Letters to the Editor
Recurrent Paroxetine-Induced Hyponatremia
Dear Editor:
Selective serotonin reuptake inhibitors (SSRIs) have been implicated in the etiology of hyponatremia. Early- and delayed-onset hyponatremia have both been reported (1). We describe a case of early-onset, recurrent hyponatremia initially arising from paroxetine treatment and later, from paroxetine extended release.
Case Report
Mrs R, aged 71 years and married, had a long history of mood and anxiety symptoms. In 2000, her internist started her on paroxetine at a dosage of 20 mg daily. A week later, she was seen in the clinic for increasing confusion, malaise, and “not feeling good.” Her sodium level was found to be 120 mmol/dL, and she was admitted to the hospital. Paroxetine was thought to be the offending agent and was stopped. Her condition improved, and she was discharged from the hospital 2 days later, with serum sodium of 129 mmol/dL.
About 3 years later, her internist rechallenged her with paroxetine, this time prescribing the extended release preparation at 12.5 mg daily, titrated later to 25 mg daily. Approximately 10 days after the titration, she was seen in the clinic with symptoms of “not feeling well” and “depression” marked by fatigue and anxiety. Her sodium level was found to be 123 mmol/dL. She was rehospitalized, and upon review, it was found that her sodium levels had been fairly stable after she stopped taking paroxetine in 2000. A workup showed increased sodium excretion and reduced serum osmolality consistent with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). She was cross-titrated to bupropion, and her sodium level at the time of discharge was 126 mmol/dL, which later improved to 133 mmol/dL on day 4 after discharge.
Discussion
Hyponatremia from SSRIs has been recognized to be more common in older patients. Stedman and others believe that there is no genetic propensity and that this effect is not dosage dependent (2). Regardless of the etiology, the effects can range from anhedonia, fatigue, and tiredness to confusion, coma, and permanent neurological injury. The literature indicates that SIADH can either manifest itself in days or take months to surface (1).
In our patient, the timeline links paroxetine to SIADH. The onset within a week of the first trial and within 2 weeks of the second trial, together with a sudden resolution only a day or 2 after discontinuation or dosage reduction leaves little else to suspect. Our case shows that a different formulation of the same drug can result in a different presentation of SIADH in the same patient.
Although hyponatremia is not common, it appears that its presentation can vary widely in different patients and even in the same patient at different times. Given its serious consequences, clinicians need to be vigilant to diagnose the condition in time and to reverse it promptly, once diagnosed.
Funding and Support
None of the authors have any financial or personal connection either to any product mentioned or to a drug company.
References
1. Arinzon ZH, Lehman YA, Fidelman ZG, Krasnyansky II. Delayed recurrent SIADH associated with SSRIs. Ann Pharmacother 2002;36:1175–7.
2. Stedman CA, Begg EJ, Kennedy MA, Roberts R, Wilkinson TJ. Cytochrome P450 2D6 genotype does not predict SSRI (fluoxetine or paroxetine) induced hyponatraemia. Hum Psychopharmacol 2002;17:187–90.
Asif R Malik, MD
Pamela K Wolf, Pharm D, RPh
Saj Ravasia, MD, CCFP, FRCPC, DABPN
Fargo, North Dakota
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