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Apoptotic and proliferative index after Alpha-1-adrenoceptor antagonist and/or finasteride treatment in benign
Tibet Erdoğru1, M Akif Ciftcioglu, Ibrahim Emreoglu
1Department of Urology, Faculty of Medicine, Akdeniz University, Antalya, Turkey. drtibet@netone.com.tr
Introduction:
The induction of apoptosis has emerged as a potential target for optimization of the medical management of benign prostatic hyperplasia (BPH), recently. The influence of alpha1-adrenoceptor antagonist (alpha1-ARA), 5-alpha reductase inhibitor and their combination on prostatic cell apoptotic and proliferative indices of benign hyperplastic prostate gland were investigated.
Materials And Methods:
A total of 49 male patients with BPH (mean age: 66.5 years) treated with alpha1-ARA and/or finasteride were retrospectively evaluated. Patients treated with alpha1-ARA (doxazosin n = 12 and terazosin n = 10), finasteride (n = 9) and combination of finasteride and alpha1-ARA (n = 9) were enrolled in the study. Primary antibodies were Ki-67 and proliferating cell nuclear antigen for the evaluation of proliferation in prostate stromal and epithelial cells. In situ apoptotic DNA fragmentation was evaluated using TUNEL assay.
Results:
All treatment groups had no significant changes in the rate of prostate stromal and epithelial cell proliferation. Epithelial apoptotic index (AI) was not statistically significant for finasteride vs. alpha1- ARA, alpha1-ARA vs. finasteride + alpha1-ARA and finasteride + alpha1-ARA vs. finasteride groups. While alpha1-ARA was more effective than finasteride on stromal apoptosis, alpha1-ARA-induced stromal apoptosis was not significantly different from alpha1-ARA plus finasteirde treatment.
Conclusion:
Not only androgen variabilities but also alterations in sympathetic neurotransmission with age could have important implications for pathophysiological prostate growth. The combination of finasteride and alpha1-ARA is not superior to alpha1-ARA therapy with their similar epithelial and stromal apoptotic effects with unaffected cell proliferation.
Insights
Alpha1-adrenoceptor antagonists (alpha1-ARA) and finasteride impact benign prostatic hyperplasia (BPH) cell apoptosis similarly. Combination therapy offers no superior apoptotic or proliferative benefits over alpha1-ARA alone for BPH treatment.
Area of Science:
- Urology
- Pharmacology
- Cell Biology
Background:
- Benign prostatic hyperplasia (BPH) management is exploring apoptosis induction.
- Alpha1-adrenoceptor antagonists (alpha1-ARA) and 5-alpha reductase inhibitors are key BPH treatments.
- Investigating their impact on prostate cell apoptosis and proliferation is crucial.
Purpose of the Study:
- To evaluate the effects of alpha1-ARA, finasteride, and their combination on BPH cell apoptosis and proliferation.
- To compare the efficacy of monotherapy versus combination therapy in modulating prostatic indices.
Main Methods:
- Retrospective analysis of 49 BPH patients treated with alpha1-ARA, finasteride, or both.
- Assessment of cell proliferation using Ki-67 and proliferating cell nuclear antigen (PCNA) markers.
- Evaluation of apoptosis via TUNEL assay for in situ DNA fragmentation.
Main Results:
- No significant changes in stromal or epithelial cell proliferation were observed across treatment groups.
- Epithelial apoptotic index showed no statistically significant differences between finasteride and alpha1-ARA groups, or combination therapy.
- Alpha1-ARA demonstrated greater stromal apoptosis induction than finasteride, with no significant difference compared to combination therapy.
Conclusions:
- Age-related sympathetic neurotransmission changes, alongside androgen variations, may influence BPH.
- Combination therapy of finasteride and alpha1-ARA is not superior to alpha1-ARA monotherapy for BPH.
- Both therapies exhibit similar effects on epithelial and stromal apoptosis with unaffected cell proliferation.
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