Mason Rebecca S, Rybchyn Mark S, Brennan-Speranza Tara C, Fraser David R
Physiology, Bosch Institute, School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, 2006, Australia.
School of Public Health, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, 2006, Australia.
Fac Rev. 2020 Dec 3;9:19. doi: 10.12703/r/9-19. eCollection 2020.
Severe vitamin D deficiency-25-hydroxyvitamin D (25OHD) concentrations below around 25-30 nmol/L-may lead to growth plate disorganization and mineralization abnormalities in children (rickets) and mineralization defects throughout the skeleton (osteomalacia) and proximal muscle weakness. Both problems are reversed with vitamin D treatment. Apart from this musculoskeletal dysfunction at very low vitamin D levels, there is apparent inconsistency in the available data about whether concentrations of 25OHD below around 50 nmol/L cause muscle function impairment and increase the risk of fracture. This narrative review provides evidence to support the contention that improving vitamin D status, up to around 50 nmol/L, plays a small causal role in optimizing bone and muscle function as well as reducing overall mortality.
严重维生素D缺乏——25-羟维生素D（25OHD）浓度低于约25 - 30 nmol/L——可能导致儿童生长板紊乱和矿化异常（佝偻病）、全身骨骼矿化缺陷（骨软化症）以及近端肌无力。这两个问题通过维生素D治疗均可得到逆转。除了在极低维生素D水平下出现的这种肌肉骨骼功能障碍外，关于25OHD浓度低于约50 nmol/L是否会导致肌肉功能损害并增加骨折风险，现有数据明显不一致。这篇叙述性综述提供了证据，支持以下观点：将维生素D状态改善至约50 nmol/L，在优化骨骼和肌肉功能以及降低总体死亡率方面起很小的因果作用。
