Leonard Mary B, Feldman Harold I, Shults Justine, Zemel Babette S, Foster Bethany J, Stallings Virginia A
Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
N Engl J Med. 2004 Aug 26;351(9):868-75. doi: 10.1056/NEJMoa040367.
Glucocorticoids suppress bone formation, impair growth, and induce obesity. We determined the effects of long-term treatment with glucocorticoids on bone mineral content in children with glucocorticoid-sensitive nephrotic syndrome, a disorder with minimal known independent effects on bone.
We performed dual-energy x-ray absorptiometry of the whole body and spine in 60 children and adolescents with the nephrotic syndrome and 195 control subjects. We used linear regression analysis of log-transformed values to compare the bone mineral content in patients with that in controls.
Patients had received an average of 23,000 mg of glucocorticoids and were shorter (P=0.008) and had a greater body-mass index (P<0.001) than controls. The bone mineral content of the spine, adjusted for bone area, age, sex, degree of maturation (Tanner stage), and race, did not differ significantly between patients and controls (ratio, 0.99; 95 percent confidence interval, 0.96 to 1.02; P=0.51). After adjustment for the z score for body-mass index, the bone mineral content of the spine was significantly lower in patients than in controls (0.96; 95 percent confidence interval, 0.92 to 0.99; P=0.01). Whole-body bone mineral content, adjusted for height, age, sex, degree of maturation, and race, was significantly higher in patients than in controls (ratio, 1.11; 95 percent confidence interval, 1.05 to 1.18; P<0.001); however, the addition of the z score for body-mass index to the model eliminated the association with the nephrotic syndrome (ratio, 0.99; 95 percent confidence interval, 0.94 to 1.03; P=0.55).
Intermittent treatment with high-dose glucocorticoids during growth does not appear to be associated with deficits in the bone mineral content of the spine or whole body relative to age, bone size, sex, and degree of maturation. Glucocorticoid-induced increases in body-mass index were associated with increased whole-body bone mineral content and maintenance of the bone mineral content of the spine.
糖皮质激素会抑制骨形成、阻碍生长并导致肥胖。我们确定了长期使用糖皮质激素治疗对糖皮质激素敏感型肾病综合征患儿骨矿物质含量的影响,该疾病对骨骼的已知独立影响极小。
我们对60例肾病综合征患儿及青少年和195名对照者进行了全身和脊柱的双能X线吸收测定。我们使用对数转换值的线性回归分析来比较患者与对照者的骨矿物质含量。
患者平均接受了23,000毫克糖皮质激素治疗,身高低于对照者(P = 0.008),体重指数高于对照者(P < 0.001)。在根据骨面积、年龄、性别、成熟度(坦纳分期)和种族进行调整后,患者与对照者脊柱的骨矿物质含量无显著差异(比值为0.99;95%置信区间为0.96至1.02;P = 0.51)。在根据体重指数的z评分进行调整后,患者脊柱的骨矿物质含量显著低于对照者(0.96;95%置信区间为0.92至0.99;P = 0.01)。在根据身高、年龄、性别、成熟度和种族进行调整后,患者全身的骨矿物质含量显著高于对照者(比值为1.11;95%置信区间为1.05至1.18;P < 0.001);然而,在模型中加入体重指数的z评分后消除了与肾病综合征的关联(比值为0.99;95%置信区间为0.94至1.03;P = 0.55)。
在生长期间间歇性使用高剂量糖皮质激素似乎与相对于年龄、骨大小、性别和成熟度而言脊柱或全身的骨矿物质含量不足无关。糖皮质激素引起的体重指数增加与全身骨矿物质含量增加及脊柱骨矿物质含量维持有关。