Ikeda K, Moriyasu H, Yasaka M, Oita J, Yamaguchi T
Rinsho Shinkeigaku. 1994 Sep;34(9):911-3.
We report an 82-year-old retired man who developed syndrome of inappropriate secretion of ADH (SIADH) caused by sodium valproate (VPA). He had been taking VPA for treatment of symptomatic epilepsy due to cardioembolic stroke. Although he was clinically asymptomatic, he was found to have decreased level of serum sodium concentration (128 mEq/l). Association of hyponatremia, normal urinary sodium concentration, high urine osmolality and increased concentration of serum ADH strongly suggested the presence of SIADH. There were no underlying disorders which can cause SIADH, such as malignant neoplasm with autonomous ADH release, non-malignant pulmonary diseases and active disorders of the central nervous system. Eight days after discontinuation of VPA administration serum sodium level increased (142 mEq/l) to the normal level. Then, we started the administration of VPA again to confirm that VPA was responsible for developing hyponatremia. As a result, he developed SIADH with hyponatremia (128 mEq/l) again, which improved after discontinuation of the administration. Therefore, we concluded that the SIADH might have been caused by administration of VPA. This is the first report on adverse effect of VPA causing SIADH.
我们报告一例82岁退休男性，因丙戊酸钠（VPA）引发抗利尿激素分泌不当综合征（SIADH）。他因心源性栓塞性卒中导致症状性癫痫而一直服用VPA。尽管他临床上无症状，但发现其血清钠浓度水平降低（128 mEq/l）。低钠血症、尿钠浓度正常、高尿渗透压以及血清抗利尿激素浓度升高共同强烈提示存在SIADH。不存在可导致SIADH的潜在疾病，如伴有自主性抗利尿激素释放的恶性肿瘤、非恶性肺部疾病以及中枢神经系统的活动性疾病。停用VPA给药8天后，血清钠水平升至正常水平（142 mEq/l）。然后，我们再次开始给予VPA以确认VPA是导致低钠血症的原因。结果，他再次出现伴有低钠血症（128 mEq/l）的SIADH，停药后病情改善。因此，我们得出结论，SIADH可能是由VPA给药引起的。这是关于VPA导致SIADH不良反应的首例报告。
