BACKGROUND: --Hyponatremia is frequently seen during the treatment of acute lymphoblastic leukemia: its causes are numerous. This work aims to present a case in whom hyponatremia was possibly due to an increased secretion of atrial natriuretic factor. CASE REPORT: --A 3 week-old baby was admitted because of malignant hemopathy. A diagnosis of acute lymphoblastic leukemia was rapidly made and the patient was firstly given alkaline diuresis, urate-oxidase and corticosteroids. Vincristine and daunorubicin were associated one week later. Insertion of a central intravenous line in the right subclavicular artery failed so that this catheter was finally inserted into the left jugular vein. Natremia was 126 mmol/l at that time and dramatically decreased within 24 hours to 109 mmol/l without net changes in water and electrolytic input. At that time, sodium urinary excretion was 6 mmol/kg/day (diuresis: 420 mlF/day). There was no hemodynamic changes, nor digestive or cardiac manifestations. Ultrasonography showed that the left superior cava vein drained into the right cardiac atrium. The catheter was withdrawn and the patient was given sodium supplementation permitting complete and definitive cure of hyponatremia within 2 days. CONCLUSIONS: --All usual causes of hyponatremia having been ruled out in this patient, we postulate that hyponatremia was due to direct stimulation of atrial natriuretic peptide through an increase in atrial pressure secondary to the catheter insertion near the cardiac atrium.
BACKGROUND: --Hyponatremia is frequently seen during the treatment of acute lymphoblastic leukemia: its causes are numerous. This work aims to present a case in whom hyponatremia was possibly due to an increased secretion of atrial natriuretic factor. CASE REPORT: --A 3 week-old baby was admitted because of malignant hemopathy. A diagnosis of acute lymphoblastic leukemia was rapidly made and the patient was firstly given alkaline diuresis, urate-oxidase and corticosteroids. Vincristine and daunorubicin were associated one week later. Insertion of a central intravenous line in the right subclavicular artery failed so that this catheter was finally inserted into the left jugular vein. Natremia was 126 mmol/l at that time and dramatically decreased within 24 hours to 109 mmol/l without net changes in water and electrolytic input. At that time, sodium urinary excretion was 6 mmol/kg/day (diuresis: 420 mlF/day). There was no hemodynamic changes, nor digestive or cardiac manifestations. Ultrasonography showed that the left superior cava vein drained into the right cardiac atrium. The catheter was withdrawn and the patient was given sodium supplementation permitting complete and definitive cure of hyponatremia within 2 days. CONCLUSIONS: --All usual causes of hyponatremia having been ruled out in this patient, we postulate that hyponatremia was due to direct stimulation of atrial natriuretic peptide through an increase in atrial pressure secondary to the catheter insertion near the cardiac atrium.