MON-331 Hypomagnesemia: A Preventable Electrolyte Disturbance from Epidermal Growth Factor Receptor Inhibitors

Abstract

Chemotherapy is a part of the treatment regimen for many different types of cancers and plays a foundational role in treating cancers. With an advent of epidermal growth factor (EGFR) inhibitor and its promising results, it has been widely incorporated in cancer treatment regimen. However, this monoclonal antibody has potential adverse drug reactions especially renal tubular toxicity. Since magnesium is one of the electrolytes that is highly regulated by renal tubular cells, hypomagnesemia is a common electrolyte disturbance in cancer patients. However, the cause of hypomagnesemia may be overlooked. Adequate magnesium supplement in a timely manner can prevent the consequences of hypomagnesemia. We report a case of an elderly man with newly diagnosed squamous cell carcinoma of the tongue with persistent hypomagnesemia after initiation of cetuximab. Magnesium supplement prevented severe hypomagnesemia and maintained serum magnesium. A 77-year-old Caucasian man with stage 3 chronic kidney disease was diagnosed with p16+ poorly differentiated invasive squamous cell carcinoma (cT2-3N2Mx) with basaloid features on the base of the tongue and received cetuximab. He developed acute kidney injury with an elevated serum creatinine up to 2 mg/dL from the baseline serum creatinine of 1.5 to 1.7 mg/dL. He had poor oral intake due to oropharyngeal lesions requiring nutritional supplementation via gastrostomy tube and intermittent intravenous 0.9% sodium chloride infusion. Since starting cetuximab, he had intermittent diarrhea and muscle weakness. Magnesium oxide 400 mg oral daily was an since initiation of cetuximab when serum magnesium a to decrease to 1.7 mg/dL. Throughout in timely months of cetuximab therapy, he had persistent borderline hypomagnesemia with a serum magnesium of 1.4 to 2.2 mg/dL despite receiving an increased magnesium oxide of 400 mg twice a day. Fractional excretion of magnesium (FEMg) was 12.2%. After completion of cetuximab therapy, his serum magnesium became normalized and serum creatinine trended down to 1.6 mg/dL. N/A Our patient started having hypomagnesemia since he received cetuximab therapy. Although there are several potential causes of hypomagnesemia including poor oral intake and diarrhea, high FEMg indicates renal magnesium wasting. Muscle weakness can a by persistent hypomagnesemia. Cetuximab, an EGFR inhibitor, causes impaired distal tubular magnesium reabsorption by inhibiting EGFR receptor at the basolateral membrane of the distal renal tubular epithelial cells which lead to inadequate activation of magnesium channel TRPM6, and subsequently renal magnesium loss. With an increase in the prevalence of malignancy, new chemotherapy agents have been incorporated widely in the cancer treatment, especially EFGR inhibitors. Magnesium plays an important role in maintaining normal cell function and hypomagnesemia results in neuromuscular, cardiovascular and metabolic manifestations. Therefore, proactive magnesium supplement can mitigate these serious consequences of hypomagnesemia until the chemotherapy is completed and hypomagnesemia is normalized.