Tauchmanovà Libuse, Pivonello Rosario, De Martino Maria Cristina, Rusciano Andrea, De Leo Monica, Ruosi Carlo, Mainolfi Ciro, Lombardi Gaetano, Salvatore Marco, Colao Annamaria
Department of Molecular and Clinical Endocrinology and Oncology, Federico II University of Naples, Naples, Italy.
Eur J Endocrinol. 2007 Sep;157(3):359-66. doi: 10.1530/EJE-07-0137.
Glucocorticoid-induced osteoporosis is the most frequent cause of secondary osteoporosis. Nevertheless, limited data are available on bone status in patients with endogenous cortisol excess. This study is aimed at investigating the role of sex steroids and severity of hypercortisolism on bone mineral density (BMD) and prevalence of vertebral fractures in female patients.
Cross-sectional, case-control study.
Seventy-one consecutive women were enrolled: 36 with overt hypercortisolism (26 with ACTH-secreting pituitary adenoma and 10 with cortisol-secreting adrenal tumor) and 35 with subclinical hypercortisolism due to adrenal incidentalomas. They were compared with 71 matched controls.
At diagnosis, we measured serum cortisol, FSH, LH, estradiol, testosterone, androstenedione and DHEAS, and urinary cortisol excretion. BMD was determined by dual energy X-ray absorptiometry at the lumbar spine and femoral neck. Vertebral fractures were investigated by a semiquantitative scoring method.
Between women with overt and subclinical hypercortisolism BMD values and prevalence of any vertebral (69 vs 57%, P = 0.56), clinical (28 vs 11.4%, P = 0.22), and multiple vertebral fractures (36 vs 31%, P = 0.92) did not differ. Among patients with subclinical hypercortisolism, amenorrhoic women had a lower BMD (P = 0.035) and more frequent vertebral fractures (80 vs 40%; P = 0.043) when compared with the eumenorrhoic ones. Among women with overt hypercortisolism, there was no difference in lumbar BMD (P = 0.37) and prevalence of fractures (81 vs 60%; P = 0.26) between those amenorrhoic and eumenorrhoic. By logistic regression analysis, lumbar spine BMD values and cortisol-to-DHEAS ratio were the best predictors of vertebral fractures (P < 0.01).
Vertebral fractures are very common in women with endogenous cortisol excess, regardless of its severity. The deleterious effects of hypercortisolism on the spine may be partly counterbalanced by DHEAS increase at any degree of cortisol excess, and by preserved menstrual cycles in women with subclinical but not in those with overt hypercortisolism.
糖皮质激素性骨质疏松是继发性骨质疏松最常见的病因。然而，关于内源性皮质醇增多症患者骨状况的数据有限。本研究旨在调查性激素和皮质醇增多症严重程度对女性患者骨密度（BMD）及椎体骨折患病率的作用。
横断面病例对照研究。
纳入71例连续的女性：36例为显性皮质醇增多症（26例为分泌促肾上腺皮质激素的垂体腺瘤，10例为分泌皮质醇的肾上腺肿瘤），35例为肾上腺意外瘤所致亚临床皮质醇增多症。将她们与71例匹配的对照进行比较。
诊断时，测定血清皮质醇、促卵泡激素（FSH）、促黄体生成素（LH）、雌二醇、睾酮、雄烯二酮和硫酸脱氢表雄酮（DHEAS），以及尿皮质醇排泄量。采用双能X线吸收法测定腰椎和股骨颈的骨密度。采用半定量评分法调查椎体骨折情况。
显性和亚临床皮质醇增多症女性之间，骨密度值以及任何椎体骨折（69%对57%，P = 0.56）、临床骨折（28%对11.4%，P = 0.22）和多发性椎体骨折（36%对31%，P = 0.92）的患病率均无差异。在亚临床皮质醇增多症患者中，与月经正常的女性相比，闭经女性的骨密度较低（P = 0.035）且椎体骨折更频繁（80%对40%；P = 0.043）。在显性皮质醇增多症女性中，闭经和月经正常者之间腰椎骨密度（P = 0.37）和骨折患病率（81%对60%；P = 0.26）无差异。通过逻辑回归分析，腰椎骨密度值和皮质醇与DHEAS比值是椎体骨折的最佳预测指标（P < 0.01）。
内源性皮质醇增多症女性中椎体骨折非常常见，无论其严重程度如何。在任何程度的皮质醇增多症中，DHEAS增加以及亚临床皮质醇增多症女性（而非显性皮质醇增多症女性）保留的月经周期可能部分抵消皮质醇增多症对脊柱的有害影响。
