Department of Medicine, Endocrinology Division, University of Padua, Via Ospedale 105, Padua, 35128, Italy.
Department of Cardiac, Thoracic and Vascular Sciences, Biostatistics, Epidemiology and Public Health Unit, University of Padua, Via Loredan 18, Padua, 35131, Italy.
Endocrine. 2018 Feb;59(2):319-329. doi: 10.1007/s12020-017-1380-8. Epub 2017 Aug 9.
to assess bone damage and metabolic abnormalities in patients with Addison's disease given replacement doses of glucocorticoids and mineralocorticoids.
A total of 87 patients and 81 age-matched and sex-matched healthy controls were studied. The following parameters were measured: urinary cortisol, serum calcium, phosphorus, creatinine, 24-h urinary calcium excretion, bone alkaline phosphatase, parathyroid hormone, serum CrossLaps, 25 hydroxyvitamin D, and 1,25 dihydroxyvitamin D. Clear vertebral images were obtained with dual-energy X-ray absorptiometry in 61 Addison's disease patients and 47 controls and assessed using Genant's classification.
Nineteen Addison's disease patients (31.1%) had at least one morphometric vertebral fracture, as opposed to six controls (12.8%, odds ratio 3.09, 95% confidence interval 1.12-8.52). There were no significant differences in bone mineral density parameters at any site between patients and controls. In Addison's disease patients, there was a positive correlation between urinary cortisol and urinary calcium excretion. Patients with fractures had a longer history of disease than those without fractures. Patients taking fludrocortisone had a higher bone mineral density than untreated patients at all sites except the lumbar spine.
Addison's disease patients have more fragile bones irrespective of any decrease in bone mineral density. Supra-physiological doses of glucocorticoids and longer-standing disease (with a consequently higher glucocorticoid intake) might be the main causes behind patients' increased bone fragility. Associated mineralocorticoid treatment seems to have a protective effect on bone mineral density.
评估给予糖皮质激素和盐皮质激素替代剂量的 Addison 病患者的骨损伤和代谢异常。
共研究了 87 例患者和 81 例年龄和性别匹配的健康对照者。测量了以下参数:尿皮质醇、血清钙、磷、肌酐、24 小时尿钙排泄量、骨碱性磷酸酶、甲状旁腺激素、血清 CrossLaps、25 羟维生素 D 和 1,25 二羟维生素 D。在 61 例 Addison 病患者和 47 例对照者中,使用双能 X 射线吸收法获得清晰的椎体图像,并使用 Genant 分类进行评估。
19 例(31.1%)Addison 病患者至少有一处形态计量学椎体骨折,而对照组为 6 例(12.8%),比值比为 3.09,95%置信区间为 1.12-8.52。患者与对照组之间任何部位的骨密度参数均无显著差异。在 Addison 病患者中,尿皮质醇与尿钙排泄呈正相关。有骨折的患者疾病史比无骨折的患者更长。服用氟氢可的松的患者除腰椎外,各部位的骨密度均高于未治疗的患者。
无论骨密度是否降低,Addison 病患者的骨骼都更脆弱。超生理剂量的糖皮质激素和更长时间的疾病(随之而来的糖皮质激素摄入增加)可能是患者骨脆弱性增加的主要原因。联合使用盐皮质激素治疗似乎对骨密度有保护作用。