Valero M A, Leon M, Ruiz Valdepeñas M P, Larrodera L, Lopez M B, Papapietro K, Jara A, Hawkins F
Services of Endocrinology, University Hospital 12 de Octubre, Madrid, Spain.
Bone Miner. 1994 Jul;26(1):9-17. doi: 10.1016/s0169-6009(08)80158-4.
Osteoporosis is a well-known side-effect of chronic treatment with glucocorticoids. We have studied vertebral bone mineral density (BMD) and biochemical markers of bone metabolism in 30 patients diagnosed of Addison's disease (AD) to determine the effect of long-term replacement treatment with hydrocortisone (30 mg/day) or prednisone (7.5 mg/day). Lumbar bone mineral density was measured with dual energy X-ray absorptiometry in L-1-4 in two occasions, separated by 12 months. BMD in premenopausal women and men with AD was similar to healthy controls and postmenopausal women had slightly lower results. Rate of change of bone density followed up over a period of 12 months was -0.82%. Bone loss was not influenced by duration or type of steroid treatment. Biochemical parameters, serum calcium, alkaline phosphatase, osteocalcin, procollagen type I, PTH and 25(OH)vitamin D were within normal limits. Our results show that in patients with AD, after replacement with low doses of glucocorticoids there is no significative trabecular bone loss neither modifications in bone formation markers.
骨质疏松症是糖皮质激素长期治疗众所周知的副作用。我们研究了30例诊断为艾迪生病（AD）患者的椎骨骨密度（BMD）和骨代谢生化标志物，以确定氢化可的松（30毫克/天）或泼尼松（7.5毫克/天）长期替代治疗的效果。采用双能X线吸收法在两个时间点测量L-1至L-4节段的腰椎骨密度，间隔12个月。绝经前女性和男性AD患者的骨密度与健康对照相似，绝经后女性的结果略低。随访12个月期间骨密度变化率为-0.82%。骨质流失不受类固醇治疗持续时间或类型的影响。生化参数、血清钙、碱性磷酸酶、骨钙素、I型前胶原、甲状旁腺激素和25（OH）维生素D均在正常范围内。我们的结果表明，在AD患者中，低剂量糖皮质激素替代治疗后，没有明显的小梁骨丢失，骨形成标志物也没有改变。
