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HYPONATREMIA IN AN OLDER PATIENT

1999; Wiley; Volume: 47; Issue: 8 Linguagem: Inglês

10.1111/j.1532-5415.1999.tb01307.x

1532-5415

R. E. Kelly, Harry Robinson, T. R. O. Beringer,

Electroconvulsive Therapy Studies

To the Editor: We read with interest the letter by Levsky and Schwartz entitled “Sertraline-Induced Hyponatremia in an Older Patient”.1 We report a case of hyponatremia occurring after only two doses of paroxetine, another selective serotonin reuptake inhibitor (SSRI). In October 1998, a 73-year-old previously independent woman was admitted to the hospital with a 2-day history of confusion, dizziness, and nausea. Three days previously her general practitioner had prescribed paroxetine 10 mgs (1/2 tablet) daily for depressive symptoms, and the patient had taken 10 mgs daily for 2 successive days. Symptoms had started 24 hours after the initial dose. For several years, the patient had been taking indapamide 2.5 mgs daily and atenolol 25 mgs daily for hypertension. On examination, the patient had a blood pressure of 180/90 mm Hg and a pulse rate of 80 beats per minute. Her mental score was 8/10. Physical examination was otherwise unremarkable. Serum sodium recorded on the day paroxetine was prescribed was 130 mmol/L (135–145 mmol/L). On admission to the hospital 72 hours later, the serum sodium was markedly reduced to 106 mmol/L. Paroxetine and indapamide were discontinued. Fluid restriction of 1000 mL was initiated. The patient's symptoms and confusion slowly resolved, and 11 days later the serum sodium level had risen to 124 mmol/L. At follow-up 2 months later, the serum sodium was normal at 138 mmol/L. On admission the serum osmolality was 218 mmol/kg (285–290 mmol/kg), and the urinary osmolality was 553 mmol/kg (250–1250 mmol/kg) with an antidiuretic hormone (ADH) level of 7.7 pmol/L. This ADH level is high compared with the reduced serum osmolality and inappropriately high urinary osmolality, supporting a diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH). Serum potassium and calcium as well as renal, thyroid, and liver function tests were normal. The patient was unwilling to consent to a rechallenge with paroxetine. The temporal relationship between the introduction of paroxetine and subsequent hyponatremia strongly implicates paroxetine as the cause of her inappropriate ADH secretion. This is supported by her recovery following withdrawal of paroxetine. Although an uncommon side effect, hyponatremia with SSRIs is widely reported. Goddard and Patton reported a patient with hyponatremia associated with paroxetine therapy in 1992.2 By January 1998, 107 cases of SIADH presumed secondary to paroxetine have been reported to the Committee on Safety of Medicines. The side effect is seen almost exclusively in older patients. In 1997, Woo and Smyth3 reviewed 25 published case reports of SSRI-induced SIADH, five attributable to paroxetine.2,4–6 To summarize all 25 reports, the median age of patients was 75 years, the median serum sodium concentration was 118 mmol/L, and the initial presentation ranged from 3 days to 4 months after commencing treatment. The older patients took between 10 and 14 days to recover, and the length of therapy or severity of hyponatremia did not influence the recovery time. We strongly support Levsky and Schwartz in their recommendations that serum sodium be monitored during therapy with SSRIs, but we suggest, if possible, that serum sodium be checked before commencing therapy and again within 1 week.