Stokes Caroline S, Volmer Dietrich A
a Department of Medicine II, Saarland University Medical Center, Saarland University, Kirrberger Str. 100, 66421 Homburg, Germany.
b Institute of Bioanalytical Chemistry, Saarland University, Saarbrücken, Germany.
Appl Physiol Nutr Metab. 2016 Dec;41(12):1311-1317. doi: 10.1139/apnm-2016-0196.
Recently, hepatic immaturity was cited as a possible reason for high levels of the C-3 epimer of 25-hydroxyvitamin (25(OH)D) in premature infants: however what role, if any, the liver plays in controlling epimer concentrations is unknown. This study assesses 3-epi-25-hydroxyvitamin D (3-epi-25(OH)D) levels during the course of cholecalciferol supplementation in adults with chronic liver diseases (CLD). Vitamin D metabolites were analyzed in 65 CLD patients with 25(OH)D <30 ng/mL who received 20 000 IU cholecalciferol/week for 6 months. The primary outcome assessed serum 25(OH)D and 3-epi-25(OH)D in response to supplementation. Corresponding values from 16 CLD patients with sufficient vitamin D levels receiving no supplementation were compared. The epimer was detected in all samples and at lower relative concentrations with lower vitamin D baseline status, i.e., severe vitamin D deficiency (<10 ng/mL) as compared with deficient (10-19.9 ng/mL), insufficient (20-29.9 ng/mL), or sufficient (≥30 ng/mL) vitamin D levels (2.4% vs. 4.8%, 5.2%, 5.8%, respectively; P < 0.001). Similar relative concentrations for 3-epi-25(OH)D, ranging from 4.3%-7.1% (absolute concentrations: 1.1-4.0 ng/mL; all P < 0.001), were obtained in response to cholecalciferol in all supplemented patients, regardless of inadequacy threshold. Epimer levels significantly decreased (P = 0.007) in unsupplemented patients, coinciding with decreasing serum 25(OH)D concentrations over time. No epimer differences between patients with (n = 17) or without (n = 48) cirrhosis were demonstrated. The 3-epi-25(OH)D was present in serum of all patients at comparable levels to those reported by others. Epimer levels increased linearly with increasing 25(OH)D levels after supplementation. However, no effect of cirrhosis on epimer concentrations was observed.
最近，肝脏不成熟被认为是早产儿25-羟基维生素（25(OH)D）的C-3差向异构体水平较高的一个可能原因：然而，肝脏在控制差向异构体浓度方面所起的作用（如果有）尚不清楚。本研究评估了慢性肝病（CLD）成人补充胆钙化醇过程中3-表-25-羟基维生素D（3-epi-25(OH)D）的水平。对65例25(OH)D<30 ng/mL的CLD患者进行了维生素D代谢物分析，这些患者接受20000 IU胆钙化醇/周，持续6个月。主要结局评估了补充维生素D后血清25(OH)D和3-epi-25(OH)D的变化。比较了16例维生素D水平充足且未接受补充的CLD患者的相应值。在所有样本中均检测到差向异构体，与维生素D基线状态较低时相比，其相对浓度较低，即与维生素D缺乏（10 - 19.9 ng/mL）、不足（20 - 29.9 ng/mL）或充足（≥30 ng/mL）状态相比，严重维生素D缺乏（<10 ng/mL）时的相对浓度分别为2.4%、4.8%、5.2%、5.8%（P<0.001）。在所有补充维生素D的患者中，无论不足阈值如何，补充胆钙化醇后3-epi-25(OH)D的相对浓度相似，范围为4.3% - 7.1%（绝对浓度：1.1 - 4.0 ng/mL；所有P<0.001）。未补充维生素D的患者中差向异构体水平显著下降（P = 0.007），这与血清25(OH)D浓度随时间下降一致。在有（n = 17）或无（n = 48）肝硬化的患者之间未显示出差向异构体差异。所有患者血清中的3-epi-25(OH)D水平与其他人报告的水平相当。补充维生素D后，差向异构体水平随25(OH)D水平升高呈线性增加。然而，未观察到肝硬化对差向异构体浓度的影响。
