Endocrine Abstracts

Introduction: Hyponatraemia is one of the most common electrolyte abnormalities that may be drug-induced either as a result of inappropriate antidiuretic hormone secretion (SIADH) or excessive sodium loss. SIADH is diagnosed on the basis of low plasma osmolarity associated with inappropriately concentrated urine.

Case report: A 67-year-old woman was admitted to hospital because of progressive confusion and perseveration. Her medical history included bipolar disorder, arterial hypertension and gastritis. Her drug therapy on admission was chlorpromazine (Prazine), sertaline (Zoloft), fluphenazine (Moditen), lisinopril (Laaven), and pantoprazole (Controloc). On physical examination the patient appeared euvolemic without evidence of congestion or dehydration. The CT scan of the brain and chest X-ray were normal. Laboratory tests revealed severe hyponatraemia (111 mmol/l) and the infusion of a 3% saline was administered. Approximately 24 h after admission the patient’s serum sodium increased to 120 mmol/l and her mental status improved. Hyponatraemia, low serum osmolarity (258 mOsm/kg), high urine osmolarity (398 mOsm/kg), high urine sodium (64 mmol/l) together with normal renal, thyroid and adrenal function, all supported diagnosis of SIADH. Therefore, fluid restriction was instituted and her chronic drug therapy suspended. Serum sodium level increased progressively and low doses of new psychotropics re-initiated (risperidone and escitalopram). At the time of hospital discharge, serum sodium level was 133 mmol/l. A follow-up serum sodium 3 weeks after discharge was within the limits of normal range.

Conclusion: Effective clinical management of drug-induced hyponatraemia can be handled through understanding of the underlying pathophysiologic mechanisms and awareness of the adverse effects of certain pharmaceutical compounds on serum sodium levels.