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

VITAMIN D INSUFFICIENCY AS AN INTERVAL CAUSE OF DIMINISHED BONE MINERAL DENSITY
维生素 D 不足是骨矿物质密度降低的间歇性原因
批准号:
7606111
负责人:
John S Adams
金额:
$1.37万
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-02-01 至 2007-11-30

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中文摘要
翻译
这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者(PI)可能从另一个NIH来源获得了主要资金, 因此可以在其他CRISP条目中表示。所列机构为 研究中心,而研究中心不一定是研究者的研究机构。 本研究旨在评估对双磷酸盐类药物治疗骨质疏松症无反应的患者中间歇性维生素D缺乏症的患病率。 符合预定义的“无反应”标准的患者将接受维生素D缺乏症筛查,在发现缺乏症的情况下,将更换维生素D,以观察是否恢复对双膦酸盐的反应。 双膦酸盐是一类用于治疗骨质疏松症或骨质疏松症的药物。一种特殊类型的X射线称为DEXA扫描通常每年进行一次,以查看患者是否对这些药物有反应。通常情况下,在服用这些药物时,骨密度(BMD)会增加。在双磷酸盐治疗时骨密度下降表明可能已经形成了骨质疏松症的另一个所谓的继发性原因。一个这样的次要原因是维生素D不足的发展。本研究旨在回答以下两个问题: 1.在BMD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反弹增加? 预计该研究将确定骨健康依赖于双膦酸盐给药的一组患者中维生素D不足的患病率。还预计,在那些维生素D水平低的患者中,补充维生素D将改善他们的BMD。我们相信,所提出的研究问题可以在标准的病人护理设置回答。也就是说,这项研究将不需要任何干预或程序超出通常需要在骨诊所。 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起着关键作用,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的白色血细胞,以分析维生素D治疗前后的基因变化。我们可以用临床采集的血液样本来做这件事。
英文摘要
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.
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