育龄妇女补充维生素 D3 后对甲状旁腺激素的反应:一项随机、双盲、安慰剂对照试验。

Plasma parathyroid hormone response to vitamin D3 supplementation among women of reproductive age: A randomized double-blind placebo-control trial.

机构信息

Division of Nutrition and Dietetics, International Medical University, Kuala Lumpur, Malaysia.

Faculty of Medicine and Health Sciences, University of Auckland, Auckland, New Zealand.

出版信息

PLoS One. 2022 Nov 10;17(11):e0276506. doi: 10.1371/journal.pone.0276506. eCollection 2022.

Abstract

While vitamin D inadequacy occurs worldwide, there is a lack of consensus internationally on the optimum plasma levels of 25(OH)D to maximally suppress the level of parathyroid hormone toward reducing bone loss. This study aimed to investigate the response of intact parathyroid hormone (iPTH) to vitamin D3 supplementation among Malaysian women of reproductive age in a randomised double-blind placebo-control trial [NMRR-15-479-25680]. A total of 106 women who fulfilled the study inclusion criteria were randomly assigned to receive daily one of these three supplement doses (i) 600 IU vitamin D3 + 500 mg calcium; (ii) 1200 IU vitamin D3 + 500 mg calcium; or (iii) 4000 IU vitamin D3 + 500 mg calcium. The placebo group received daily 500 mg calcium. The outcome examined was change in plasma iPTH concentration in response to daily vitamin D3 supplementation for 16 weeks. Fasting blood sample was obtained at baseline and post-supplementation. A total of 78 subjects (73.6%) completed the intervention. None of the supplementation groups brought about any detectable suppression of iPTH concentration post-supplementation. Vitamin D3 supplementation resulted in overall increase in plasma 25(OH)D levels, but only the 4000 IU/day group showed a significant dose effect post-supplementation (mean 49.7 ± 26.5 nmol/L) compared to placebo (29.3 ± 13.3 nmol/L). The lack of iPTH suppression is attributed to high prevalence of vitamin D insufficiency at baseline and the supplementation regimen was inadequate to raise the 25(OH)D level to cause PTH suppression. Inadequate calcium intake of the participants was also a likely contributing factor to the result. As prolonged vitamin D insufficiency and hypocalcaemia could lead to a compensatory rise in PTH resulting in accelerated bone loss, as well as posing increasing risks of non-skeletal morbidities, further clinical trials with an adequately powered sample size should be undertaken over an appropriate study duration to verify the results obtained in this study.

摘要

虽然维生素 D 不足在全球范围内普遍存在,但国际上对于最大程度抑制甲状旁腺激素水平以减少骨丢失的最佳血浆 25(OH)D 水平仍缺乏共识。本研究旨在通过一项随机、双盲、安慰剂对照试验 [NMRR-15-479-25680] ,调查维生素 D3 补充对马来西亚育龄妇女的完整甲状旁腺激素 (iPTH) 的反应。共有 106 名符合研究纳入标准的女性被随机分配接受以下三种补充剂剂量中的一种,每天一次:(i) 600IU 维生素 D3 + 500mg 钙;(ii) 1200IU 维生素 D3 + 500mg 钙;或 (iii) 4000IU 维生素 D3 + 500mg 钙。安慰剂组每天服用 500mg 钙。研究的结果是检测 16 周内每日维生素 D3 补充对血浆 iPTH 浓度的变化。在基线和补充后采集空腹血样。共有 78 名受试者(73.6%)完成了干预。补充剂组均未检测到 iPTH 浓度的任何可察觉抑制。维生素 D3 补充剂使血浆 25(OH)D 水平总体升高,但只有每天 4000IU 组在补充后表现出显著的剂量效应(平均 49.7 ± 26.5 nmol/L),与安慰剂组(29.3 ± 13.3 nmol/L)相比。iPTH 抑制不足归因于基线时维生素 D 不足的高患病率,以及补充方案不足以将 25(OH)D 水平提高到抑制 PTH 的水平。参与者钙摄入量不足也可能是导致结果的一个因素。由于长期维生素 D 不足和低钙血症可能导致甲状旁腺激素代偿性升高,从而加速骨丢失,并增加非骨骼疾病的风险,因此应该进行进一步的临床试验,样本量足够大,研究时间适当,以验证本研究的结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e6d/9648839/43467e26960c/pone.0276506.g001.jpg

相似文献

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索