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Plasma Levels and Therapeutic Effect of 25-Hydroxycholecalciferol in Epileptic Patients taking Anticonvulsant Drugs

机译:服用抗惊厥药物的癫痫患者血浆中25-羟胆钙化固醇的水平和治疗效果

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摘要

Plasma levels of 25-hydroxycholecalciferol (25-HCC) were measured by a specific competitive protein-binding assay. Mean levels in both normal London adults and adolescent schoolchildren were 16 ng/ml and the mean level in a group of epileptic patients on high-dosage anticonvulsant therapy was 5 ng/ml, (difference from normals P < 0·001). Two further epileptic patients, with well-marked anticonvulsant osteomalacia, were treated with small doses of 25-HCC during full metabolic balance studies; rapid healing followed administration of 25-HCC by mouth in doses of 10-45 μg daily, which is well below the effective dose range of calciferol in this condition. These findings provided further evidence that anticonvulsant osteomalacia results from hepatic enzyme induction which, by increasing the metabolism of cholecalciferol to inactive compounds, lowers 25-HCC levels in patients whose dietary vitamin D intake and exposure to sunlight are otherwise adequate. Results also indicated that under certain circumstances 25-HCC may have considerably stronger antirachitic potency in man than has hitherto been recognized.
机译:通过特异性竞争蛋白结合测定法测量血浆25-羟胆钙化固醇(25-HCC)的水平。伦敦正常成年人和青少年学童的平均水平均为16 ng / ml,接受高剂量抗惊厥治疗的一组癫痫患者的平均水平为5 ng / ml(与正常人的差异P <0·001)。在充分的代谢平衡研究期间,另外两名癫痫患者伴有明显的抗惊厥性骨软化症,接受了小剂量的25-HCC治疗;每天口服10-45μg剂量的25-HCC可以迅速治愈,这远低于在这种情况下钙化甾醇的有效剂量范围。这些发现提供了进一步证据,证明抗惊厥性骨软化症是由肝酶诱导产生的,通过增加胆钙化固醇代谢成非活性化合物的代谢,可以降低饮食中维生素D摄入量和阳光充足的患者的25-HCC水平。结果还表明,在某些情况下,25-HCC可能比迄今公认的对人具有更强的抗树根作用。

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