Jones G, Sambrook P N
Bone and Mineral Research Division, Garvan Institute for Medical Research, St Vincent's Hospital, Sydney, Australia.
Drug Saf. 1994 Jun;10(6):480-9. doi: 10.2165/00002018-199410060-00006.
Calcium homeostasis depends upon the interplay of intestinal calcium absorption, renal excretion and skeletal mobilisation of calcium, mediated through bone formation and resorption, which are closely coupled in the adult skeleton. Serum calcium is extremely important for maintenance of normal cellular functions and is regulated by the major calciotropic hormones, parathyroid hormone (PTH), 1,25-dihydroxy-vitamin D and calcitonin. Certain drugs can interfere with calcium metabolism by effects at different stages in calcium metabolism, and a knowledge of the mechanism of drug action is generally helpful in understanding the various resultant clinical skeletal syndromes. Corticosteroids, for example, have profound effects at multiple stages of calcium metabolism, resulting in decreased bone formation and enhanced bone resorption leading to accelerated osteoporosis. Drugs such as aluminium and anticonvulsants impair mineralisation, leading to osteomalacia. Other drugs, such as fluoride, are employed for their known effects on bone, but in excess dosage can be harmful by producing mineralisation defects. Management of these conditions will be discussed in this review.
钙稳态取决于肠道钙吸收、肾脏排泄以及骨骼对钙的动员之间的相互作用，这些过程通过骨形成和骨吸收来介导，在成人骨骼中它们紧密相关。血清钙对于维持正常细胞功能极为重要，并受主要的钙调节激素甲状旁腺激素（PTH）、1,25-二羟维生素D和降钙素的调节。某些药物可通过影响钙代谢的不同阶段来干扰钙代谢，了解药物作用机制通常有助于理解由此产生的各种临床骨骼综合征。例如，皮质类固醇在钙代谢的多个阶段具有深远影响，导致骨形成减少和骨吸收增强，进而导致骨质疏松加速。铝和抗惊厥药等药物会损害矿化，导致骨软化症。其他药物，如氟化物，因其对骨骼的已知作用而被使用，但过量使用可能会因产生矿化缺陷而有害。本文将讨论这些情况的管理。
