权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

TREATMENT FOR OSTEOPOROSIS OF THE HIP

髋部骨质疏松症的治疗

基本信息

批准号：
2769316
负责人：
John CHRISTOPHER GALLAGHER
金额：
$ 38.08万
依托单位：
CREIGHTON UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
1991
资助国家：
美国
起止时间：
1991-09-30 至 2001-08-31
项目状态：
已结题

项目摘要

Bone loss from the proximal femur continues into the nineties and low bone mass leads to an increased susceptibility to fracture. The risk of fracture accelerates between age 80-90 so that 33% of women and 17% of men sustain a hip fracture. Hip fractures cause an immediate 15% mortality, and will cost 20 billion dollars annually within 20 years. Two major factors play a role in the bone loss. Estrogen deficiency after the menopause is associated with increased bone loss from the femur. In the mid sixties a second factor emerges - malabsorption of calcium, which increases the degree of negative calcium balance causing secondary hyperparathyroidism and bone loss. By correcting estrogen deficiency and malabsorption of calcium it may be possible to reverse bone loss from the proximal femur. In order to test this hypothesis, 500 osteopenic women aged between 65-77 years will be treated with either estrogen, 1 alpha- hydroxyvitamin D2 (1 alpha-OH-D2) or a combination of estrogen and 1 alpha- OH-D2 for 3 years in an attempt to reverse bone loss from the proximal femur. It is suggested that estrogen will inhibit bone resorption and 1 alpha-OH-D2 will stimulate bone formation, and that the combination will be more effective than single therapy. The study will be double blind and placebo controlled. The primary outcome will be bone mineral density of the proximal femur, however, other areas of the skeleton will be measured so that any effect of therapy which might cause redistribution of bone mineral from cortex to trabecular sites can be detected. Loss of cortical bone could increase fracture susceptibility. Reversing bone loss from the proximal femur from age 65 for several years could maintain bone density above the fracture threshold and significantly reduce the risk of fracture. Not only would this provide considerable individual health benefits, but also greatly reduce health care costs.

股骨近端的骨丢失持续到90年代和低骨量肿块会增加骨折的易感性。存在以下风险骨折在80-90岁之间加速，33%的女性和17%的男性造成髋部骨折。髋部骨折会立即导致15%的死亡率，并将在20年内每年耗资200亿美元。有两个主要因素在骨质流失中起作用。雌激素缺乏症后更年期与股骨骨丢失增加有关。在……里面 60年代中期出现了第二个因素--钙吸收不良，这是增加负钙平衡的程度，导致继发性甲状旁腺机能亢进症和骨质流失。通过纠正雌激素缺乏和钙吸收不良有可能逆转骨量减少。股骨近端。为了验证这一假设，500名骨质疏松症女性年龄在65-77岁之间的人将接受雌激素治疗，1α- 羟基维生素D2(1α-OH-D2)或雌激素和1α-维生素D2的组合物- Oh-D2治疗3年，试图扭转近端的骨丢失大腿骨。提示雌激素可抑制骨吸收，1 Alpha-OH-D2会刺激骨形成，这种结合将是比单一疗法更有效。这项研究将是双盲的，安慰剂对照。主要结果将是股骨近端的骨密度，但是，骨骼的其他区域将被测量，以便可能导致骨矿物质从皮质重新分配到可检测到骨小梁部位。皮质骨丢失可能会增加断裂敏感性。从65岁起逆转股骨近端几年的骨丢失可以将骨密度维持在骨折阈值以上，并显著降低骨折风险。这不仅将提供相当大的个人健康受益，也大大降低了医疗成本。