Zelissen P M, Croughs R J, van Rijk P P, Raymakers J A
Department of Endocrinology, University Hospital Utrecht, The Netherlands.
Ann Intern Med. 1994 Feb 1;120(3):207-10. doi: 10.7326/0003-4819-120-3-199402010-00005.
To study the influence of glucocorticoid replacement therapy on bone mineral density.
Cross-sectional.
University hospital in the Netherlands.
91 patients with Addison disease who had been receiving glucocorticoid replacement therapy for a mean of 10.6 years (range, 0.5 to 36.5 years).
Bone mineral density of the lumbar spine and both femoral necks using a dual-energy x-ray absorptiometer and basal serum concentrations of adrenocorticotropin, gonadal hormones, and adrenal androgens.
Decreased bone mineral density (less than 2 standard deviations [SD] of the mean value of an age-matched reference population) was found in 10 of 31 men (32%; 95% Cl, 17% to 51%) and in 4 of 60 women (7%; Cl, 2% to 16%). No statistically significant differences were found between men and women with regard to age, duration of glucocorticoid substitution, or glucocorticoid dose, either in absolute quantities or when expressed per kilogram of body weight. However, in men with decreased bone mineral density, the daily hydrocortisone dose per kilogram of body weight (0.43 +/- 0.08 mg/kg; mean +/- SD) was significantly (P = 0.032) higher than in men with normal bone mineral density (0.35 +/- 0.10 mg/kg). After correction for possible confounding variables, a significant linear correlation was found between hydrocortisone dose per kilogram of body weight and bone mineral density of the lumbar spine in the men (regression coefficient, -0.86; Cl, -1.60 to -0.13; P = 0.029) but not in the women.
Long-term treatment with standard replacement doses of glucocorticoids may induce bone loss in men with Addison disease. Adjustment of glucocorticoid therapy to the lowest acceptable dose is mandatory in Addison disease, and regular measurement of bone mineral density may be helpful in identifying men at risk for the development of osteoporosis.
研究糖皮质激素替代疗法对骨密度的影响。
横断面研究。
荷兰的大学医院。
91例艾迪生病患者，平均接受糖皮质激素替代治疗10.6年（范围0.5至36.5年）。
使用双能X线吸收仪测量腰椎和双侧股骨颈的骨密度，以及促肾上腺皮质激素、性腺激素、肾上腺雄激素的基础血清浓度。
31名男性中有10名（32%；95%可信区间，17%至51%）和60名女性中有4名（7%；可信区间，2%至16%）骨密度降低（低于年龄匹配参考人群平均值的2个标准差[SD]）。男性和女性在年龄、糖皮质激素替代治疗持续时间或糖皮质激素剂量方面，无论是绝对量还是按每千克体重计算，均未发现统计学上的显著差异。然而，骨密度降低的男性每千克体重的氢化可的松每日剂量（0.43±0.08mg/kg；平均值±标准差）显著高于（P = 0.032）骨密度正常的男性（0.35±0.10mg/kg）。在校正可能的混杂变量后，发现男性每千克体重的氢化可的松剂量与腰椎骨密度之间存在显著的线性相关性（回归系数，-0.86；可信区间，-1.60至-0.13；P = 0.029），而女性则未发现。
用标准替代剂量的糖皮质激素进行长期治疗可能会导致艾迪生病男性出现骨质流失。在艾迪生病中，将糖皮质激素治疗调整至最低可接受剂量是必要的，定期测量骨密度可能有助于识别有骨质疏松症发生风险的男性。
