Godang K, Ueland T, Bollerslev J
Department of Medical Endocrinology, National University Hospital, N-0027 Oslo, Norway.
Eur J Endocrinol. 1999 Aug;141(2):126-31. doi: 10.1530/eje.0.1410126.
It is well established that chronic excess of glucocorticoids has negative effects on bone and collagen turnover, and that secondary osteoporosis is a known clinical complication of endogenous Cushing's syndrome (CS). The aim of the present study was to evaluate bone dimension and bone mineral content in relation to biochemical markers of bone and collagen turnover, in a consecutive series of 23 patients with endogenous CS (18 with pituitary adenoma and 5 with adrenal tumor; 17 women, 6 men; mean age 39.7+/-2.8 (S.E. M.) and 44.3+/-3.1 years respectively), compared with 23 age-, sex- and body mass index-matched healthy controls. Bone mineral densities were uniformly reduced in the different regions analyzed: lumbar spine (16.1%, P<0.001), femoral neck (15.2%, P<0.001), total body (11.5%, P<0.001), and the subregions of arms (8.4%, P<0.05), legs (10.1%, P<0.05) and trunk (15.8%, P<0.001). Similar results were observed for bone mineral content, although these were less prominent. The calculated area was significantly decreased in trunk (13.8%, P<0.01) and total body (11.6%, P<0.05). Serum levels of osteocalcin were significantly decreased (28%, P<0.03) in patients with CS. No significant differences were observed for the formative markers carboxyterminal propeptide of type I procollagen and aminoterminal propeptide of type I procollagen. Markers of bone resorption, serum Crosslaps and carboxyterminal cross-linked telopeptide of type I collagen were increased in patients compared with controls, although only significantly for Crosslaps (P<0.02). No correlations between formative and resorptive markers were found in the patients, but in controls, the formative markers were positively correlated with resorptive markers. In conclusion, bone dimension and bone mineral content of the entire skeleton are found to be decreased in endogenous CS. As judged by biochemical markers of bone remodeling, this is caused by decreased bone formation and an increased bone resorption.
长期过量的糖皮质激素对骨骼和胶原蛋白代谢具有负面影响，继发性骨质疏松是内源性库欣综合征（CS）已知的临床并发症，这一点已得到充分证实。本研究的目的是评估23例连续的内源性CS患者（18例垂体腺瘤患者和5例肾上腺肿瘤患者；17例女性，6例男性；平均年龄分别为39.7±2.8（标准误）岁和44.3±3.1岁）的骨尺寸和骨矿物质含量，并与23例年龄、性别和体重指数相匹配的健康对照者进行比较，同时分析其与骨和胶原蛋白代谢生化标志物的关系。在所分析的不同区域，骨矿物质密度均一致降低：腰椎（降低16.1%，P<0.001）、股骨颈（降低15.2%，P<0.001）、全身（降低11.5%，P<0.001）以及手臂各亚区域（降低8.4%，P<0.05）、腿部（降低10.1%，P<0.05）和躯干（降低15.8%，P<0.001）。骨矿物质含量也观察到类似结果，尽管不太明显。计算得出的面积在躯干（降低13.8%，P<0.01）和全身（降低11.6%，P<0.05）显著减小。CS患者血清骨钙素水平显著降低（降低28%，P<0.03）。I型前胶原羧基末端前肽和I型前胶原氨基末端前肽等形成标志物未观察到显著差异。与对照组相比，患者的骨吸收标志物血清交联C末端肽和I型胶原羧基末端交联肽有所升高，不过仅交联C末端肽有显著差异（P<0.02）。患者中未发现形成标志物与吸收标志物之间存在相关性，但在对照组中，形成标志物与吸收标志物呈正相关。总之，内源性CS患者整个骨骼的骨尺寸和骨矿物质含量均降低。从骨重塑的生化标志物判断，这是由骨形成减少和骨吸收增加所致。
