- © 2008 Canadian Medical Association
Saleh Alqahtani and colleagues have provided a welcome reminder that hyperammonemia is a common side effect of valproate therapy.1 However, I am not convinced that hyperammonemia is a benign asymptomatic condition. I wonder whether the sedation that is often seen as a side effect of valproate therapy is in fact a symptom of low-grade encephalopathy.
In the past year, 2 of my patients with bipolar disorder who were taking valproate complained of foul-smelling urine. Both described the odour as strong, and when I smelled their urine myself I was unable to come up with a better descriptor. Blood ammonia levels were elevated in both patients. Both patients noted that the smell disappeared when they were switched to a different medication (oxcarbazepine), and they felt that their mental clarity improved as well.
If strong-smelling urine is indeed a sign of valproate-related hyperammonemia, it is simple enough to ask patients who take valproate whether they are experiencing this side effect. If they are, and if their blood ammonia level is elevated, the need for valproate therapy should be reassessed.
The authors' recommendations for managing valproate-related hyperammonemic encephalopathy are prudent, but I wonder if they missed half the picture. Does valproate therapy unmask underlying conditions such as urea- cycle disorders or fatty-acid-oxidation disorders? Did the authors look for these conditions in their patient? If not, why not? More importantly, how should family physicians begin investigating these possibilities? What tests should the physician in the trenches order to screen for these conditions once suspicions are raised?
Footnotes
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Competing interests: None declared.
REFERENCE
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