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.
Life-threatening hyponatremia caused by vinblastine
ZAVAGLI, Giorgio
Primo
;RICCI, GiorgioSecondo
;MAPELLI, GiorgioPenultimo
;ABBASCIANO, Vincenzo CataldoUltimo
1988
Abstract
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.File | Dimensione | Formato | |
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