医学
非那雄胺
增生
川地34
泌尿科
前列腺
血管内皮生长因子
免疫染色
缺氧(环境)
经尿道前列腺电切术
免疫组织化学
病理
内科学
血管内皮生长因子受体
癌症
有机化学
化学
氧气
生物
遗传学
干细胞
作者
A. Lekas,Andreas C. Lazaris,Michael Chrisofos,Athanasios Papatsoris,Dimitrios Lappas,Efstratios Patsouris,Charalampos Deliveliotis
出处
期刊:Urology
[Elsevier]
日期:2006-08-01
卷期号:68 (2): 436-441
被引量:32
标识
DOI:10.1016/j.urology.2006.03.038
摘要
Objectives To assess the effects of finasteride on angiogenetic and hypoxia markers in benign prostatic hyperplasia. Methods A total of 178 patients aged 51 to 85 years (mean 68.7) with benign prostatic hyperplasia and awaiting transurethral prostate resection were prospectively randomized into a group of patients receiving finasteride (group 1; 88 patients) and a group of patients who received no medication until transurethral prostate resection (group 2; 90 patients). Tissue specimens were immunohistochemically stained with monoclonal antibodies against CD34 for microvessel density (MVD), vascular endothelial growth factor (VEGF), and hypoxia inducible factor-1alpha (HIF-1α). Results Blood loss during transurethral prostate resection was significantly higher in group 2 compared with group 1 (P <0.001). The distribution of CD34 immunostaining was mainly at the suburethral prostate. MVD, VEGF, and HIF-1α values were significantly lower statistically (P <0.001) in group 1 compared with group 2. In the finasteride group (group 1), the positive correlation of the immunoreactivity of CD34 and HIF-1α, VEGF and HIF-1α, and VEGF and CD34 was statistically significant (P <0.001). In the same group, MVD and VEGF and HIF-1α expression correlated statistically with the treatment duration. Conclusions Finasteride administration in benign prostatic hyperplasia results in statistically significant suppression of MVD, VEGF, and HIF-1α in a time-dependent manner.
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