Chiodini I, Torlontano M, Carnevale V, Trischitta V, Scillitani A
Unit of Endocrinology and Diabetology, Department of Medical Sciences, Fondazione Ospedale Maggiore Policlinico, IRCCS, University of Milan, Milan, Italy.
J Endocrinol Invest. 2008 Mar;31(3):267-76. doi: 10.1007/BF03345601.
Overt endogenous glucocorticoid excess is a well-recognized cause of bone loss and osteoporotic fractures. Cortisol excess inhibits bone formation, increases bone resorption, impairs calcium absorption from the gut, and affects the secretion of several hormones (in particular gonadotropins and GH), cytokines, and growth factors, influencing bone metabolism. The glucocorticoid excess mainly affects trabecular bone, leading to vertebral fractures in up to 70% of patients. Osteoporotic fractures may be the presenting symptom of an otherwise silent glucocorticoid excess and can precede the diagnosis of hypercortisolism by up to 2 yr. The removal of glucocorticoid excess leads to a recovery of bone mass which is, however, often incomplete and delayed, although it reduces the risk of osteoporotic fractures. Bisphosphonate therapy has been suggested to be useful in maintaining bone mass in these patients. Subclinical hypercortisolism, a condition of impaired hypothalamic- adrenal-axis homeostasis without the classical signs and symptoms of glucocorticoid excess, is a recently defined entity, which has been shown to be associated to increased bone resorption, bone loss, and high prevalence of vertebral fractures regardless of gonadal status. However, data about the effect of this subtle glucocorticoid excess on bone are still scarce and conflicting. Moreover, it is not yet known whether removing the cause of subclinical hypercortisolism leads to a recovery of bone mass and reduces the risk of osteoporotic fractures. Finally, recent data suggest that subclinical hypercortisolism is a common and underrated finding in patients with established osteoporosis. In summary, it is crucial to evaluate the risk of osteoporosis and fractures in patients with glucocorticoid excess; on the other hand, it also seems advisable to screen for glucocorticoid excess patients with osteoporotic fractures without known secondary causes of osteoporosis.
明显的内源性糖皮质激素过多是公认的骨质流失和骨质疏松性骨折的原因。皮质醇过多会抑制骨形成、增加骨吸收、损害肠道对钙的吸收，并影响多种激素（特别是促性腺激素和生长激素）、细胞因子和生长因子的分泌，从而影响骨代谢。糖皮质激素过多主要影响小梁骨，导致高达70%的患者发生椎体骨折。骨质疏松性骨折可能是隐匿性糖皮质激素过多的首发症状，且可在皮质醇增多症诊断前长达2年出现。去除过多的糖皮质激素可使骨量恢复，然而，尽管这降低了骨质疏松性骨折的风险，但骨量恢复往往不完全且延迟。双膦酸盐治疗已被认为对维持这些患者的骨量有用。亚临床皮质醇增多症是一种下丘脑-肾上腺轴稳态受损的情况，无糖皮质激素过多的典型体征和症状，是最近定义的一种病症，已显示无论性腺状态如何，其都与骨吸收增加、骨质流失和椎体骨折的高患病率相关。然而，关于这种轻微糖皮质激素过多对骨骼影响的数据仍然稀少且相互矛盾。此外，尚不清楚去除亚临床皮质醇增多症的病因是否会导致骨量恢复并降低骨质疏松性骨折的风险。最后，最近的数据表明亚临床皮质醇增多症在已确诊的骨质疏松症患者中是一种常见且被低估的发现。总之，评估糖皮质激素过多患者的骨质疏松和骨折风险至关重要；另一方面，对于无已知继发性骨质疏松病因的骨质疏松性骨折患者筛查糖皮质激素过多似乎也是可取的。
