Christiansen C, Rodbro P, Munck O
Br Med J. 1975 May 17;2(5967):363-5. doi: 10.1136/bmj.2.5967.363.
In 54 epileptic outpatients treated for at least one year with anticonvulsants the bone mineral content (B.M.C.), an estimate of total body calcium, and serum calcium were measured before and during treatment with three doses of cholecalciferol (vitamin D3; 200, 100, and 50 mu-g daily) and 25-hydroxycholecalciferol (25-OHD3; 40, 20, and 10 mu-g daily) for 12 weeks. The results, when compared with the effects of calciferol (vitamin D2; 200, 100, and 50 mu-g daily) in 40 epileptic outpatients, showed different actions in anticonvulsant osteomalacia of vitamin D2 on the one hand and vitamin D3 and 25-OHD3 on the other. In the patients who received vitamin D2 an increase in B.M.C. was found whereas serum calcium was unchanged. The patients who received vitamin D3 or 25-OHD3 showed an increase in serum calcium but unchanged values of B.M.C. The results suggest that liver enzyme induction cannot alone explain anticonvulsant osteomalacia.
对54例接受抗惊厥药物治疗至少一年的癫痫门诊患者,在使用三种剂量的胆钙化醇(维生素D3;每日200、100和50μg)和25-羟胆钙化醇(25-OHD3;每日40、20和10μg)治疗12周之前及治疗期间,测量了骨矿物质含量(B.M.C.,全身钙含量的估计值)和血清钙。与40例癫痫门诊患者使用钙化醇(维生素D2;每日200、100和50μg)的效果相比,结果显示维生素D2、维生素D3和25-OHD3在抗惊厥性骨软化症中的作用不同。接受维生素D2的患者骨矿物质含量增加,而血清钙未改变。接受维生素D3或25-OHD3的患者血清钙增加,但骨矿物质含量值未改变。结果表明,肝酶诱导不能单独解释抗惊厥性骨软化症。