Abstract
Many studies as well as case reports have acknowledged hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone (SISADH) as known side-effects of selective serotonin-re-uptake inhibitors (SSRIs) such as fluoxetine and sertraline [1, 2], and inhibitors of serotonin and norepinephrine re-uptake (SSRIs and SNRIs) such as duloxetine [3]. Hyponatremia has also been reported with reboxetine [4], an SNRI, but this is probably the first reported case of hyponatremia from atomoxetine (Strattera, Eli Lily and Co., Indianapolis, IN, USA) which is also an SNRI.
The patient was a 32-year-old man with a history of attention-deficit–hyperactivity disorder who presented to an outpatient psychiatric clinic for evaluation. The patient reported that his previous psychiatrist retired so he was referred to this clinic for evaluation. The patient said that he had been taking atomoxetine 60 mg for the last 2 months and that he had achieved good results from the medication and thought that it had really helped him with concentration. The patient also reported that had been much less impulsive after starting atomoxetine. The patient reported a past trial of Adderal XR (Shire Pharmaceuticals, Basingstoke, UK) and said that he was afraid of becoming addicted to stimulants and that was why his psychiatrist switched him to atomoxetine.
During evaluation the patient complained of nausea and fatigue, especially for last few weeks. No other psychiatric symptoms were reported by the patient, nor medical concerns or any past medical problems.
The patient was maintained on the same dose of atomoxetine and was referred to Primary Care Physician (PCP) for his nausea and malaise. One week later the patient's primary care physician called regarding the patient's low sodium level. PCP had done the lab work. All other results were normal except low sodium level at 122 mmol L–1. The patient record suggested that the sodium level measured 1 year previously was 141 mmol L–1. PCP could not find any other justification for low sodium level except medication-induced SIADH. And the only medication the patient was currently taking was atomoxetine. Based on the suspicion that atomoxetine might be causing the low sodium level, it was discontinued and the patient was asked to schedule a follow-up visit in 1 week.
When seen 1 week later the patient reported improvement in his nausea and fatigue. Repeat sodium level was 130 and 2 weeks later was 140 mmol L–1. The patient was switched back to Adderal XR (at his request) 2 weeks after stopping atomoxetine.
The mechanism of SIADH induced by serotonergic and norepinephrine-acting medications is not clear. Although animal studies do suggest that both serotonin and norepinephrine stimulate antidiuretic hormone [5], and that this might explain the SIADH induced by the inhibitory mechanism of the SSRI, or SNRI medications.
However, as shown by the present case report, atomoxetine can also cause low sodium level and therefore patients need to be monitored for this possible outcome.