DULOXETINE, A SEROTONIN and norepinephrine reuptake inhibitor, has recently been approved for treatment of stress urinary incontinence in Europe. We report a case of severe urinary retention requiring urinary catheterization associated with treatment of depression with duloxetine and quetiapine.
A 36-year-old Asian man with no medical, urogenital, or psychiatric illness histories, presented with depression accompanying insomnia. He was treated with escitalopram 20 mg/d and trazodone 100 mg/d for 4 weeks but his symptoms continued. On the 24th treatment day, quetiapine immediate release (IR) 150 mg/d replaced trazodone. On the 28th treatment day, duloxetine 30 mg/d replaced escitalopram. Two days later, duloxetine dosage was escalated to 60 mg/d, and he immediately started to develop urination difficulty and hesitancy. Alfuzosin, a uroselective α1-blocker, was prescribed (10 mg/d), but his urination difficulty continued. Therefore, both quetiapine and duloxetine were discontinued and were switched to mirtazapine 30 mg. Despite these efforts, on the 34th treatment day (6 days after duloxetine initiation and 1 day after duloxetine discontinuation), the urination difficulty progressed to complete urinary retention with residual urine amounting to 900 mL. Subsequently, urinary catheterization had to be carried out for 16 days before his urination function became normalized.
To our knowledge, there is only one published report of severe urinary retention associated with duloxetine (in combination with olanzapine) in a patient with depression. In this previous report, the urinary retention resolved within 1 week after duloxetine discontinuation. However, the patient in our case experienced much more severe urinary retention that did not improve with duloxetine discontinuation and further required more than 16 days of urinary catheterization and a uroselective α1-blocker.
Duloxetine has minimal anticholinergic properties, and it improves urinary incontinence by inhibiting serotonin and norepinephrine reuptake in Onuf's nucleus, located in the sacral spinal cord.[1, 3] Both α-receptors and serotonin 5-HT2 receptors located in the Onuf's nucleus facilitate the storage reflex by contracting the urethral external sphincter muscle. Likewise, increased serotonin and norepinephrine due to duloxetine administration might have caused the voiding dysfunction in our patient. It cannot be completely ruled out that quetiapine, an agent with significant antihistaminic and antimuscarinic properties, might have been the cause because quetiapine-induced urinary retention has also been reported previously. However, our patient was taking a much lower dose of quetiapine than the patient in the previous case report (150 mg/d vs 1800–2400 mg/d). Obtaining the patient's serum drug level might have helped clarify this controversy regarding the exact cause. However, we were unable to perform such an examination, which is an important limitation of our report. Regardless of possible debates concerning the exact contributing factor, the fact that such a complication occurred in a young male patient with no urological illness is of concern. Thus, this case suggests increased attention on urinary function may be needed, when using duloxetine in particular, if drugs with high anticholinergic properties are combined.