Audran M
Presse Med. 1994 Feb 12;23(6):271-3.
Long-term corticosteroid therapy is the most frequent and most severe cause of iatrogenic osteoporosis. Hypocalcaemia, subsequent to the induced negative calcium balance, may lead to secondary hyperparathyroidism. Corticosteroids also affect bone itself, probably by disrupting the production of growth factors. Bone resorption increases and bone formation decreases leading to a reduction in total bone mass. The relative immobilization resulting from the corticoid-induced myopathy or the underlying disease may accelerate the process. On the average, after one year of treatment, 5% of the bone mass is lost, and loss may reach as much as 10 to 30% at certain sites. Nearly 40% of all subjects on long-term corticosteroids suffer fractures. Other iatrogenic causes include anticonvulants which perturb phosphocalcium metabolism, 1-thyroxin which leads to bone loss when administered for hormone substitution, gonadotropin-releasing hormone antagonists which inhibit the hypophyseal-ovarian axis, tamoxifen (used in the treatment of breast cancer) which has an oestrogen-like effect, and other circumstances such as chemotherapy and long-term heparin. The gravity of iatrogenic osteroporosis thus requires preventive measures. Calcium and vitamin D supplements can compensate for impaired intestinal absorption of calcium but have no effect on bone density. One-alpha hydroxyl derivatives have been suggested but their effect remains controversial. Calcitriol can prevent bone loss in the lumbar vertebrae but hypercalcaemia occurs in one-fourth of the cases, limiting its use. Recent reports have shown that anti-oestroclastic agents may be useful. Nandrolone decaonate would have a favourable effect on bone loss but also causes virilization. In patent osteoporosis, fluorine can be combined with calcium resulting in increased lumbar bone density. Calcitonin and calcium can also be combined to induce a rise in bone density. The long-term effects of these treatments in terms of reduced fracture risk remain to be determined. A better understanding of the adverse effects of the different classes of corticosteroids is essential for optimal treatment. In cases requiring long-term therapy implicating the risk of iatrogenic osteoporosis, bone density quantitation can be a valuable means of evaluating bone loss, and of adapting preventive or corrective measures.
长期使用皮质类固醇疗法是医源性骨质疏松最常见、最严重的病因。因钙负平衡导致的低钙血症可能会引发继发性甲状旁腺功能亢进。皮质类固醇还会影响骨骼本身，可能是通过干扰生长因子的产生。骨吸收增加而骨形成减少，导致骨总量降低。由皮质激素诱发的肌病或基础疾病导致的相对活动减少可能会加速这一进程。平均而言，治疗一年后，骨量会流失5%，某些部位的流失量可能高达10%至30%。近40%长期使用皮质类固醇的患者会发生骨折。其他医源性病因包括扰乱磷钙代谢的抗惊厥药、用于激素替代治疗时导致骨质流失的左甲状腺素、抑制垂体-卵巢轴的促性腺激素释放激素拮抗剂、具有雌激素样作用的他莫昔芬（用于治疗乳腺癌），以及化疗和长期使用肝素等其他情况。因此，医源性骨质疏松的严重性需要采取预防措施。补充钙和维生素D可以弥补肠道对钙吸收的受损，但对骨密度没有影响。有人提出使用1-α羟基衍生物，但其效果仍存在争议。骨化三醇可以预防腰椎的骨质流失，但四分之一的病例会出现高钙血症，限制了其使用。最近的报告表明，抗破骨细胞药物可能有用。癸酸诺龙对骨质流失可能有有利影响，但也会导致男性化。在原发性骨质疏松中，氟可以与钙结合，从而增加腰椎骨密度。降钙素和钙也可以联合使用以提高骨密度。这些治疗在降低骨折风险方面的长期效果仍有待确定。更好地了解不同类别皮质类固醇的不良反应对于优化治疗至关重要。在需要长期治疗且存在医源性骨质疏松风险的情况下，骨密度定量可以作为评估骨质流失以及调整预防或纠正措施的重要手段。
