Kruse K, Kracht U, Göpfert G
Neuropediatrics. 1982 Feb;13(1):3-9. doi: 10.1055/s-2008-1059588.
The response of kidney and bone to parathyroid extract (PTE) was investigated in 8 epileptic children on long-term treatment with primidone in combination with phenytoin or other anticonvulsant drugs. The results indicate a dissociation between normal and cyclic AMP excretion and disturbed renal handling of phosphate which resembles type II pseudohypoparathyroidism suggesting an anticonvulsant drug related inhibition of cyclic AMP-induced phosphaturia. It is speculated that antiepileptic drugs may provoke renal conservation of phosphate which may explain the relative low incidence of manifest rickets or osteomalacia in site of low 25-hydroxy-vitamin D levels in epileptic patients. A normal bone response of PTE indicates that antiepileptic treatment with phenobarbital and phenytoin does not affect PTH-stimulated bone resorption in the investigated patients.
对8名长期服用扑米酮联合苯妥英或其他抗惊厥药物治疗的癫痫患儿,研究了肾脏和骨骼对甲状旁腺提取物(PTE)的反应。结果表明,正常和环磷酸腺苷排泄之间存在分离,肾脏对磷酸盐的处理受到干扰,这类似于II型假性甲状旁腺功能减退,提示抗惊厥药物相关的环磷酸腺苷诱导的磷尿抑制。据推测,抗癫痫药物可能会促使肾脏保留磷酸盐,这可能解释了癫痫患者尽管25-羟基维生素D水平较低,但明显佝偻病或骨软化症的发病率相对较低的原因。PTE的正常骨反应表明,在所研究的患者中,苯巴比妥和苯妥英的抗癫痫治疗不影响甲状旁腺激素刺激的骨吸收。