Basha B, Rao D S, Han Z H, Parfitt A M
Bone and Mineral Metabolism Research Laboratory, Bone and Joint Center, Henry Ford Health System, Detroit, Michigan, USA.
Am J Med. 2000 Mar;108(4):296-300. doi: 10.1016/s0002-9343(99)00460-x.
Osteomalacia due to vitamin D depletion is believed to be rare in the United States because of the routine fortification of milk and other dairy products with vitamin D. We present a series of patients with histologically verified osteomalacia due to vitamin D depletion to emphasize the need for more careful and systematic surveillance of patients at risk of this metabolic bone disease.
Between 1989 and 1994, 17 patients with osteomalacia due to vitamin D depletion were seen in the Bone and Mineral Division of Henry Ford Health System, Detroit. All patients had a transiliac bone biopsy after in vivo double tetracycline labeling. Biochemical indexes of vitamin D nutritional status, parathyroid function, markers of bone turnover, and bone mineral density were assessed at the time of bone biopsy. The duration of symptoms, the lag between the cause of vitamin D depletion and the development of symptoms, and the radiologic findings were recorded.
Osteomalacia was suspected by the referring physician in only 4 of the 17 patients, although a gastrointestinal disorder that can lead to vitamin D depletion was present in every patient. Thirteen of the patients had sustained at least one osteoporotic fracture (wrist, spine, or hip), and most had low appendicular and axial bone mineral density. All patients had one or more biochemical abnormalities consistent with vitamin D depletion. In 4 patients, a progressive rise in the serum alkaline phosphatase level was recorded but was not investigated until the patient presented with bone pain, muscle weakness, or fracture.
Osteomalacia due to vitamin D depletion appears not to be suspected or diagnosed promptly in susceptible patients, perhaps because their physicians were not sufficiently aware of this condition.
由于牛奶和其他乳制品常规添加维生素D，在美国，维生素D缺乏所致的骨软化症被认为较为罕见。我们报告一组经组织学证实为维生素D缺乏所致骨软化症的患者，以强调对这种代谢性骨病高危患者需要更仔细、系统地进行监测。
1989年至1994年间，底特律亨利·福特医疗系统骨与矿物质科诊治了17例维生素D缺乏所致骨软化症患者。所有患者在进行体内双四环素标记后接受了髂骨活检。在骨活检时评估维生素D营养状况、甲状旁腺功能、骨转换标志物及骨密度的生化指标。记录症状持续时间、维生素D缺乏原因与症状出现之间的间隔时间以及放射学检查结果。
尽管17例患者均存在可导致维生素D缺乏的胃肠道疾病，但转诊医生仅对其中4例怀疑有骨软化症。13例患者至少发生过一次骨质疏松性骨折（腕部、脊柱或髋部），大多数患者四肢和轴向骨密度较低。所有患者均有一项或多项与维生素D缺乏相符的生化异常。4例患者血清碱性磷酸酶水平呈进行性升高，但直到患者出现骨痛、肌肉无力或骨折才进行检查。
维生素D缺乏所致骨软化症在易感患者中似乎未被及时怀疑或诊断，可能是因为其医生对这种情况认识不足。
