Abstract / Summary
Abstract Central nervous system germinoma is highly curable, but very late relapse and chronic endocrine sequelae can complicate salvage treatment. Herein, we report a 22-year-old man with central diabetes insipidus and panhypopituitarism who developed biopsy-proven pure germinoma in the right intraorbital optic nerve 12 years after treatment for childhood suprasellar germinoma. The optic nerve lesion was outside the initial irradiation field. A hemorrhagic right middle cerebellar peduncle lesion was radiographically suspicious but unbiopsied; angiography showed no detectable vascular lesion. During ifosfamide, cisplatin, and etoposide salvage chemotherapy, symptomatic grade 4 hypotonic hyponatremia developed (serum sodium 118.4 mEq/L; osmolality 236 mOsm/kg). On rechallenge, recorded urine output rose from 1.40 L/day on cycle 2 day 0 to 4.25 L/day on day 3 and 9.75 L/day on day 4, accompanied by high spot urinary sodium concentrations. Desmopressin, hydrocortisone, and levothyroxine were continued. Because oral intake, intravenous volumes, net balance, objective volume status, and fractional urate excretion were unavailable, the episode was classified as a chemotherapy-associated mixed sodium–water disturbance with a suspected salt-wasting component rather than confirmed renal salt wasting. Hypertonic saline, isotonic fluids, oral salt, and serial serum/urine monitoring were used. Recurrent toxicity prompted discontinuation of cisplatin and ifosfamide and a switch to carboplatin plus etoposide. The high-output pattern was attenuated, although grade 3 hyponatremia persisted. This supportive strategy enabled completion of curative-intent chemotherapy and craniospinal irradiation. At the 1-year imaging assessment, complete response was maintained.