Shafer R B, Nuttall F Q
J Clin Endocrinol Metab. 1975 Dec;41(06):1125-9. doi: 10.1210/jcem-41-6-1125.
Calcium and folic acid absorption were studied in 28 adult male epileptics on chronic anticonvulsant therapy. In 16 patients on diphenylhydantoin alone, calcium absorption was abnormal in 9. In 12 patients on both diphenylhydantoin and phenobarbital, calcium absorption was abnormal in 3 patients. Folic acid (3H-PGA) absorption was normal in all but one patient, while serum folate (less than 6.4 ng/ml) was reduced in all patients. Hypocalcemia (less than 8.5 mg/100 ml) occurred in only 2 patients, while serum alkaline phosphatase was elevated in 7 patients. These findings support the proposal that rickets and osteomalacia reported in patients on chronic anticonvulsant therapy results from reduced calcium absorption. The effect of these drugs appears to be the acceleration of the metabolism of vitamin D and an increase in the excretion of polar metabolites. This may result in reduced levels of 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol which are necessary for normal absorption of calcium. Since calcium absorption may be impaired secondary to a relative vitamin D deficiency, a supplemental increase in vitamin D intake by patients on anticonvulsant drugs is recommended.
对28名接受慢性抗惊厥治疗的成年男性癫痫患者的钙和叶酸吸收情况进行了研究。在仅服用苯妥英钠的16名患者中,9人钙吸收异常。在同时服用苯妥英钠和苯巴比妥的12名患者中,3人钙吸收异常。除1名患者外,所有患者的叶酸(3H-PGA)吸收均正常,而所有患者的血清叶酸(低于6.4 ng/ml)均降低。仅2名患者出现低钙血症(低于8.5 mg/100 ml),而7名患者血清碱性磷酸酶升高。这些发现支持了以下观点:慢性抗惊厥治疗患者中报告的佝偻病和骨软化症是由钙吸收减少所致。这些药物的作用似乎是加速维生素D的代谢并增加极性代谢产物的排泄。这可能导致正常钙吸收所必需的25-羟胆钙化醇和1,25-二羟胆钙化醇水平降低。由于钙吸收可能因相对维生素D缺乏而受损,建议抗惊厥药物治疗的患者补充增加维生素D的摄入量。