Single-dose Tamsulosin Induces Reversible Azoospermia and Ejaculatory Dysfunction Suggesting Potential for on-demand...

Ejaculatory alterations are among the most frequent sexual side effects of α₁-adrenergic antagonists. Although often attributed to retrograde ejaculation, recent evidence indicates that tamsulosin primarily disrupts seminal emission, occasionally leading to transient azoospermia. This study evaluated the frequency, timing, and reversibility of ejaculatory and seminal changes following a single oral dose of 0.8 mg tamsulosin in healthy men.

Thirty-one healthy male volunteers (aged 18-45 years) underwent a baseline semen analysis, followed by six additional collections at 1-3 week intervals. Each collection was performed at a different post-dose time point, spaced every 4 hours, to construct a 24-hour post-administration profile. Semen parameters were assessed according to WHO criteria, and post-ejaculatory urine was examined to detect retrograde ejaculation. Temporal variations were analyzed using repeated-measures ANOVA, with effect sizes estimated by Cohen's d.

Seminal volume decreased significantly in 93.6% of participants, with aspermia in 80.7%, peaking 12 h after ingestion (p<0.001, d=2.05). Sperm concentration declined markedly, with azoospermia in 80.7% (p<0.001, d=1.59) and normalized after wash-out in 2 days. No retrograde ejaculation was observed. Adverse effects were mild and self-limited. A single 0.8 mg dose of tamsulosin caused a consistent, time-dependent disruption of seminal emission, producing transient azoospermia rather than retrograde ejaculation.

A single 0.8 mg dose of tamsulosin transiently suppressed seminal emission, leading to reversible azoospermia within 12 hours most recovered by 24h, and all recovered within 48h. Its predictable, reversible effect supports caution in men seeking conception and further exploration as an on-demand male contraceptive model.