摘要（日本） 糖皮质激素诱导性骨质疏松（GIOP）的发生机制分为局部和全身作用。在局部作用中，GIOP重要机制之一是激素对骨形成有直接抑制作用，而全身作用机制是，由于激素抑制钙吸收和增加钙排泄，导致钙负性平衡，诱发继发性甲状旁腺功能亢进所致。本综述还介绍了GIOP的其他机制。从临床方面来说，本综述还评价了GIOP的血清学标记物，作为骨形成的标记物，骨钙素、I型前胶原N-末端肽和骨特异性碱性磷酸酶在GIOP降低，而作为骨吸收的标记物，I型胶原 N-末端肽和抗酒石酸酸性磷酸酶5b在GIOP增高，临床指南推荐，双膦酸酸盐是GIOP治疗的首选药物。重组的人甲状旁腺激素1-34——特立帕肽（Teriparatide）是有高骨折风险患者的治疗选择。抗核因子- β配体(RANKL)受体激活剂——狄诺塞麦（Denosumab）已批准为绝经后骨质疏松的治疗药物，临床试验证实对GIOP也有效。
附原文：Abstract Mechanisms of glucocorticoid-induced osteoporosis (GIOP) are categorized into local and systemic effects. In the local mechanisms, direct inhibitory effect of glucocorticoid on bone formation is thought to be one of the important mechanisms of GIOP. In contrast, secondary hyperparathyroidism induced by negative balance of calcium due to inhibition of absorption and increase of excretion is an important systemic mechanism of GIOP. Other mechanisms of GIOP are also shown in this review. From clinical points of view, serum markers for evaluation of GIOP have been discussed. Osteocalcin, procollagen type I N-terminal peptide, and bone-specific alkaline phosphatase as markers of bone formation are decreased in GIOP. Collagen I N-terminal telopeptide and tartrate resistent acid phosphatase isoform. 5b as markers of bone resorption are increased in GIOP. Clinical guidelines have recommended that bisphosphonate is the first choice for the treatment of GIOP. Teriparatide is recombinant human parathyroid hormone 1-34, which should be considered as a therapeutic option for those at high risk of bone fracture. Denosumab, an anti receptor activator of nuclear factor-β ligand approved as a drug for postmenopausal osteoporosis was also effective for GIOP in clinical trials.
引自：Kaneko K, Kawai S.Mechanisms and therapeutics of glucocorticoid-induced osteoporosis, 2011;34(3):138-48.