Lee Paul, Greenfield Jerry R
Department of Endocrinology, St Vincent's Hospital and Diabetes and Metabolism Branch, Garvan Institute of Medical Research, Sydney, NSW, Australia.
Clin Endocrinol (Oxf). 2015 Aug;83(2):157-61. doi: 10.1111/cen.12730. Epub 2015 Feb 16.
Addison's disease is associated with low bone mineral density and increased risk of hip fractures. Causes are multifactorial, contributed by underlying adrenocortical hormonal deficiency, associated autoimmune endocrinopathies, electrolyte disturbances and, in some patients, supraphysiologic glucocorticoid replacement. Recent realization of physiologic cortisol production rate has revised downwards glucocorticoid replacement dosages. Meanwhile, new research has emerged suggesting complex interplay between sodium and calcium homoeostasis under the influence of mineralocorticoid and parathyroid hormone that may impact bone health. As the prevalence of Addison's disease is rising, and osteoporosis and fractures are associated with significant morbidity and increased mortality, attention to bone preservation in Addison's disease is of clinical relevance and importance. We suggest an approach to bone health in Addison's disease integrating physiologic adrenocortical hormonal replacement with electrolyte and mineral homoeostasis optimization.
艾迪生病与低骨矿物质密度及髋部骨折风险增加相关。其病因是多因素的，由潜在的肾上腺皮质激素缺乏、相关的自身免疫性内分泌病、电解质紊乱以及在一些患者中使用超生理剂量的糖皮质激素替代治疗所致。近期对生理皮质醇产生率的认识已下调了糖皮质激素替代剂量。与此同时，新的研究表明，在盐皮质激素和甲状旁腺激素的影响下，钠和钙稳态之间存在复杂的相互作用，这可能会影响骨骼健康。随着艾迪生病患病率的上升，且骨质疏松症和骨折与显著的发病率及死亡率增加相关，关注艾迪生病患者的骨骼保护具有临床相关性和重要性。我们建议采用一种针对艾迪生病骨骼健康的方法，将生理肾上腺皮质激素替代与电解质和矿物质稳态优化相结合。
