamin D deficiency rickets in children.

Plasma concentrations of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D), and 24,25-dihydroxyvitamin D (24,25-(OH)2D) were determined in 17 children with vitamin D deficiency rickets before therapy was started. Thirteen of them also had these tests repeated during treatment. The median 25-OHD concentration was at the lower limit of the reference range before, but increased distinctly within one week of treatment with 1 700-4 000 IU vitamin D per day (17 vs. 37 nmol/l, p less than 0.01). 24,25-(OH)2D was undetectable in twelve of the patients before therapy. Detectable concentrations were in the range of 1.7 to 3.5% of the corresponding 25-OHD levels throughout the study, and the two metabolites were closely correlated (r = 0.84, p less than 0.0005). The median 1,25-(OH)2D concentration was near the average of the reference range before, but increased to well above the upper limit of normal within one week of treatment (121 vs. 368 pmol/l, p less than 0.01). The levels were largely normal after 10 weeks of therapy, as were the plasma concentrations of calcium, phosphate, and alkaline phosphatase. Parathyroid activity, as judged by serum parathyroid hormone or urinary cyclic AMP concentrations, was stimulated in 11 of 12 children studied prior to treatment. It is concluded that there may be no clear-cut differences between normal nad rachitic values of the different vitamin D metabolites under practical clinical conditions. A low 25-OHD level combined with evidence of a stimulated parathyroid activity, and a rise of 1,25-(OH)2D levels to supernormal values following a few days of vitamin D therapy may be diagnostic clues.

Serum concentrations of vitamin D metabolites in exclusively breast-fed infants at 70 degrees north.

The effect of prolonged breast-feeding on the serum concentrations of vitamin D metabolites, calcium, phosphate, and alkaline phosphatase was studied longitudinally in 7 infants from Northern Norway. They were exclusively breast-fed for a median of 7 1/2 months. Three of the mothers were supplemented with vitamin D throughout lactation. All but one of the infants had 25-hydroxyvitamin D (25-OHD) levels in the rachitic range (less than 20 nmol/l) on at least one occasion. Vitamin D supplementation of the mother had no apparent effect on the infants' 25-OHD levels, but the values increased during summer. The infant who had the lowest 25-OHD levels also had decreased 1,25-dihydroxyvitamin D (1,25-(OH)2D) concentrations, while the others maintained 1,25-(OH)2D levels within normal limits. 24,25-(OH)2D concentrations were undetectable when the 25-OHD levels were below 35 nmol/l, but the two metabolites were closely correlated for higher values of 25-OHD. Low 25-OHD levels were associated with decreased phosphate concentrations at 6 months. The calcium levels were normal throughout the study period of one year, as were all but two of the alkaline phosphatase values. Although none of the infants had clinical or biochemical evidence of rickets, the results suggest that the vitamin D supply from human milk is inadequate, and that routine vitamin D supplementation is advisable for breast-fed infants who are deprived of sunlight exposure.

Serum concentrations of vitamin D metabolites in maternal and umbilical cord blood of Libyan and Norwegian women.

The serum concentrations of the vitamin D metabolites 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D) and 24,25-dihydroxyvitamin D (24,25-(OH)2D), and vitamin D binding protein, calcium, phosphate and alkaline phosphatase were determined in 19 grand multiparous Libyan women at delivery, and in the umbilical cord blood of 14 of their babies. The results were compared with similarly collected data from 22 vitamin D-supplemented Norwegian mother-infant pairs. The median 25-OHD and 24,25-(OH)2D concentrations were significantly lower for the Libyan group (maternal 25-OHD: 34 vs 112 nmol/l; cord 25-OHD: 20 vs 76 nmol/l; maternal 24,25-(OH)2D: 0.6 vs 4.1 nmol/l; cord 24,25-(OH)2D: 0.4 vs 2.7 nmol/l, P less than 0.001 for all differences). In both groups the 25-OHD and 24,25-(OH)2D levels in maternal as well as in cord blood were closely associated (P less than 0.001). The median 1,25-(OH)2D level was similar for the two maternal groups (198 vs 194 pmol/l), but slightly lower for the Libyan than for the Norwegian cord samples (80 vs 93 pmol/l, P = 0.04). A calculated free 1,25-(OH)2D concentration (not bound to vitamin D binding protein) did not differ between the two maternal or cord groups. Calcium and phosphate concentrations were similar for the respective maternal and cord samples, while the median alkaline phosphatase level of cord blood was slightly higher for the Libyan group (P = 0.04). The results suggest that calcium and phosphate homoeostasis of pregnant women and their fetuses can be maintained despite wide variations in vitamin D supply and numerous repeated pregnancies.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma concentrations of vitamin D metabolites in unsupplemented breast-fed infants.

Plasma concentrations of the vitamin D metabolites 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D and 25,26-dihydroxyvitamin D were determined in 12 solely breast-fed infants 4 days and 6 weeks after birth. They were not exposed to sunlight, but the mothers received an average of 600 IU vitamin D2 per day during the study period. The mothers' 25-hydroxyvitamin D levels did not change significantly (medians 42 and 58 nmol/l), but the median level dropped from 26 to 15 nmol/l in the infants (P less than 0.001). There was a close correlation between maternal and infant levels at 4 days (r = 0.95). The babies with the highest initial levels showed the most marked decrease by 6 weeks. The median concentrations of 24,25-dihydroxyvitamin D and 25,26-dihydroxyvitamin D decreased similarly from 1.7 to 0.8 and 0.63 to 0.35 nmol/l respectively, (P less than 0.001). The 1,25-dihydroxyvitamin D levels were within normal limits as were plasma calcium, phosphorus, and alkaline phosphatase. The data suggest that fetal stores of vitamin D may be rapidly depleted, and that breast milk may be inadequate as the only source of vitamin D, even for breast-fed infants of vitamin D-supplemented mothers.

Effect of season and vitamin D supplementation on plasma concentrations of 25-hydroxyvitamin D in Norwegian infants.

Plasma concentrations of 25-hydroxyvitamin D (25OHD) were determined in 81 vitamin D supplemented or unsupplemented infants at the end of winter. The values were compared with maternal levels and with concentrations found in 22 unsupplemented infants at the end of summer. The 25OHD levels of the neonates were lower, but closely related to maternal values (r = 0.95, p less than 0.0005). Unsupplemented breast-fed infants had lower 25OHD levels at 6 weeks than at 4 days (16 +/- 7 vs. 32 +/- 15 nmol/l, mean +/- 1 SD, p less than 0.0005). The mean 25OHD level of vitamin D supplemented 6-12 months old infants was intermediate between those of the unsupplemented nursed groups and the unsupplemented children studied during summer (53 +/- 28 vs. 85 +/- 28 nmol/l, p less than 0.0005). Six weeks old infants who had received a milk formula containing 400 IU vitamin D3 per liter had levels similar to the latter group (92 +/- 21 nmol/l). The data suggest that the vitamin D stores acquired during fetal life, or from ultraviolet light exposure during the summer, may be inadequate to maintain safe levels of 25OHD throughout the winter, but that a daily supplement of 400 IU is adequate to establish concentrations in the summer range.

Plasma concentrations of 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D, and 25,26-dihydroxyvitamin D in the first year of life.

Plasma concentrations of 1,25-dihydroxyvitamin D [1,25-(OH)2D], 24,25-dihydroxyvitamin D [24,25-(OH)2D], and 25,26-dihydroxyvitamin D [25,26-(OH)2D] were determined in 80 healthy infants of 4 days, 6 weeks, 6 months, and 12 months of age. The 4-day-old babies received breast milk, while the 6-week-old infants were either exclusively breast or formula fed. The older infants were on mixed diets and received daily vitamin D supplements. The levels were analyzed with regard to age and the concentrations of 25-hydroxyvitamin D (25OHD), calcium, phosphate, magnesium, and alkaline phosphatase and were compared with adult levels of vitamin D metabolites. The median 1,25-(OH)2D concentration was highest at 4 days of age and lowest at 6 weeks, but, except for the 6-week-old group, all had higher levels than the adults (6 weeks, P less than 0.1; others, P less than 0.01). 1,25-(OH)2D and 25OHD levels showed significant correlation only at 4 days (r = 0.74; P less than 0.0005), and there were no consistent relationships between 1,25-(OH)2D and the other variables. The median concentration of 24,25-(OH)2D was lower (P less than 0.01), while the 25,26-(OH)2D value was similar to that in the adults. Both were, however, positively related to the 25OHD level [24,25-(OH)2D, r = 0.82; 25,26-(OH)2D, r = 0.65; P less than 0.0005], as in the adults. The ratio of 24,25-(OH)2D to 25OHD was lower beyond 4 days of life than in the adults (medians, 3.4% vs. 5.1%; P less than 0.02). The data suggest that 1,25-(OH)2D synthesis has relative priority over 24,25-(OH)2D production during infancy compared with that in adulthood.

Vitamin D metabolism in normal and hypoparathyroid pregnancy and lactation. Case report.

Plasma concentrations of vitamin D metabolites in 17 non-pregnant women, 22 pregnant women at delivery, and in eight lactating women 3 and 16 days after delivery, were compared with those in a postpartum hypoparathyroid patient treated with 1 alpha-hydroxyvitamin D (1 alpha-OHD). The mean concentration of 1,25-dihydroxyvitamin D [1,25-(OH)2 D] was 203 (SD 61) pmol/l in the pregnant, and 86 (SD 27) pmol/l in the non-pregnant women (P less than 0.0005). The levels 3 and 16 days after delivery were similar [57 (11) compared with 62 (19) pmol/l], and lower than the non-pregnant value (P less than 0.01). The 25-hydroxyvitamin D (25-OHD) concentration remained unchanged between the 3rd and 16th days after delivery, whereas the 24,25-dihydroxyvitamin D [24,25-(OH)2D] level increased from 2.7 (SD 1.8) to 3.7 (SD 2.3) nmol/l (P less than 0.025). The patient temporarily required an increased supplement of l alpha-OHD during pregnancy, but a dose which was appropriate before pregnancy resulted in marked hypercalcaemia and a rise of 1,25-(OH)2D concentration within 16 days of delivery despite lactation. The results suggest that the metabolic need for the active vitamin D metabolite 1,25-(OH)2D is increased during pregnancy and rapidly reduced during early lactation in healthy and hypoparathyroid women.

Plasma concentrations of vitamin D metabolites in a case of rickets of prematurity.

Rickets was diagnosed in an extremely low-birthweight infant 16 weeks after birth. She had a normal plasma concentration of 25-hydroxyvitamin D, a relatively low level of 24,25-dihydroxyvitamin D, and a markedly elevated 1,25-dihydroxyvitamin D level compared with adult standards. The plasma concentrations of the vitamin D metabolites were, however, indistinguishable from those of healthy preterm infants who received a similar diet of human milk and vitamins. The results indicate that rickets was not caused by vitamin D deficiency or by abnormal vitamin D metabolism, but by calcium and/or phosphate deficiency, and that the calcium and phosphorous content of human milk may be inappropriately low for very low-birthweight infants.

Vitamin D nutritional status of premature infants supplemented with 500 IU vitamin D2 per day.

The vitamin D nutritional status of premature infants was assessed by determining plasma 25-hydroxyvitamin D concentrations before and during supplementation with 500 IU vitamin D2 per day. Fifty-one samples were collected from 25 healthy infants fed breast milk and a vitamin D3 fortified formula. Gestational age was 32.2 +/- 2.4 weeks (mean +/- 1 SD). 25-hydroxyvitamin D levels before supplementation correlated well with maternal values (r = 0.81). The infants' mean plasma concentration increased from 30.6 +/- 13.7 nmol/l (mean +/- 1 SD) after birth to 46.3 +/- 10.5 nmol/l after 9 +/- 1 days (p less than 0.0025), and to 65.3 +/- 16.6 nmol/l after 37 +/- 10 days of vitamin D2 treatment (p less than 0.0005). 25-hydroxyvitamin D2 and 25-hydroxyvitamin D3 were determined separately, and it appeared that the rise was accounted for by the D2 fraction while 25-hydroxyvitamin D3 concentrations were unchanged. The results demonstrate that vitamin D2 is well absorbed and hydroxylated in the 25 position by premature infants free of associated disease, and that a supplementation of 500 IU per day in addition to breast milk and a regular vitamin D fortified formula is adequate to rapidly establish 25-hydroxyvitamin D levels within the normal adult range.