Habener J F, Mahaffey J E
Annu Rev Med. 1978;29:327-42. doi: 10.1146/annurev.me.29.020178.001551.
A rapidly growing understanding of the biochemical and physiological processes that underlie the metabolism of vitamin D has provided new insights into the pathogenesis of oestomalacia. Many of the vitamin D--resistant osteomalacia syndromes can now be explained on the basis of defects in the metabolic conversion of vitamin D to the biologically active dihydroxylated metabolite 1,25(OH)2D and perhaps, in some instances, to impairement of the actions of 1,25(OH)2D on target tissues. The availability of this new information has made possible the synthesis of 1-hydroxylated forms of the vitamin for therapeutic use in states of vitamin D resistance. Although many questions regarding the pathogenesis and most effective approaches in the management of osteomalacia remain unanswered, considerable progress has been made in this direction as a result of continued research on the subject.
对维生素D代谢所涉及的生化和生理过程的迅速深入了解，为骨软化症的发病机制提供了新的见解。现在，许多维生素D抵抗性骨软化综合征可以基于维生素D向具有生物活性的二羟基化代谢物1,25(OH)2D的代谢转化缺陷来解释，在某些情况下，可能还与1,25(OH)2D对靶组织作用的受损有关。这些新信息的可得性使得合成维生素的1-羟基化形式用于维生素D抵抗状态的治疗成为可能。尽管关于骨软化症发病机制和最有效治疗方法的许多问题仍未得到解答，但由于对该主题的持续研究，在这方面已经取得了相当大的进展。
