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Abstract: PUB216

Oxaliplatin-Induced Hypomagnesemia

Session Information

Category: Trainee Case Report

  • 1500 Onco-Nephrology

Authors

  • Khanin, Yuriy, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Sachdeva, Mala, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Uppal, Nupur N., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
Introduction

Platinum based chemotherapy is used in the treatment of several malignancies including lung, colorectal, ovarian, breast, head/neck, bladder and testicular cancers. We present a case of profound electrolyte disturbances in the setting of oxaliplatin therapy.

Case Description

78-year-old Caucasian male diagnosed with pancreatic cancer three months prior to admission, on oxaliplatin therapy, presented to emergency room with new onset atrial fibrillation. He was afebrile, hemodynamically stable, and without respiratory distress. He endorsed a history of chronic diarrhea since beginning chemotherapy, however he began to have weakness and dizziness three days prior to admission. Laboratory analysis revealed hypokalemia: 2.9mmol/L, hypomagnesemia: 0.8mg/dL, hypocalcemia: 6.2mg/dL with ionized calcium of 0.8mmol/L. Urine magnesium (Mg) was 10.2mg/dL, and urinary fractional excretion of Mg was calculated to be 2.75%, consistent with renal Mg wasting. The atrial fibrillation resolved after adequate repletion of electrolytes, and he was transitioned from intravenous to oral supplements. He was discharged home on oral calcium carbonate, magnesium oxide, and potassium chloride supplements. Repeat labs one week post hospitalization showed stable potassium of 4.2 mmol/L and calcium 9.3mg/dl, however hypomagnesemia persisted to 1.3mg/dL, requiring an increase in Mg supplementation.

Discussion

Platinum based chemotherapy agents including cisplatin and to a lesser extent carboplatin have been known to cause electrolyte disturbances, in particular hypomagnesemia. However, case reports of oxaliplatin associated magnesium wasting are limited. This can be partially explained by the fact that oxaliplatin is protein bound and cannot readily accumulate in the kidney tubules to mediate nephrotoxicity, as is the case with carboplatin which is not protein bound. Magnesium deficiency is an under recognized entity, however it can precipitate potentially fatal cardiovascular dysfunction. Clinicians need to be aware of this potential adverse effect related to oxaliplatin therapy, as its prompt diagnosis and treatment can prevent the associated complications.