Duran M J, Borst G C, Osburne R C, Eil C
Am J Med. 1984 Jan;76(1):151-4. doi: 10.1016/0002-9343(84)90764-2.
A 24-year-old woman presented with clinical features suggesting hypoparathyroidism: tetany, basal ganglia calcification, and a history of a seizure disorder. Hypocalcemia was present on admission despite therapy with calcium and vitamin D. Hormonal evaluation revealed undetectable parathormone levels and a normal cyclic AMP and phosphaturic response to parathormone infusion, suggesting the diagnosis of idiopathic hypoparathyroidism. Additional testing, however, revealed hypomagnesemia and elevated urinary magnesium levels. Normomagnesemia could not be consistently achieved despite oral magnesium administration. When the serum magnesium level was temporarily normalized via intravenous magnesium supplementation, parathormone levels rose into the normal range. These data indicate that the patient's hypomagnesemia was most likely due to renal magnesium loss. The normalization of her parathormone level during magnesium replenishment, along with the parathormone infusion data, suggests that this patient's hypomagnesemia was responsible for decreased parathormone synthesis and/or secretion, while target tissue responsiveness to parathormone was maintained.
一名24岁女性出现了提示甲状旁腺功能减退的临床特征:手足搐搦、基底节钙化以及癫痫病史。尽管接受了钙和维生素D治疗,但入院时仍存在低钙血症。激素评估显示甲状旁腺激素水平检测不到,且对甲状旁腺激素输注的环磷酸腺苷和磷尿反应正常,提示特发性甲状旁腺功能减退的诊断。然而,进一步检查发现低镁血症和尿镁水平升高。尽管口服镁剂,正常血镁水平仍无法持续维持。当通过静脉补充镁剂使血清镁水平暂时恢复正常时,甲状旁腺激素水平升至正常范围。这些数据表明,患者的低镁血症很可能是由于肾脏排镁所致。在补充镁期间甲状旁腺激素水平恢复正常,以及甲状旁腺激素输注数据表明,该患者的低镁血症导致甲状旁腺激素合成和/或分泌减少,而靶组织对甲状旁腺激素的反应性得以维持。