A Rare Case of Low-Dose Cyclophosphamide-Induced Symptomatic Hyponatremia

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Introduction: We report a case of severe acute symptomatic hyponatremia with generalized tonic clonic seizures after the first cycle of adjuvant chemotherapy with cyclophosphamide. Case Description: We present a case of 62-year-old woman who was diagnosed with breast cancer and underwent lumpectomy followed by first cycle of chemotherapy with cyclophosphamide, dexamethasone, and doxorubicin. She received low dose, 15 mg/kg or 1,030 mg IV Cyclophosphamide. On the day of chemotherapy her sodium was 144 mEq/L. The next day the patient had a seizure at home. While in the Emergency Department she had another witnessed seizure. On physical examination vital signs were normal, patient showed altered mental status with no focal deficits. Laboratory: Serum sodium 127 mEq/L, CBC was normal; LFT and other electrolytes were in a normal range. Her head CT was normal. Patient's urine osmolarity was 432 mmol/L and urine sodium was 116 mmol/L. These findings were suggestive of SIADH. Infusion of 300 ml of NaCl 3% and water restriction improved the symptoms and corrected hyponatremia within 24 hours. Discussion: Hyponatremia is a known but rare complication of cyclophosphamide. Initially it was thought that only high doses of cyclophosphamide (>40 mg/kg) could induce hyponatremia. However, cases of low-dose cyclophosphamide (<20 mg/kg), have been reported, though uncommon. We report a rare case of low dose cyclophosphamide-induced symptomatic hyponatremia. Our patient's rapid decline of sodium could have precipitated the seizure. Using hypertonic saline, hyponatremia resolved, and symptoms improved without neurological deficits. Cyclophosphamide-induced hyponatremia was first reported by Moses et al demonstrating antidiuretic hormone-like effect of Cyclophosphamide to retain water. More recent studies suggest a direct toxic effect of cyclophosphamide or its metabolites on renal collecting tubules and/or an antidiuretic hormone-like activity of cyclophosphamide metabolites. Thus, development of SIADH has been accepted as one of the mechanisms for cyclophosphamide-induced hyponatremia. Thus, physicians should have a low threshold to suspect cyclophosphamide-induced hyponatremia which can be life threatening.

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