Vitamin D insufficiency and skeletal development in utero.
Vitamin D insufficiency and skeletal development in utero.
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DOI：
10.1002/jbmr.2
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发表时间：
2010-01
期刊：
影响因子：
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通讯作者：
Adams JS
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文献类型：
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作者：
Hewison M;Adams JS
在过去的10年里，我们对什么是正常的维生素D状态的看法经历了实质性的修改。在此之前，次佳维生素D的定义是在非常基本的水平上，即是否有相关的骨骼疾病(即儿童软骨病和成人骨软化症)。因此，维生素D缺乏症是由血清25-羟基维生素D(25-OHD)浓度低于25 NM(10 ng/mL)来确定的，任何高于25-OHD的浓度都是“正常”的。然而，随着观察到钙稳态的几个参数继续与血清25-OHD水平相关，直到浓度高达约80 NM(32 ng/mL)，这一点已经改变。(1，2)这意味着只有当25-OHD浓度高于这一水平时，才能达到最佳的维生素D状态；根据这些修正后的参数，我们得出的结论是，维生素D缺乏是一种全球现象，全世界估计有10亿人的25-OHD水平低于最佳水平。(3)一些群体似乎比其他群体，尤其是孕妇，面临更大的维生素D缺乏风险。(4-8)在宾夕法尼亚州匹兹堡进行的一项研究表明，74%到95%的黑人孕妇和46%到62%的白人孕妇维生素D不足。(5)值得注意的是，在怀孕早期，几乎45%的非裔美国母亲的25-OHD水平低于37.5 NM。(5)这些流行病学数据引发的一个关键问题涉及怀孕期间维生素D不足的生理影响。在最新一期的《华尔街日报》上，Mahon和他的同事们通过一项针对孕妇的前瞻性纵向研究解决了这个问题。在这项研究中，他们描述了孕妇维生素D状况对胎儿骨骼发育的宫内测量的影响。(9)维生素D不足和维生素D缺乏的确切定义仍然存在一些争议。在某些情况下，维生素D缺乏被定义为25-OHD的血清浓度低于50 NM，而维生素D充足是指25-OHD水平大于75 NM。(10)因此，介于这些值之间的25-OHD的血清浓度对应于上述维生素D不足。在Mahon及其同事描述的对424名孕妇的研究中，(9)作者根据英国国家饮食和营养调查数据，将适量定义为25-OHD浓度大于70 NM。维生素D缺乏被定义为小于25 NM的25-OHD，有趣的是，作者随后将干预的25-OHD血清浓度细分为两组：“临界”(50-70 NM)和“不足”(25-50 NM)，为母亲维生素D状态的生理影响提供了另一种视角。
Over the last 10 years, our perception of what constitutes normal vitamin D status has undergone a substantial revision. Prior to this, suboptimal vitamin D was defined at a very basic level by the presence or absence of associated bone disease (ie, rickets in children and osteomalacia in adults). As a consequence, vitamin D deficiency was determined by serum concentrations of 25-hydroxyvitamin D (25-OHD) of less than 25 nM (10 ng/mL), and anything higher was ‘‘normal.’’However, this has changed with the observation that several parameters of calcium homeostasis continue to correlate with serum levels of 25-OHD up to concentrations as high as approximately 80 nM (32 ng/mL).(1, 2) The implication is that optimal vitamin D status is achieved only at 25-OHD concentrations above this; anything less is suboptimal or ‘‘insufficient.’’Based on these revised parameters, it has been concluded that vitamin D insufficiency is a global phenomenon, with an estimated 1 billion people worldwide having suboptimal levels of 25-OHD.(3) Some groups appear to be at greater risk of vitamin D insufficiency than others, notably pregnant women.(4–8) In a study carried out in Pittsburgh, PA, Bodnar and colleagues showed that 74% to 95% of pregnant black women and 46% to 62% of pregnant white women were vitamin D insufficient.(5) Notably, during early pregnancy, almost 45% of the African-American mothers had 25-OHD levels that were less than 37.5 nM.(5) A key question arising from these epidemiologic data concerns the physiologic impact of vitamin D insufficiency during pregnancy. In the current issue of the Journal, Mahon and colleagues have addressed this through a prospective longitudinal study of pregnant women in which they have characterized the impact of maternal vitamin D status on in utero measures of fetal skeletal development.(9) The precise definition of what constitutes vitamin D insufficiency versus vitamin D deficiency is still subject to some debate. In some instances, vitamin D deficiency is defined as a serum concentration of 25-OHD of less than 50 nM, whereas vitamin D sufficiency refers to a 25-OHD level of greater than 75 nM.(10) As a result, serum concentrations of 25-OHD of between these values correspond to the aforementioned vitamin D insufficiency. In the study of 424 pregnant women described byMahon and colleagues,(9) the authors have defined sufficiency as being 25-OHD concentrations greater than 70 nM based on National Diet and Nutrition Survey data from the United Kingdom. Vitamin D deficiency was defined as being less than 25 nM 25-OHD, and interestingly, the authors then subdivided intervening serum concentrations of 25-OHD into two groups:‘‘borderline’’(50 to 70 nM) and ‘‘insufficient’’(25 to 50 nM), providing an additional perspective on the physiologic impact of maternal vitamin D status.