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To the Editor: Selective serotonin reuptake inhibiting (SSRI) antidepressants commonly produce iatrogenic sexual dysfunction (1, 2). It is uncommon for spontaneous remission of this side effect to occur, even after taking the SSRI for years (3). A variety of augmentation strategies have been proposed to reverse SSRI-induced sexual dysfunction (4). Sildenafil has been used to reverse SSRI-induced anorgasmia in a woman (5). Vardenafil, a phosphodiesterase type-5 inhibitor, is indicated in the treatment of male erectile disorder. I report here a case of SSRI-induced anorgasmia in a woman that was reversed by vardenafil.
Ms. A was a 37-year-old Caucasian woman who was successfully treated for panic disorder without agoraphobia and for generalized anxiety disorder with sertraline, 100 mg/day, for over 2 years after difficulty tolerating trials of alprazolam and clonazepam. Unfortunately, she developed anorgasmia from the sertraline within 3 months of reaching this dose. A dose reduction to 50 mg/day led to relapse, although her anorgasmia improved. Sildenafil augmentation 1 hour before sexual activity reversed her anorgasmia but only at the 100-mg dose; the 50-mg dose was ineffective. The anorgasmia persisted if she forgot to take sildenafil. The cost, however, was prohibitive because the drug was not covered by her health insurance. She was interested in trying vardenafil instead because it cost less than sildenafil. She found that vardenafil in the 10-mg strength was not only effective in reversing anorgasmia but was also more affordable because she could break the 20-mg pills in half. Ms. A could not detect any difference in the onset of action, the duration of effect, or adverse reactions from vardenafil compared to what she felt while taking sildenafil. Vardenafil has continued to be effective when she uses it once or twice a week for 9 months to date without any difficulty tolerating it.
This case report describes a woman with SSRI-induced anorgasmia and no other sexual complaints who had this side effect reversed by vardenafil. It is possible that this response was a placebo effect, although it is unlikely since this side effect persisted with a low dose of sildenafil. Larger-scale placebo-controlled studies would be helpful in determining the effect size and whether other opportunities exist for using vardenafil to reverse SSRI-induced sexual dysfunction.
At this point, vardenafil has been approved by the Food and Drug Administration only for use in men. Further studies in women with primary or secondary sexual dysfunction may reveal other populations and medical conditions that are responsive to vardenafil treatment. This report suggests that augmentation with vardenafil may assist some patients with SSRI-induced sexual dysfunction.
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