Zavagli G, Ricci G, Tataranni G, Mapelli G, Abbasciano V
Istituto di Patologia Medica, Università di Ferrara, Italy.
Med Oncol Tumor Pharmacother. 1988;5(1):67-9. doi: 10.1007/BF03003183.
Some days after the administration of a third bolus of ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) a patient affected by immunoblastic lymphoma underwent a neurotoxic crisis. The episode lasted 1 week and was followed by a dramatic fall in plasma sodium (104 mEq I-1), associated with a proportionally lesser decrease in plasma chloride and phosphate. Despite the lowest plasma osmolality, detectable levels of circulating ADH were present. After 36 h the hyponatremic episode improved after the infusion of hypertonic sodium chloride. Nevertheless the patient lapsed into a hypotonic coma. The urinary concentrations of the main tubular enzymes (gamma-glutamyltranspeptidase, N-acetyl-glucosaminidase, alpha-glucosidase) proved very high and successively decreased slowly. The most likely cause of such hyponatremic episode is vinblastine. The drug acted through: (a) an already known inappropriate release of ADH, and (b) a hitherto unreported tubular lesion, which impaired the reabsorption of sodium and other coupled solutes.
在给予第三剂ABVD(阿霉素、博来霉素、长春花碱、达卡巴嗪)几天后,一名患有免疫母细胞淋巴瘤的患者发生了神经毒性危机。该发作持续了1周,随后血浆钠急剧下降(104 mEq I-1),同时血浆氯和磷酸盐的下降幅度相对较小。尽管血浆渗透压最低,但仍存在可检测水平的循环抗利尿激素(ADH)。36小时后,输入高渗氯化钠后低钠血症发作有所改善。然而,患者陷入了低渗性昏迷。主要肾小管酶(γ-谷氨酰转肽酶、N-乙酰氨基葡萄糖苷酶、α-葡萄糖苷酶)的尿浓度非常高,随后逐渐缓慢下降。这种低钠血症发作最可能的原因是长春花碱。该药物通过以下方式起作用:(a)已知的ADH不适当释放,以及(b)一种迄今未报道的肾小管病变,该病变损害了钠和其他偶联溶质的重吸收。