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一名既往闭经的骨质疏松症跑步运动员骨密度恢复正常。

Normalization of bone density in a previously amenorrheic runner with osteoporosis.

作者信息

Fredericson Michael, Kent Kyla

机构信息

Department of Orthopaedic Surgery, Division of Physical Medicine and Rehabilitation, Stanford University School of Medicine, CA 94305, USA.

出版信息

Med Sci Sports Exerc. 2005 Sep;37(9):1481-6. doi: 10.1249/01.mss.0000177561.95201.8f.

Abstract

PURPOSE

To examine changes in bone mineral density (BMD) and bone mineral content (BMC) in relation to pharmacological and nutritional interventions in a distance runner diagnosed with the female athlete triad of disordered eating, amenorrhea, and osteoporosis.

METHODS

BMD of the lumbar spine (L2-L4) and total proximal femur were measured from ages 22.9 to 30.8 yr using dual x-ray absorptiometry (DXA).

RESULTS

At age 22.9, the patient presented with primary amenorrhea, low body weight (BMI: 15.8 kg.m(-2)), and low BMD in the spine (74% of normal, T score: -2.50) and hip (80% of normal, T score: -1.54). For the next 2 yr, the patient took oral contraceptives to induce menses, but continued to maintain a low weight. Her BMD remained unchanged. At age 25.1 yr, she decided to gain weight and improve her nutrition, resulting in small increases in spinal BMD (+1.1%), hip BMD (+1.6%), and total body BMC (+7.6%) in 4 months. From ages 25.4 to 30.8 yr, the patient continued to gain weight, eventually reaching a healthy BMI of 21.3 kg.m(-2); correspondingly, since baseline, her BMD had increased 25.5% in the spine and 19.5% in the hip, bringing her BMD to within normal values (spine: 94% of normal, hip: 96% of normal).

CONCLUSION

This case illustrates that even if skeletal development is interrupted in adolescence, there is still the potential for "catch-up" in BMD well into the third decade of life. Reversal of large bone density deficits in this patient can be attributed to improved nutrition and weight gain but not to hormone replacement.

摘要

目的

研究一名被诊断患有饮食失调、闭经和骨质疏松三联征的女性长跑运动员,其骨矿物质密度(BMD)和骨矿物质含量(BMC)在药物和营养干预后的变化情况。

方法

使用双能X线吸收法(DXA)测量该患者在22.9岁至30.8岁期间腰椎(L2-L4)和股骨近端的BMD。

结果

22.9岁时,该患者出现原发性闭经、体重过低(体重指数:15.8kg·m⁻²),脊柱BMD低(正常的74%,T值:-2.50),髋部BMD低(正常的80%,T值:-1.54)。在接下来的2年里,患者服用口服避孕药诱导月经,但体重仍维持在较低水平,其BMD保持不变。25.1岁时,她决定增加体重并改善营养,4个月内脊柱BMD增加了1.1%,髋部BMD增加了1.6%,全身BMC增加了7.6%。从25.4岁到30.8岁,患者体重持续增加,最终达到健康的体重指数21.3kg·m⁻²;相应地,自基线以来,她的脊柱BMD增加了25.5%,髋部BMD增加了19.5%,使其BMD恢复到正常范围内(脊柱:正常的94%,髋部:正常的96%)。

结论

该病例表明,即使青春期骨骼发育中断,在生命的第三个十年仍有BMD“追赶”的潜力。该患者骨密度大幅 deficits 的逆转可归因于营养改善和体重增加,而非激素替代。 (注:原文中“large bone density deficits”表述不太准确,可能是“large bone density decrease”之类的意思,但按要求未做修改)

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