Hahn T J, Halstead L R, DeVivo D C
Calcif Tissue Int. 1979 Aug 24;28(1):17-22. doi: 10.1007/BF02441213.
Vitamin D and mineral metabolism status was examined in five children maintained chronically on combined ketogenic diet-anticonvulsant drug therapy (KG), and the results compared to those obtained in 18 patients treated with anticonvulsant drugs alone (AD) and 15 normal controls. KG patients exhibited biochemical findings of vitamin D deficiency osteomalacia: decreased serum 25-hydroxyvitamin D (25OHD) and calcium concentrations, elevated serum alkaline phosphatase and parathyroid hormone concentrations, decreased urinary calcium and increased urinary hydroxyproline excretion, and decreased bone mass. Although the KG and AD groups demonstrated similar reductions in serum 25OHD concentration, the KG patients exhibited a significantly greater reduction in bone mass. In response to vitamin D supplementation (5000 IU/day), mean bone mass in the KG group increased by 8.1 +/- 0.9% (P less than 0.001) over a 12-month period. These results suggest that ketogenic diet and anticonvulsant drug therapy have additive deleterious effects on bone mass and that these effects are partially reversible by vitamin D treatment.
对长期采用生酮饮食 - 抗惊厥药物联合治疗(KG)的5名儿童的维生素D和矿物质代谢状况进行了检查,并将结果与18名单独接受抗惊厥药物治疗(AD)的患者以及15名正常对照者的结果进行了比较。KG组患者表现出维生素D缺乏性骨软化症的生化表现:血清25 - 羟维生素D(25OHD)和钙浓度降低,血清碱性磷酸酶和甲状旁腺激素浓度升高,尿钙减少,尿羟脯氨酸排泄增加,骨量减少。虽然KG组和AD组血清25OHD浓度均有相似程度的降低,但KG组患者的骨量减少更为显著。在补充维生素D(5000 IU/天)后,KG组的平均骨量在12个月内增加了8.1±0.9%(P<0.001)。这些结果表明,生酮饮食和抗惊厥药物治疗对骨量有累加的有害影响,并且这些影响可通过维生素D治疗部分逆转。