Tamsulosin

Medina-Pizaño MY, et al. Life Sciences, 2025, 379, 123859.

Tamsulosin was evaluated for its antifibrotic effects in a thioacetamide (TAA)-induced cirrhosis rat model. In vitro, LX-2 hepatic stellate cells (HSCs) were activated by norepinephrine (NE), followed by treatment with tamsulosin. Cell viability, retinol content, and expression of α-SMA and collagen I were assessed via molecular assays and microscopy. Tamsulosin significantly inhibited NE-induced HSC activation, proliferation, and migration. In vivo, male Wistar rats received TAA for 4 weeks to induce fibrosis, followed by oral tamsulosin for 4 weeks. Liver histology, function tests, and in situ perfusion were performed. Tamsulosin reduced hepatic collagen I deposition, improved liver function, and prevented portal hypertension without inducing systemic hypotension. These findings demonstrate the efficacy of tamsulosin in modulating HSC activity and alleviating fibrotic progression, highlighting its potential as a targeted therapy for cirrhosis-related complications.

Seyedinnavadeh S, et al. The American Journal of Surgery, 2025, 247, 116455.

A randomized clinical trial evaluated the prophylactic efficacy of Tamsulosin in reducing postoperative urinary retention (POUR) in 179 male patients (>50 years) undergoing unilateral inguinal hernioplasty under spinal anesthesia. Group A (n=87) received 0.4 mg Tamsulosin orally 8 hours preoperatively and again 6-12 hours postoperatively. Group B (n=92) received a placebo on the same schedule. The incidence of POUR within 24 hours post-surgery was recorded, and statistical analysis was performed using SPSS version 18. Although POUR occurred less frequently in the Tamsulosin group (10.3% vs. 16.3%), the difference was not statistically significant (p = 0.242). Logistic regression further showed no significant correlation between Tamsulosin administration and POUR prevention. These results suggest that Tamsulosin, despite its mechanism of relaxing urethral smooth muscle, does not significantly prevent POUR under the tested conditions.

Nguyen M-H, et al. Heliyon, 2025, 11(3), e41768.

In this retrospective cohort study, the impact of Tamsulosin on glycemic control was investigated in comparison to Finasteride among men with type 2 diabetes and benign prostatic hyperplasia (BPH). Utilizing nationwide pharmaceutical dispensing and hospitalization databases in New Zealand, the study enrolled new users of Tamsulosin (n=580) and Finasteride (n=1,259). Propensity score-based inverse probability treatment weighting was applied to balance baseline characteristics. Cox proportional hazards models estimated the relative risk of poor glycemic control. Median follow-up periods were 1.6 and 2.4 years, respectively. The incidence of glycemic deterioration was 564 per 10,000 person-years in Tamsulosin users versus 409 for Finasteride. However, no statistically significant difference was found (HR 1.27, 95% CI: 0.95-1.72). Sensitivity analyses addressed potential confounders and protopathic bias. These findings indicate that Tamsulosin use does not confer an elevated long-term risk of impaired glucose regulation in diabetic patients.