VITAMIN D INSUFFICIENCY AS AN INTERVAL CAUSE OF DIMINISHED BONE MINERAL DENSITY

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 这项研究旨在评估双膦酸类药物治疗骨质疏松症无效的患者中间歇性维生素D缺乏的患病率。符合预先定义的“无反应”标准的患者将接受维生素D缺乏筛查，在发现缺乏的情况下，将更换维生素D，以观察这是否能恢复对双膦酸类药物的反应。 双膦酸盐是一类用于治疗骨质脆弱或骨质疏松症的药物。一种名为DEXA扫描的特殊类型的X射线通常每年进行一次，以观察患者是否对这些药物有反应。正常情况下，服用这些药物会增加骨骼的密度(BMD)。接受双膦酸类药物治疗时，骨密度下降，这表明另一个所谓的继发性骨质疏松症可能已经形成。其中一个次要原因是维生素D不足。本研究的目的是回答以下两个问题： 1.骨密度下降的患者中维生素D缺乏的频率是多少？ 2.在维生素D缺乏和BMD下降的患者中，补充维生素D是否会导致BMD回升？ 预计这项研究将确定一组患者中维生素D缺乏的患病率，这些患者的骨骼健康依赖于双膦酸类药物的使用。还预计，在那些维生素D含量较低的患者中，补充维生素D将改善他们的骨密度。我们相信，拟议的研究问题可以在标准患者护理的背景下得到回答。也就是说，这项研究不需要任何超出骨诊所正常要求的干预或程序。 除了在骨骼健康中的作用外，维生素D在我们的免疫系统中也发挥着关键作用，有助于对抗感染。因此，作为一项单独的研究，我们希望研究储存的血液样本中的白细胞，以分析维生素D治疗前后的基因变化。我们可以通过临床原因收集的血液样本来做到这一点。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This study is designed to assess the prevalence of interval Vitamin D deficiency in patients not responding to therapy with bisphosphonates for the treatment of osteoporosis. Patients meeting pre-defined criteria of "non-response" will be screened for vitamin D deficiency, and in those cases where deficiency is found, will have vitamin D replaced in order to see if this restores response to bisphosphonates. Bisphosphonates are a class of medications used to treat weak bones or osteoporosis. A special type of x-ray known as a DEXA Scan is usually done annually to see whether patients are responding to these medicines. Normally, there is an increase in the density of the bones (BMD) while on these medicines. A decline in bone density while on bisphosphonate treatment suggests a separate so-called ¿¿secondary¿¿ cause of osteoporosis may have developed. One such secondary cause is the development of vitamin D insufficiency. The purpose of this study is to answer the following two questions: 1. What is the frequency of vitamin D deficiency in patients who have had a decline in BMD? 2. In patients with vitamin D deficiency and a decline in BMD, does replacement of vitamin D cause a rebound increase in BMD ? It is expected that the study will determine the prevalence of vitamin D insufficiency in a group of patients whose bone health is dependent on the administration of bisphosphonates. It is also anticipated that in those patients who have low vitamin D, replacing it will improve their BMD. We believe that the proposed research questions can be answered in the setting of standard patient care. That is to say, this research will not require any interventions or procedures beyond what is normally required in a bone clinic. In addition to its role in bone health, vitamin D plays a key role in our immune system, helping fight infection. Accordingly, as a separate study, we wish to study the white blood cells of stored samples of blood to analyze gene changes before and after treatment with vitamin D. We can do this with samples of blood collected for clinical reasons.