Browsing INFANT Research Centre by Subject "25-hydroxyvitamin D"
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- ItemEstimation of the maternal vitamin D intake that maintains circulating 25-hydroxyvitamin D in late gestation at a concentration sufficient to keep umbilical cord sera >= 25-30 nmol/L: a dose-response, double-blind, randomized placebo-controlled trial in pregnant women at northern latitude(Oxford University Press, 2018) O'Callaghan, Karen M.; Hennessy, Áine; Hull, George L. J.; Healy, Karina; Ritz, Christian; Kenny, Louise C.; Cashman, Kevin D.; Kiely, Mairead E.; European CommissionBackground: In the absence of dose-response data, Dietary Reference Values for vitamin D in nonpregnant adults are extended to pregnancy. Objective: The aim was to estimate vitamin D intake needed to maintain maternal 25-hydroxyvitamin D [25(OH)D] in late gestation at a concentration sufficient to prevent newborn 25(OH)D <25-30 nmol/L, a threshold indicative of increased risk of nutritional rickets. Design: We conducted a 3-arm, dose-response, double-blind, randomized placebo-controlled trial in Cork, Ireland (51.9 degrees N). A total of 144 white-skinned pregnant women were assigned to receive 0, 10 (400 IU), or 20 (800 IU) mu g vitamin D-3/d from <= 18 wk of gestation. Vitamin D metabolites at 14, 24, and 36 wk of gestation and in cord sera, including 25(OH)D-3, 3-epi-25(OH)D-3, 24,25(OH)(2)D-3, and 25(OH)D-2 were quantified by liquid chromatography-tandem mass spectrometry. A curvilinear regression model predicted the total vitamin D intake (from diet and antenatal supplements plus treatment dose) that maintained maternal 25(OH)D in late gestation at a concentration sufficient to maintain cord 25(OH)D at >= 25-30 nmol/L. Results: Mean +/- SD baseline 25(OH)D was 54.9 +/- 10.7 nmol/L. Total vitamin D intakes at the study endpoint (36 wk of gestation) were 12.1 +/- 8.0, 21.9 +/- 5.3, and 33.7 +/- 5.1 mu g/d in the placebo and 10-mu g and 20-mu g vitamin D-3 groups, respectively; and 25(OH)D was 24.3 +/- 5.8 and 29.2 +/- 5.6 nmol/L higher in the 10- and 20-mu g groups, respectively, compared with placebo (P < 0.001). For maternal 25(OH)D concentrations >= 50 nmol/L, 95% of cord sera were >= 30 nmol/L and 99% were > 25 nmol/L. The estimated vitamin D intake required to maintain serum 25(OH)D at >= 50 nmol/L in 97.5% of women was 28.9 mu g/d. Conclusions: Thirty micrograms of vitamin D per day safely maintained serum 25(OH)D concentrations at >= 50 nmol/L in almost all white-skinned women during pregnancy at a northern latitude, which kept 25(OH)D at > 25 nmol/L in 99% and >= 30 nmol/L in 95% of umbilical cord sera.
- ItemExploring the concept of functional vitamin D deficiency in pregnancy: impact of the interaction between 25-hydroxyvitamin D and parathyroid hormone on perinatal outcomes(Oxford University Press, 2018) Hemmingway, Andrea; Kenny, Louise C.; Malvisi, Lucio; Kiely, Mairead E.; Seventh Framework Programme; Health Research Board; Science Foundation Ireland; European Regional Development FundBackground: Associations of vitamin D with perinatal outcomes are inconsistent and few studies have considered the wider calcium metabolic system. Objectives: We aimed to explore functional vitamin D deficiency in pregnancy by investigating associations between vitamin D status, parathyroid hormone (PTH), and perinatal outcomes. Design: SCOPE (Screening for Pregnancy Endpoints) Ireland is a prospective cohort study of low-risk, nulliparous pregnant women. We measured serum 25-hydroxyvitamin D [25(OH)D] and PTH at 15 wk of gestation in 1754 participants. Results: Mean ± SD 25(OH)D was 56.6 ± 25.8 nmol/L (22.7 ± 10.3 ng/mL) and geometric mean (95% CI) PTH was 7.84 pg/mL (7.7, 8.0 pg/mL) [0.86 pmol/L (0.85, 0.88 pmol/L)]. PTH was elevated in 34.3% of women who had 25(OH)D <30 nmol/L and in 13.9% of those with 25(OH)D ≥75 nmol/L. Whereas 17% had 25(OH)D <30 nmol/L, 5.5% had functional vitamin D deficiency, defined as 25(OH)D <30 nmol/L with elevated PTH. Elevated mean arterial pressure (MAP), gestational hypertension, pre-eclampsia, and small-for-gestational-age (SGA) birth were confirmed in 9.2%, 11.9%, 3.8%, and 10.6% of participants, respectively. In fully adjusted regression models, neither low 25(OH)D nor elevated PTH alone increased the risk of any individual outcome. The prevalence of elevated MAP (19.1% compared with 9.7%) and SGA (16.0% compared with 6.7%) were highest (P < 0.05) in those with functional vitamin D deficiency compared with the reference group [25(OH)D ≥75 nmol/L and normal PTH]. The adjusted prevalence ratio (PR) and RR (95% CIs) for elevated MAP and SGA were 1.83 (1.02, 3.27) and 1.53 (0.80, 2.93), respectively. There was no effect of functional vitamin D deficiency on the risk of gestational hypertension (adjusted RR: 1.00; 95% CI: 0.60, 1.67) or pre-eclampsia (adjusted RR: 1.17; 95% CI: 0.32, 4.20). Conclusion: The concept of functional vitamin D deficiency, reflecting calcium metabolic stress, should be considered in studies of vitamin D in pregnancy. The SCOPE pregnancy cohort is registered at http://www.anzctr.org.au as ACTRN12607000551493.
- ItemInteractions between vitamin D status, calcium intake and parathyroid hormone concentrations in healthy white-skinned pregnant women at northern latitude(MDPI AG, 2018) Hemmingway, Andrea; O'Callaghan, Karen M.; Hennessy, Áine; Hull, George; Cashman, Kevin D.; Kiely, Mairead E.; Seventh Framework ProgrammeAdverse effects of low vitamin D status and calcium intakes in pregnancy may be mediated through functional effects on the calcium metabolic system. Little explored in pregnancy, we aimed to examine the relative importance of serum 25-hydroxyvitamin D (25(OH)D) and calcium intake on parathyroid hormone (PTH) concentrations in healthy white-skinned pregnant women. This cross-sectional analysis included 142 participants (14 ± 2 weeks’ gestation) at baseline of a vitamin D intervention trial at 51.9 °N. Serum 25(OH)D, PTH, and albumin-corrected calcium were quantified biochemically. Total vitamin D and calcium intakes (diet and supplements) were estimated using a validated food frequency questionnaire. The mean ± SD vitamin D intake was 10.7 ± 5.2 μg/day. With a mean ± SD serum 25(OH)D of 54.9 ± 22.6 nmol/L, 44% of women were <50 nmol/L and 13% <30 nmol/L. Calcium intakes (mean ± SD) were 1182 ± 488 mg/day and 23% of participants consumed <800 mg/day. The mean ± SD serum albumin-adjusted calcium was 2.2 ± 0.1 mmol/L and geometric mean (95% CI) PTH was 9.2 (8.4, 10.2) pg/mL. PTH was inversely correlated with serum 25(OH)D (r = −0.311, p < 0.001), but not with calcium intake or serum calcium (r = −0.087 and 0.057, respectively, both p > 0.05). Analysis of variance showed that while serum 25(OH)D (dichotomised at 50 nmol/L) had a significant effect on PTH (p = 0.025), calcium intake (<800, 800–1000, ≥1000 mg/day) had no effect (p = 0.822). There was no 25(OH)D-calcium intake interaction effect on PTH (p = 0.941). In this group of white-skinned women with largely sufficient calcium intakes, serum 25(OH)D was important for maintaining normal PTH concentration.
- ItemSystematic review of vitamin D and hypertensive disorders of pregnancy(MDPI AG, 2018) O'Callaghan, Karen M.; Kiely, Mairead E.; Seventh Framework ProgrammeThis narrative systematic review evaluates growing evidence of an association between low maternal vitamin D status and increased risk of hypertensive disorders. The inclusion of interventional, observational, and dietary studies on vitamin D and all hypertensive disorders of pregnancy is a novel aspect of this review, providing a unique contribution to an intensively-researched area that still lacks a definitive conclusion. To date, trial evidence supports a protective effect of combined vitamin D and calcium supplementation against preeclampsia. Conflicting data for an association of vitamin D with gestational hypertensive disorders in observational studies arises from a number of sources, including large heterogeneity between study designs, lack of adherence to standardized perinatal outcome definitions, variable quality of analytical data for 25-hydroxyvitamin D (25(OH)D), and inconsistent data reporting of vitamin D status. While evidence does appear to lean towards an increased risk of gestational hypertensive disorders at 25(OH)D concentrations <50 nmol/L, caution should be exercised with dosing in trials, given the lack of data on long-term safety. The possibility that a fairly narrow target range for circulating 25(OH)D for achievement of clinically-relevant improvements requires further exploration. As hypertension alone, and not preeclampsia specifically, limits intrauterine growth, evaluation of the relationship between vitamin D status and all terms of hypertension in pregnancy is a clinically relevant area for research and should be prioritised in future randomised trials.