Koo W W, Antony G, Stevens L H
Am J Dis Child. 1984 Feb;138(2):172-5. doi: 10.1001/archpedi.1984.02140400054013.
Radiologic and biochemical abnormalities associated with nutritional hypophosphatemic rickets were discovered in a 945-g preterm infant despite daily supplementation with 800 to 1,600 IU of ergocalciferol (vitamin D2) and an elevated serum 25-hydroxyvitamin D concentration. Vitamin D supplementation was stopped, and the rickets was corrected by phosphorus supplement alone with the use of a unique technique of long-term, continuous nasogastric phosphorus infusion. Normophosphatemia was rapidly achieved and effectively maintained. Hypocalcemia did not occur at rates of infusion of 100 mg of elemental phosphorus per day. The data are consistent with specific phosphorus deficiency as the cause of rickets in this infant, rather than insufficient vitamin D intake or disturbed vitamin D metabolism. We speculated that continuous phosphorus infusion prevents the intermittent hyperphosphatemia of bolus phosphorus supplement and that continuous phosphorus infusion may be useful in the treatment of other hypophosphatemic states of infancy.
一名945克的早产婴儿尽管每日补充800至1600国际单位的麦角钙化醇（维生素D2）且血清25-羟基维生素D浓度升高，但仍出现了与营养性低磷性佝偻病相关的放射学和生化异常。停止补充维生素D，仅通过使用长期、持续鼻饲磷输注的独特技术补充磷来纠正佝偻病。迅速实现并有效维持了正常血磷水平。每天输注100毫克元素磷时未发生低钙血症。这些数据表明，该婴儿佝偻病的病因是特定的磷缺乏，而非维生素D摄入不足或维生素D代谢紊乱。我们推测，持续磷输注可预防大剂量补充磷时出现的间歇性高磷血症，且持续磷输注可能对治疗婴儿期的其他低磷血症状态有用。
