%0 Journal Article
%T Assessment of Ondansetron-Associated Hypokalemia in Pediatric Oncology Patients
%A Elsa Fiedrich
%A Vikram Sabhaney
%A Justin Lui
%A Maury Pinsk
%J ISRN Oncology
%D 2012
%R 10.5402/2012/798239
%X Objectives. Ondansetron is a 5-hydroxytryptamine (5-HT3, serotonin) receptor antagonist used as antiemetic prophylaxis preceding chemotherapy administration. Hypokalemia is a rare complication of ondansetron, which may be underreported due to confounding emesis and chemotherapy-induced tubulopathy. We performed a prospective cohort study to determine if ondansetron caused significant hypokalemia independently as a result of renal potassium wasting. Methods. Twelve patients were recruited, with ten completing the study. Blood and urine samples were collected before and after ondansetron administration in patients admitted for intravenous (IV) hydration and chemotherapy. Dietary histories and IV records were analyzed to calculate sodium and potassium balances. Results. We observed an expected drop in urine osmolality, an increase in urine sodium, but no statistically significant change in sodium or potassium balance before and after ondansetron. Conclusion. Ondansetron does not cause significant potassium wasting in appropriately hydrated and nutritionally replete patients. Careful monitoring of serum potassium is recommended in patients with chronic nutritional or volume status deficiencies receiving this medication. 1. Introduction Ondansetron is an antiemetic used as an adjunctive to chemotherapy in pediatric oncology patients. It is a selective 5-HT3 receptor antagonist which has an excellent safety profile and is efficacious [1, 2]. A side effect infrequently reported is the development of hypokalemia [3]. Hypokalemia may be a result of ondansetron itself [3¨C5], an effect of chemotherapy on renal tubular function [6], a result of emesis-induced alkalosis [7], or a combination of factors. Based on in vitro data, ondansetron has the capacity to cause hypokalemia by affecting renal tubular physiology [4]. Ondansetron acts at two levels in the nephron. First, at the level of the Loop of Henle, ondansetron downregulates the Na+-K+-2Cl-(NKCC2) cotransporter, which results in increased sodium delivery to the distal nephron. This in turn necessitates K+ excretion, via the ROMK potassium channel to facilitate the electroneutral reabsorption of sodium via the epithelial sodium channel (ENaC) from the distal nephron, leading to K+ wasting. Second, throughout the nephron, and in particular the distal tubule, ondansetron upregulates the Na+-K+ ATPase. This exacerbates the renal K wasting by lowering intracellular sodium levels in distal tubular cells expressing ENaC thereby further increasing tubular sodium entry at this segment. This ultimately requires
%U http://www.hindawi.com/journals/isrn.oncology/2012/798239/