Bone Metabolism Unit, Creighton University School of Medicine, Omaha, Nebraska 68131, USA.
Ann Intern Med. 2012 Mar 20;156(6):425-37. doi: 10.7326/0003-4819-156-6-201203200-00005.
Serum 25-hydroxyvitamin D (25-[OH]D) is considered the best biomarker of clinical vitamin D status.
To determine the effect of increasing oral doses of vitamin D(3) on serum 25-(OH)D and serum parathyroid hormone (PTH) levels in postmenopausal white women with vitamin D insufficiency (defined as a 25-[OH]D level ≤50 nmol/L) in the presence of adequate calcium intake. These results can be used as a guide to estimate the Recommended Dietary Allowance (RDA) (defined as meeting the needs of 97.5% of the population) for vitamin D(3).
Randomized, placebo-controlled trial. (ClinicalTrials.gov registration number: NCT00472823)
Creighton University Medical Center, Omaha, Nebraska.
163 healthy postmenopausal white women with vitamin D insufficiency enrolled in the winter or spring of 2007 to 2008 and followed for 1 year.
Participants were randomly assigned to receive placebo or vitamin D(3), 400, 800, 1600, 2400, 3200, 4000, or 4800 IU once daily. Daily calcium supplements were provided to increase the total daily calcium intake to 1200 to 1400 mg.
The primary outcomes were 25-(OH)D and PTH levels at 6 and 12 months.
The mean baseline 25-(OH)D level was 39 nmol/L. The dose response was curvilinear and tended to plateau at approximately 112 nmol/L in patients receiving more than 3200 IU/d of vitamin D(3). The RDA of vitamin D(3) to achieve a 25-(OH)D level greater than 50 nmol/L was 800 IU/d. A mixed-effects model predicted that 600 IU of vitamin D(3) daily could also meet this goal. Compared with participants with a normal body mass index (<25 kg/m(2)), obese women (≥30 kg/m(2)) had a 25-(OH)D level that was 17.8 nmol/L lower. Parathyroid hormone levels at 12 months decreased with an increasing dose of vitamin D(3) (P = 0.012). Depending on the criteria used, hypercalcemia occurred in 2.8% to 9.0% and hypercalciuria in 12.0% to 33.0% of participants; events were unrelated to dose.
Findings may not be generalizable to other age groups or persons with substantial comorbid conditions.
A vitamin D(3) dosage of 800 IU/d increased serum 25-(OH)D levels to greater than 50 nmol/L in 97.5% of women; however, a model predicted the same response with a vitamin D(3) dosage of 600 IU/d. These results can be used as a guide for the RDA of vitamin D(3), but prospective trials are needed to confirm the clinical significance of these results.
National Institute on Aging.
血清 25-羟维生素 D（25-（OH）D）被认为是临床维生素 D 状况的最佳生物标志物。
确定在摄入足够的钙的情况下，增加维生素 D（3）的口服剂量对绝经后维生素 D 不足（定义为 25-（OH）D 水平≤50nmol/L）的白人女性血清 25-（OH）D 和甲状旁腺激素（PTH）水平的影响。这些结果可用于估计维生素 D（3）的推荐膳食允许量（RDA）（定义为满足 97.5%人群的需求）。
随机、安慰剂对照试验。（临床试验.gov 注册号：NCT00472823）
内布拉斯加州奥马哈市克赖顿大学医学中心。
163 名健康的绝经后白人女性，于 2007 年至 2008 年冬季或春季入组，并随访 1 年。
参与者被随机分配接受安慰剂或维生素 D（3），400、800、1600、2400、3200、4000 或 4800IU 每日一次。每日提供钙补充剂以将总日钙摄入量增加至 1200 至 1400mg。
主要结局是 6 个月和 12 个月时的 25-（OH）D 和 PTH 水平。
基线时平均 25-（OH）D 水平为 39nmol/L。剂量反应呈曲线，在接受 3200IU/d 以上维生素 D（3）的患者中趋于在约 112nmol/L 处达到平台期。达到 25-（OH）D 水平大于 50nmol/L 的维生素 D（3）的 RDA 为 800IU/d。混合效应模型预测，每天 600IU 的维生素 D（3）也可以达到这一目标。与体重指数正常（<25kg/m2）的参与者相比，肥胖女性（≥30kg/m2）的 25-（OH）D 水平低 17.8nmol/L。随着维生素 D（3）剂量的增加，甲状旁腺激素水平在 12 个月时降低（P=0.012）。根据使用的标准，2.8%至 9.0%的参与者发生高钙血症，12.0%至 33.0%的参与者发生高钙尿症；这些事件与剂量无关。
研究结果可能不适用于其他年龄组或有实质性合并症的人群。
维生素 D（3）剂量为 800IU/d 可使 97.5%的女性血清 25-（OH）D 水平升高至大于 50nmol/L；然而，模型预测相同的反应需要维生素 D（3）剂量为 600IU/d。这些结果可用于维生素 D（3）的 RDA 指导，但需要前瞻性试验来证实这些结果的临床意义。
美国国家老龄化研究所。
