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Esomeprazole/valaciclovir Hyponatraemia and hypouricaemia secondary to syndrome of inappropriate secretion of antidiuretic hormone: case report

A 78-year-old woman developed hyponatraemia and hypouricaemia secondary to syndrome of inappropriate secretion of antidiuretic hormone (SIADH) during treatment with esomeprazole and valaciclovir [dosages not stated; not all indications and routes stated]. The woman with hyponatraemia was referred to the Nephrology Department for evaluation. She was admitted 6 days previously to the otorhinolaryngology Department due to sudden onset of left facial paralysis. She had history of hypothyroidism being treated with levothyroxine sodium [levothyroxine]. Laboratory tests showed serum sodium levels of 135 mEq/L. She was diagnosed with left Bell’s palsy. She started receiving unspecified oral glucocorticoids and esomeprazole to prevent glucocorticoid-induced gastric ulcer. Additionally, she started receiving oral valaciclovir for 7 days. On hospitalisation day 6, she developed consciousness impairment. Laboratory tests revealed a serum sodium level of 103 mEq/L (hyponatraemia), a urine sodium level of 64.8 mEq/L, a urine potassium level of 43.6 mEq/L and a urine osmolality of 450 mOsm/kg H2O. Hypouricaemia occurred concomitantly with hyponatraemia. Then, she was referred to the Nephrology Department. During hospitalisation, she ate about 50% of her meals and took about 500–700mL of fluid in addition to meals. She also denied vomiting, polydipsia or diarrhoea. The vital signs were unremarkable. Physical examination revealed no peripheral oedema and no abnormal heart or respiratory sounds. Her history and physical examination indicated that she was euvolaemic. Additional laboratory investigations ruled out hypothyroidism or adrenal insufficiency. Inadequate oral intake might have contributed to the onset of hyponatraemia; however, it was unlikely that this alone caused such a sudden drop in serum sodium levels from 135 to 103 mEq/L. Antidiuretic hormone levels were elevated. Therefore, SIADH was suggested as an underlying aetiology of hyponatraemia. The woman was treated with fluid restriction and administration of 3% hypertonic sodium chloride [saline] 0.6 mL/kg/hour owing to the fact that her urine tonicity exceeded serum sodium, which indicated that free water excretion was impaired and spontaneous improvement of serum sodium levels seemed unlikely. After 2 days, serum sodium improved to 113 mEq/L with a urine sodium level of 33.1 mEq/L, a urine potassium level of 25.7 mEq/L and a urine osmolality of 386 mOsm/kg H2O. Concomitant improvement in hypouricaemia was also observed. Her urine sodium and urine osmolality were still increased. Therefore, drug-induced SIADH was suspected. Esomeprazole was considered to be the likely causative factor for SIADH and was discontinued. Valaciclovir might have accelerated the development of esomeprazole-induced SIADH. Consequently, serum sodium gradually increased with a concomitant decrease in urine osmolarity. Therefore, concentration of so