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The change in plasma 25-hydroxyvitamin D did not differ between breast-fed infants that received a daily supplement of ergocalciferol or cholecalciferol for 3 months.

ABSTRACT: The biological equivalency of ergocalciferol (D2) and cholecalciferol (D3) has been debated; several comparisons have appeared in the adult literature but are scarce in pediatrics. The objective of this study was to compare increases in plasma 25-hydroxyvitamin D [25(OH)D] concentrations and attainment of 50 and 75 mol/L status cutoffs following 3 mo of daily supplementation with D2 compared with D3. Healthy, breast-fed, 1-mo-old infants (n = 52) received 10 ?g (400 ic) of either D2 or D3 daily. At 1 and 4 mo of age, plasma 25-hydroxyergocalciferol and 25-hydroxycholecalciferol concentrations were determined by liquid chromatography tandem MS (LC-MS/MS) and total 25(OH)D by chemiluminescent immunoassay (DiaSorin Liaison). Data were analyzed using t tests and ?² by intent to treat. A total of 23% of infants were deficient (?24.9 nmol/L) at baseline and 2% at follow-up on the basis of LC-MS/MS. At 4 mo, 96% were breastfed and there were no differences in compliance, breastfeeding rates, or sun exposure among groups. The change in total 25(OH)D measured by LC-MS/MS did not differ between the D2 (17.6 ± 26.7 nmol/L) and D3 (22.2 ± 20.2 nmol/L) groups. In the combined groups, the baseline plasma 25(OH)D concentration was inversely related to the change in total 25(OH)D (r = -0.52; P < 0.001). Overall, 86% of infants met the 50 nmol/L cutoff at follow-up; however, fewer infants in the D2 group (75%) met this level compared with the D3 group (96%) (P < 0.05). Similar results were obtained by immunoassay. In conclusion, the increase in the 25(OH)D concentration among the D2 and D3 groups did not differ, suggesting daily intake of either isoform is acceptable for infants <4 mo.

SUBMITTER: Gallo S

PROVIDER: S-EPMC3969107 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature

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The change in plasma 25-hydroxyvitamin D did not differ between breast-fed infants that received a daily supplement of ergocalciferol or cholecalciferol for 3 months.

Gallo Sina S Phan Anna A Vanstone Catherine A CA Rodd Celia C Weiler Hope A HA

The Journal of nutrition 20121219 2

The biological equivalency of ergocalciferol (D2) and cholecalciferol (D3) has been debated; several comparisons have appeared in the adult literature but are scarce in pediatrics. The objective of this study was to compare increases in plasma 25-hydroxyvitamin D [25(OH)D] concentrations and attainment of 50 and 75 mol/L status cutoffs following 3 mo of daily supplementation with D2 compared with D3. Healthy, breast-fed, 1-mo-old infants (n = 52) received 10 μg (400 ic) of either D2 or D3 daily. ...[more]

PMID: 23256143

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Project description:BackgroundVariability in the 25-hydroxyvitamin D [25(OH)D] response to prenatal and postpartum vitamin D supplementation is an important consideration for establishing vitamin D deficiency prevention regimens.ObjectivesWe aimed to examine interindividual variation in maternal and infant 25(OH)D following maternal vitamin D supplementation.MethodsIn a randomized trial of maternal vitamin D supplementation (Maternal Vitamin D for Infant Growth Trial), healthy pregnant women (n = 1300) received a prenatal cholecalciferol (vitamin D-3) dose of 0, 4200, 16,800, or 28,000 IU/wk from 17 to 24 wk of gestation followed by placebo to 6 mo postpartum. A fifth group received 28,000 IU cholecalciferol/wk both prenatally and postpartum. In a subset of participants, associations of 25(OH)D with hypothesized explanatory factors were estimated in women at delivery (n = 655) and 6 mo postpartum (n = 566), and in their infants at birth (n = 502) and 6 mo of age (n = 215). Base models included initial 25(OH)D and supplemental vitamin D dose. Multivariable models were extended to include other individual characteristics and specimen-related factors. The model coefficient of determination (R2) was used to express the percentage of total variance explained.ResultsSupplemental vitamin D intake and initial 25(OH)D accounted for the majority of variance in maternal 25(OH)D at delivery and postpartum (R2 = 70% and 79%, respectively). Additional characteristics, including BMI, contributed negligibly to remaining variance (<5% increase in R2). Variance in neonatal 25(OH)D was explained mostly by maternal delivery 25(OH)D and prenatal vitamin D intake (R2 = 82%). Variance in 25(OH)D in later infancy could only partly be explained by numerous biological, sociodemographic, and laboratory-related characteristics, including feeding practices (R2 = 43%).ConclusionsPresupplementation 25(OH)D and vitamin D supplemental dose are the major determinants of the response to maternal prenatal vitamin D intake. Vitamin D dosing regimens to prevent maternal and infant vitamin D deficiency should take into consideration the mean 25(OH)D concentration of the target population.

Project description:Background and objectivesElevated concentrations of fibroblast growth factor 23 (FGF23) are postulated to promote 25-hydroxyvitamin D (25[OH]D) insufficiency in CKD by stimulating 24-hydroxylation of this metabolite, leading to its subsequent degradation; however, prospective human studies testing this relationship are lacking.Design, setting, participants, & measurementsAn open-label prospective study was conducted from October 2010 through July 2012 to compare the effect of 8 weeks of oral cholecalciferol therapy (50,000 IU twice weekly) on the production of 24,25(OH)2D3 in vitamin D-insufficient patients with CKD (n=15) and controls with normal kidney function (n=15). Vitamin D metabolites were comprehensively profiled at baseline and after treatment, along with FGF23 and other mineral metabolism parameters.ResultsVitamin D3 and 25(OH)D3 concentrations increased equivalently in the CKD and control groups following cholecalciferol treatment (median D3 change, 8.6 ng/ml [interquartile range, 3.9-25.6 ng/ml] for controls versus 12.6 ng/ml [6.9-41.2 ng/ml] for CKD [P=0.15]; 25(OH)D3 change, 39.2 ng/ml [30.9-47.2 ng/ml] for controls versus 39.9 ng/ml [31.5-44.1 ng/ml] for CKD [P=0.58]). Likewise, the absolute increase in 1α,25(OH)2D3 was similar between CKD participants and controls (change, 111.2 pg/ml [64.3-141.6 pg/ml] for controls versus 101.1 pg/ml [74.2-123.1 pg/ml] for CKD; P=0.38). Baseline and post-treatment 24,25(OH)2D3 concentrations were lower in the CKD group; moreover, the absolute increase in 24,25(OH)2D3 after therapy was markedly smaller in patients with CKD (change, 2.8 ng/ml [2.3-3.5 ng/ml] for controls versus 1.2 ng/ml [0.6-1.9 ng/ml] for patients with CKD; P<0.001). Furthermore, higher baseline FGF23 concentrations were associated with smaller increments in 24,25(OH)2D3 for individuals with CKD; this association was negated after adjustment for eGFR by multivariate analysis.ConclusionsPatients with CKD exhibit an altered ability to increase serum 24,25(OH)2D3 after cholecalciferol therapy, suggesting decreased 24-hydroxylase activity in CKD. The observed relationship between baseline FGF23 and increments in 24,25(OH)2D3 further refutes the idea that FGF23 directly contributes to 25(OH)D insufficiency in CKD through stimulation of 24-hydroxylase activity.

Dataset Information

The change in plasma 25-hydroxyvitamin D did not differ between breast-fed infants that received a daily supplement of ergocalciferol or cholecalciferol for 3 months.

Publications

The change in plasma 25-hydroxyvitamin D did not differ between breast-fed infants that received a daily supplement of ergocalciferol or cholecalciferol for 3 months.

Similar Datasets

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