Okuno S, Inaba M, Nishizawa Y, Miki T, Inoue Y, Morii H
Endocrinol Jpn. 1987 Apr;34(2):299-307. doi: 10.1507/endocrj1954.34.299.
A 64-year-old woman was admitted for evaluation of hyponatremia. She was maintained on hypertonic saline administration. Without this therapy, the serum Na concentration decreased progressively to 127 mEq/L and the plasma osmolality to 254 mOsm/Kg H2O, on Day 3. At that time, the concentration of antidiuretic hormone (ADH) was as high as 3.5 pg/ml. A skull radiogram revealed an enlarged sella turcica. Computed tomography (CT) revealed a low density in the sella, and magnetic resonance imaging revealed equal intensity of the sella turcica and the cerebrospinal fluid. A diagnosis of empty sella syndrome was made by metrizamide cisternography in conjunction with CT scanning. A diagnosis of panhypopituitarism was made by endocrine function tests. 123I-thyroidal uptake was 6% when her serum TSH was 10.9 microU/ml, suggesting that she might also have primary hypothyroidism. When this patient was given glucocorticoid before levothyroxine replacement, her serum Na concentration rose up to about 140 mEq/L and a normal relationship between her plasma ADH level (2.4 pg/ml) and plasma osmolality (281 mOsm/kg H2O) was restored. Therefore, it was suggested that ADH hypersecretion induced by the glucocorticoid deficiency might in part contribute to the development of hyponatremia. This is the case of primary empty syndrome associated with panhypopituitarism, in whom initial symptom was caused by hyponatremia.
一名64岁女性因低钠血症入院评估。她接受高渗盐水治疗。若不进行此治疗,血清钠浓度在第3天逐渐降至127 mEq/L,血浆渗透压降至254 mOsm/Kg H₂O。此时,抗利尿激素(ADH)浓度高达3.5 pg/ml。头颅X线片显示蝶鞍增大。计算机断层扫描(CT)显示蝶鞍内低密度影,磁共振成像显示蝶鞍与脑脊液信号强度相等。通过甲泛葡胺脑池造影结合CT扫描诊断为空蝶鞍综合征。通过内分泌功能检查诊断为全垂体功能减退。当她的血清促甲状腺激素(TSH)为10.9 microU/ml时,¹²³I甲状腺摄取率为6%,提示她可能还患有原发性甲状腺功能减退。在该患者左甲状腺素替代治疗前给予糖皮质激素时,她的血清钠浓度升至约140 mEq/L,血浆ADH水平(2.4 pg/ml)与血浆渗透压(281 mOsm/kg H₂O)之间恢复了正常关系。因此,提示糖皮质激素缺乏诱导的ADH分泌过多可能部分导致了低钠血症的发生。这是一例与全垂体功能减退相关的原发性空蝶鞍综合征病例,其首发症状由低钠血症引起。