TREATMENT FOR OSTEOPOROSIS OF THE HIP

髋部骨质疏松症的治疗

• 批准号: 3546452
• 负责人: John CHRISTOPHER GALLAGHER
• 金额: $ 53.9万
• 依托单位: CREIGHTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1991
• 资助国家: 美国
• 起止时间: 1991-09-30 至 1996-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3546452
• 关键词: 1,25 dihydroxycholecalciferol; blood chemistry; bone density; calcium metabolism; clinical trials; dietary calcium; disease /disorder proneness /risk; drug adverse effect; estrogens; female; femur; hip; hip fractures; human old age (65+); human subject; human tissue; interview; longitudinal human study; malabsorption; nutrition related tag; osteoporosis; pathologic bone resorption; photon absorptiometry; placebos; postmenopause; progestins; spine; urinalysis

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.

股骨近端的骨质流失持续到九十年代， 质量导致增加的对断裂的敏感性。 的风险 骨折在80-90岁之间加速，因此33%的女性和17%的男性 髋骨骨折 髋部骨折会导致15%的死亡率， 20年内每年将耗资200亿美元。 两个主要因素在骨丢失中起作用。 雌激素缺乏症 绝经期与股骨的骨丢失增加有关。 在 60年代中期出现了第二个因素-钙吸收不良， 增加负钙平衡的程度，导致继发性 甲状旁腺功能亢进和骨质流失。 通过纠正雌激素缺乏， 钙吸收不良，可能会逆转骨丢失， 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岁之间的患者将用雌激素，1 α- 羟基维生素D2（1 α-OH-D2）或雌激素和1 α-OH-D2的组合 OH-D2治疗3年，试图逆转近端骨丢失 股骨 提示雌激素可抑制骨吸收， alpha-OH-D2将刺激骨形成，并且该组合将 比单一疗法更有效。 该研究将是双盲的， 安慰剂对照。 主要结果将是股骨近端的骨矿物质密度， 然而，骨骼的其他区域将被测量， 可能导致骨矿物质从皮质重新分布到 可以检测到小梁部位。 皮质骨的丢失会增加 断裂敏感性 从65岁开始扭转股骨近端骨丢失数年 可以保持骨密度高于骨折阈值， 降低骨折的风险。 这不仅会给我们 个人健康受益，而且大大降低了医疗费用。