Adam, a 17-year-old boy, was treated with prazepam and olanzapine, 5 mg b.i.d. He was admitted to our intensive care unit after he had ingested 15 tablets (75 mg) of olanzapine and 7.5 mg of prazepam in a suicide attempt. He had no history of polydipsia. A comprehensive drug screen detected no other substances. He had mild CNS depression with otherwise normal vital signs. Within the first 24 hours of admission, Adam developed a high urinary output (5400 ml/24 hours), with diluted urine. At that time, his urine density was 1.004, his urine osmolality was 166 mosmol/kg H₂O, and his serum osmolality was 287 mosmol/kg H₂O. His sodium blood level rose from 132 mmol/liter at admission to 141 mmol/liter when Adam was polyuric. His glucose blood level was within the normal range. His blood concentration of ADH was 3.1 pg/ml (normal range=0.0–8.0), and his thyroid-stimulating hormone level was 6.01 μU/ml (normal range=0.2–3.5), with normal total triiodothyronine and thyroxine values. Adam’s polyuria corrected after the intravenous administration of 4 μg of desmopressin (and 2 μg 12 hours later). He was discharged from the intensive care unit on day 3. No recurrence of polyuria was noted at the 1-month follow-up. Magnetic resonance imaging of the hypothalamic-pituitary area, performed 2 months after discharge, was normal.