Bailey Dana, Perumal Nandita, Yazdanpanah Mehrdad, Al Mahmud Abdullah, Baqui Abdullah H, Adeli Khosrow, Roth Daniel E
Clinical Biochemistry, Department of Pediatric Laboratory Medicine, Hospital for Sick Children, Canada; Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada; Gamma-Dynacare Medical Laboratories, London, Ontario, Canada.
Department of Paediatrics, Hospital for Sick Children and University of Toronto, Toronto, Ontario, Canada.
Clin Biochem. 2014 Jun;47(9):816-22. doi: 10.1016/j.clinbiochem.2014.01.015. Epub 2014 Jan 22.
Poor vitamin D status (i.e. low serum 25-hydroxyvitamin D (25(OH)D)) has been associated with adverse clinical outcomes during pregnancy and childhood. However, the interpretation of serum 25(OH)D levels may be complicated by the presence of the C3-epimer of 25(OH)D. We aimed to quantify C3-epi-25(OH)D3 in pregnant women and fetuses, to explore the relationship of the C3-epimer between maternal and cord samples, and to establish whether infant C3-epimer abundance is explained by prenatal formation.
In a sub-study of a randomized trial of prenatal vitamin D3, 25(OH)D3 and C3-epi-25(OH)D3 were quantified by LC-MS/MS in 71 sets of mother-fetus-infant serum samples, including maternal delivery specimens, cord blood, and infant specimens acquired at 3-28 weeks of age.
Without supplementation, median concentrations of C3-epi-25(OH)D₃ were higher in infants (6.80 nmol/L) than mothers (0.45 nmol/L) and cord blood (0 nmol/L). However, there was substantial variation such that C3-epi-25(OH)D₃ accounted for up to 11% (maternal), 14% (cord), and 25% (infant) of the total 25(OH)D₃. Supplemental vitamin D₃ significantly increased maternal-fetal C3-epi-25(OH)D₃, and was a preferential source of C3-epi-25(OH)D₃ compared to basal vitamin D, possibly due to C3-epi-cholecalciferol in the supplement. Multivariate regression did not suggest transplacental transfer of C3-epi-25(OH)D₃, but rather indicated its generation within the fetal-placental unit from maternally-derived 25(OH)D₃. Neither maternal nor fetal C3-epi-25(OH)D₃ is accounted for the relatively high concentrations of infant C3-epi-25(OH)D₃, suggesting rapid postnatal generation.
C3-epi-25(OH)D₃ is present in some pregnant women and fetuses, but does not appear to be efficiently transferred transplacentally. High C3-epimer concentrations in infancy are probably due to postnatal formation rather than fetal stores.
维生素D状态不佳（即血清25-羟基维生素D（25(OH)D）水平低）与妊娠和儿童期不良临床结局相关。然而，25(OH)D的C3差向异构体的存在可能会使血清25(OH)D水平的解读变得复杂。我们旨在对孕妇和胎儿体内的C3-表-25(OH)D3进行定量，探讨母体和脐带样本中C3差向异构体的关系，并确定婴儿C3差向异构体的丰度是否由产前形成所解释。
在一项产前维生素D3随机试验的子研究中，通过液相色谱-串联质谱法（LC-MS/MS）对71组母婴血清样本中的25(OH)D3和C3-表-25(OH)D3进行定量，这些样本包括产妇分娩标本、脐带血以及3至28周龄婴儿的标本。
在未补充维生素D的情况下，婴儿体内C3-表-25(OH)D₃的中位数浓度（6.80 nmol/L）高于母亲（0.45 nmol/L）和脐带血（0 nmol/L）。然而，存在很大差异，使得C3-表-25(OH)D₃在总25(OH)D₃中所占比例高达11%（母体）、14%（脐带）和25%（婴儿）。补充维生素D₃显著增加了母婴C3-表-25(OH)D₃，与基础维生素D相比，它是C3-表-25(OH)D₃的优先来源，这可能是由于补充剂中含有C3-表-胆钙化醇。多变量回归未提示C3-表-25(OH)D₃经胎盘转运，而是表明其在胎儿-胎盘单位内由母体来源的25(OH)D₃生成。母体和胎儿的C3-表-25(OH)D₃均不能解释婴儿C3-表-25(OH)D₃的相对高浓度，这表明其在出生后快速生成。
C3-表-25(OH)D₃存在于一些孕妇和胎儿体内，但似乎不能有效地经胎盘转运。婴儿期C3差向异构体浓度高可能是由于出生后形成而非胎儿储存。
