Lemaire V, Miravet L, Bordier P, Ryckewaert A
Nouv Presse Med. 1975 Dec 20;4(44):3121-4.
A case of osteomalacia, with no cause apart from the ingestion of anti-convulsants, is reported. As was shown by a study with tritium labelled vitamin D, the metabolism of the latter was accelerated in this case in comparison with deficiency type osteomalacia. This lends support to the hypothesis that anti-convulsant medications, acting via a hepatic enzyme induction process, cause increased transformation of vitamin D into inactive metabolites, thus explaining a certain deficiency in vitamin D in treated epileptics, a deficiency state which requires treatment.
报告了一例除摄入抗惊厥药外无其他病因的骨软化症病例。正如用氚标记的维生素D进行的研究所显示的那样,与缺乏型骨软化症相比,该病例中维生素D的代谢加快。这支持了以下假设:抗惊厥药物通过肝酶诱导过程起作用,导致维生素D向无活性代谢产物的转化增加,从而解释了接受治疗的癫痫患者中存在一定程度的维生素D缺乏,这种缺乏状态需要治疗。