Jubiz W, Haussler M R, McCain T A, Tolman K G
J Clin Endocrinol Metab. 1977 Apr;44(4):617-21. doi: 10.1210/jcem-44-4-617.
Recent evidence has linked altered plasma vitamin D metabolite levels to the reported occurrence of hypocalcemia and other metabolic abnormalities in patients receiving anticonvulsant drugs. We have measured plasma levels of 25-hydroxyvitamin D (25-(OH)D) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) in institutionalized patients on diphenylhydantoin (Dilantin) and/or phenobarbital therapy. Values were compared with those obtained in institutionalized patients receiving no drugs and with normal ambulatory subjects. Although plasma 25-(OH)D levels were lower in the patients on drugs, a deficiency of 1,25-(OH)2D, the tissue active metabolite of vitamin D, was not present. These results indicate that in patients taking anticonvulsant drugs, the serum calcium, phosphorus, alkaline phosphatase and parathyroid hormone (PTH) abnormalities are not caused by a defective formation of 1,25-(OH)2D.
近期证据表明,接受抗惊厥药物治疗的患者血浆维生素D代谢产物水平改变与低钙血症及其他代谢异常的发生有关。我们测定了接受苯妥英钠(大仑丁)和/或苯巴比妥治疗的住院患者血浆25-羟维生素D(25-(OH)D)和1,25-二羟维生素D(1,25-(OH)₂D)的水平。将这些值与未接受药物治疗的住院患者以及正常门诊受试者的值进行了比较。尽管服药患者的血浆25-(OH)D水平较低,但并未出现维生素D的组织活性代谢产物1,25-(OH)₂D缺乏的情况。这些结果表明,服用抗惊厥药物的患者血清钙、磷、碱性磷酸酶和甲状旁腺激素(PTH)异常并非由1,25-(OH)₂D生成缺陷所致。