Dear Editor, A 66-year-old woman who had developed acute promyelocytic leukemia was admitted with bicytopenia and administered all-trans-retinoic acid (45 mg/m), idarubicin (12 mg/m for 3 days), and cytarabine (Ara C 100 mg/m for 5 days). She first obtained remission 40 days after the administration of induction therapy. Then she was administered two courses of consolidation therapy (first course: Ara C 200 mg/m for 5 days and mitoxantrone 7 mg/m for 3 days; second course: Ara C 150 mg/m for 5 days and daunorubicin 40 mg/m for 3 days), resulting in complete remission. Before the third course, she was administered intrathecal chemotherapy [IT; methotrexate (MTX) 15 mg, Ara C 40 mg, prednisolone (PSL) 10 mg]. Chemotherapy was performed after the administration of IT. She daily ingested almost 2,500 ml of liquid, which contained an infusion of drip, and her urine totaled from 1,600 to 3,700 ml (average of 2,600 ml). She developed hyponatremia after the administration of IT. On the 5th day of IT, the patient developed general fatigue followed by a gradual disturbance of consciousness. As indicated in Fig. 1, her serum sodium level had fallen to 109 mEq/l (normal range 135 to 147 mEq/l), and plasma osmolarity was 229.5 mOsm/kg H2O (normal range 280 to 300 mOsm/kg H2O) without edema. After treatment with hypertonic saline infusion and minocycline hydrochloride (MINO), she gradually regained consciousness. On the 7th day of IT, her serum sodium level had recovered to 130 mEq/l. Plasma osmolarity was still 277 mOsm/kg H2O, urine osmolarity was 578 mOsm/kg H2O (normal range 500 to 800 mOsm/kg H2O), and her ADH level was 1.0 pg/ml (normal range 0.3 to 3.5 pg/ml). Magnetic resonance imaging (MRI) of the pituitary gland showed only neurohypophysis (lobus posterior) (Fig. 2). Her symptoms and abnormal laboratory data completely disappeared 1 month after the IT. Inappropriate secretion of ADH (SIADH) is characterized by water retention, hyponatremia, and central nervous system symptoms. SIADH can be induced by various causes, including central nervous disorders, endocrine diseases, paraneoplastic syndromes, and anticancer agents such as vincristine and cyclophosphamide [1–4]. On the other hand, MTX and PSL have not been reported to be the causative agents of SIADH. Just a single investigator reported that one of thirteen patients with a high dosage of intravenous Ara C (3–7.5 g/m) developed SIADH, but not in a patient with IT [5]. This case lacked any viral infection or disease recurrence, and the administration of IT was only evident after the development of SIADH. One reason the patient developed SIADH is thought to reflect the Ann Hematol (2007) 86:149–150 DOI 10.1007/s00277-006-0199-9
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