cholecalciferol and Infant--Newborn--Diseases

Vitamin D has historically been considered to play a role solely in bone and calcium metabolism. Human disease associations and basic physiological studies suggest that vitamin D deficiency is plausibly implicated in adverse health outcomes including mortality, malignancy, cardiovascular disease, immune functioning and glucose metabolism. There is considerable evidence that low maternal levels of 25 hydroxyvitamin D are associated with adverse outcomes for both mother and fetus in pregnancy as well as the neonate and child. Vitamin D deficiency during pregnancy has been linked with a number of maternal problems including infertility, preeclampsia, gestational diabetes and an increased rate of caesarean section. Likewise, for the child, there is an association with small size, impaired growth and skeletal problems in infancy, neonatal hypocalcaemia and seizures, and an increased risk of HIV transmission. Other childhood disease associations include type 1 diabetes and effects on immune tolerance. The optimal concentration of 25 hydroxyvitamin D is unknown and compounded by difficulties in defining the normal range. Whilst there is suggestive physiological evidence to support a causal role for many of the associations, whether vitamin D deficiency is a marker of poor health or the underlying aetiological problem is unclear. Randomised controlled trials of vitamin D supplementation with an appropriate assessment of a variety of health outcomes are required.

Topics: Cholecalciferol; Diabetes Mellitus; Diabetes, Gestational; Female; Humans; Infant, Newborn; Infant, Newborn, Diseases; Lactation; Muscle, Skeletal; Parathyroid Hormone; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Reference Values; Skin; Vitamin D Deficiency

To determine whether maternal vitamin D supplementation, in the vitamin D deficient mother, prevents neonatal vitamin D deficiency.. Open-label randomized controlled trial.. Metropolitan Melbourne, Australia, tertiary hospital routine antenatal outpatient clinic.. Seventy-eight women with singleton pregnancies with vitamin D deficiency/insufficiency (serum 25-OH Vit D < 75 nmol/l) at their first antenatal appointment at 12-16-week gestation were recruited.. Participants were randomized to vitamin D supplementation (2000-4000 IU cholecalciferol) orally daily until delivery or no supplementation.. The primary outcome was neonatal serum 25-OH vit D concentration at delivery. The secondary outcome was maternal serum 25-OH vit D concentration at delivery.. Baseline mean maternal serum 25-OH vit D concentrations were similar (P = 0·9) between treatment (32 nmol/l, 95% confidence interval 26-39 nmol/l) and control groups (33 nmol/l, 95% CI 26-39 nmol/l). Umbilical cord serum 25-OH vit D concentrations at delivery were higher (P < 0·0001) in neonates of treatment group mothers (81 nmol/l, 95% CI; 70-91 nmol/l) compared with neonates of control group mothers (42 nmol/l, 95% CI; 34-50 nmol/l) with a strongly positive correlation between maternal serum 25-OH Vit D and umbilical cord serum 25-OH vit D concentrations at delivery (Spearman rank correlation coefficient 0·88; P < 0·0001). Mean maternal serum 25-OH Vit D concentrations at delivery were higher (P < 0·0001) in the treatment group (71 nmol/l, 95% CI; 62-81 nmol/l) compared with the control group (36 nmol/l, 95% CI; 29-42 nmol/l).. Vitamin D supplementation of vitamin D deficient pregnant women prevents neonatal vitamin D deficiency.

Topics: Administration, Oral; Adult; Cholecalciferol; Dietary Supplements; Female; Fetal Blood; Humans; Immunoassay; Infant, Newborn; Infant, Newborn, Diseases; Pregnancy; Pregnancy Complications; Tertiary Care Centers; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Vitamins

Topics: Biomarkers; Calcium; Cholecalciferol; Dietary Supplements; Female; Humans; Hyperparathyroidism, Primary; Hypocalcemia; Hypoparathyroidism; Infant, Newborn; Infant, Newborn, Diseases; Male; Pregnancy; Recurrence; Risk Factors; Seizures; Tetany; Time Factors; Treatment Outcome

Using the Haddad modified method, 25-OH-D were measured in the blood of the umbilical cord of 29 infants and in peripheral serum after 6 weeks. 16 infants were given a daily dosage of 1000 I. E., 13 infants 500 I. E. vitamin D against rickets. Further they were fed with an adapted milk containing 400 I. E. vitamin D/1. The mean cord serum values were 13 and 15 ng/ml. After treatment with 1000 I. E., 25-OH-D values around 54 ng/ml were measured after 6 weeks and under 500 I. E. daily, values of 37 ng/ml, respectively. Treatment using a dosage of 500 I. E. vitamin D combined with feeding with vitamin D fortified milk seems adequate, to prevent vitamin D depletion.

Topics: 25-Hydroxyvitamin D 2; Cholecalciferol; Dose-Response Relationship, Drug; Ergocalciferols; Humans; Infant, Newborn; Infant, Newborn, Diseases; Rickets; Vitamin D Deficiency

The necessary daily amount of vitamin D3 in premature infants was calculated by Hövels and his group as being 25 mcg (1000 I.U.). This was in agreement with our own investigations. Without vitamin D3, however, the incidence of rikkets in premature and small-for-dates newborns occurred usually at the beginning of the second month of life. Clinical signs of rickets are still absent at this time, while an increased activity of the serum alkaline phosphatase signals the beginning of the illness. Three groups of prematurely born infants received up to 50 days daily oral doses of 12.5 mcg vitamin D3 (=500 I.U.), 25 mcg vitamin D3 (=1000 I.U.) or 9 mcg 25-hydroxycholecalciferol (25-HCC), respectively, while one untreated group served as control. No differences were noted between the four groups in the serum values of calcium and phosphorus. The activity of the alkaline phosphatase tended to be higher in the untreated and the 500 I.U. groups. The differences were prouved by the chi2-test to be significant (see table 2 and 3). It appeared that 9 mcg of 25-HCC prevented the rise in alkaline phosphatase slightly better than 25 mcg of vitamin D3 (1000 I.U.). On a mcg base 25-HCC seems three times as effective as cholecalciferol. One could speculate about a delayed hydroxylation of cholecalciferol (vitamin D3) to 25-HCC.

Topics: Age Factors; Alkaline Phosphatase; Birth Weight; Calcium; Cholecalciferol; Humans; Hydroxycholecalciferols; Infant; Infant Nutritional Physiological Phenomena; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature; Nutritional Requirements; Phosphates; Rickets; Time Factors

Topics: Age Factors; Alkaline Phosphatase; Calcium; Cholecalciferol; Humans; Hypercalcemia; Infant, Newborn; Infant, Newborn, Diseases; Phosphorus; Rickets