Decreased suburethral prostatic microvessel density in finasteride treated prostates: a possible mechanism for reduced bleeding in benign prostatic hyperplasia

PURPOSE: We evaluated the influence of finasteride on prostatic microvessel density to elucidate a mechanism of decreased bleeding in finasteride treated patients with hematuria secondary to benign prostatic hyperplasia (BPH). MATERIALS AND METHODS: A total of 22 patients with clinical BPH and gross hematuria who underwent prostate reductive surgery between 1998 and 2000 were prospectively evaluated. The prostate from 10 finasteride treated and 12 untreated patients was immunohistochemically stained for CD-34. Microvessel density analysis was performed by quantifying positive stained blood vessels located within the stroma of hyperplastic nodules as well as in the suburethral portion of the prostate. RESULTS: Mean microvessel density plus or minus standard deviation in finasteride treated patients was significantly lower in the suburethral portion of the prostate versus untreated controls (14.0 +/- 2.8 versus 20.2 +/- 5.3 vessels per high power field, p <0.05). In the nodular hyperplasia there was no statistically significant difference in the treatment and control groups (mean 17.5 +/- 2.8 and 16.7 +/- 4.6 vessels per high power field, respectively). CONCLUSIONS: Finasteride significantly decreases suburethral prostatic microvessel density in patients with BPH, which may explain its efficacy for decreasing BPH associated bleeding.     

Effects of finasteride on vascular endothelial growth factor

OBJECTIVE: Finasteride has been shown to reduce prostate bleeding in patients with benign prostatic hyperplasia (BPH). The mechanisms behind this are not known, but it has been suggested that finasteride reduces bleeding by inhibiting angiogenesis in the prostate. Studies in animals have shown that castration rapidly induces involution of the prostate vasculature, and androgen-stimulated prostate growth may be angiogenesis dependent. The objective of this study was to explore the response to finasteride on the vasculature and the expression of vascular endothelial growth factor (VEGF), a potent regulatory factor of angiogenesis in human prostate tissue. MATERIAL AND METHODS: Patients with BPH were randomly assigned to 3 months of treatment either with finasteride (5 mg/day) or placebo before undergoing transurethral resection of the prostate (TURP). Prostate tissue VEGF expression was quantified by Western blot and the vascular density determined in Factor VIII immunostained tissue sections. Serum concentrations of VEGF were measured with ELISA technique. RESULTS: Patients treated with finasteride (n = 15) showed a decrease in prostate tissue VEGF(165) expression compared with placebo (n = 13) treated patients (p < 0.05), but the vascular density and the serum VEGF levels were unaffected. CONCLUSIONS: This study shows that finasteride treatment decreases VEGF expression in the human prostate.     

Dynamic contrast enhanced magnetic resonance imaging as a biological marker to noninvasively assess the effect of finasteride on prostatic suburethral microcirculation

PURPOSE: We assessed dynamic contrast enhanced magnetic resonance imaging as a biological marker of in vivo changes in microcirculation in the prostatic suburethral region. MATERIALS AND METHODS: A total of 12 male beagle dogs with spontaneous benign prostatic hyperplasia were randomly allocated to 1 control group and 1 finasteride (Merck and Co., Whitehouse Station, New Jersey) treated group. Two baseline dynamic contrast enhanced magnetic resonance imaging examinations and 3 followups were performed to assess prostate microcirculation. Treatment duration was 3 months. The pharmacokinetic parameters evaluated in prostatic suburethral areas were the maximum enhancement ratio in AU, time to maximum signal enhancement in minutes, amplitude in AU and the exchange rate constant in minutes(-1). RESULTS: After completion of the therapeutic regimen time to maximum signal enhancement was significantly longer in the finasteride group than in controls (p < 0.01). Amplitude and the exchange rate constant decreased 39% and 34%, respectively, in the finasteride group at the end of treatment, which significantly differed from results in the control group (p < 0.05). CONCLUSIONS: Dynamic contrast enhanced magnetic resonance imaging is capable of noninvasively assessing the prostatic microcirculation changes induced by finasteride. Pharmacokinetic parameters show considerable promise to be biomarkers for the development of benign prostatic hyperplasia drugs such as 5alpha-reductase inhibitors by the in vivo monitoring of microvascular changes. A relevant clinical application could be the pretreatment assessment of finasteride effectiveness to decrease perioperative bleeding at transurethral prostate resection and in treatment for hematuria.     

非那雄胺对前列腺增生组织中CD34、VEGF及bFGF表达的影响

目的:探讨非那雄胺对前列腺增生组织中CD34、VEGF及bFGF表达的影响。方法:应用免疫组化LDP法检测40例服药的(非那雄胺组)和40例未服药的(对照组)前列腺增生组织中CD34、VEGF和bFGF的表达。结果:非那雄胺组前列腺增生组织中血管数目为(63±1.7)个,对照组为(129±2.4)个,两组差别有统计学意义(P<0.01)。非那雄胺组前列腺增生组织中VEGF及bFGF的表达与对照组相比明显减弱,两组差别有统计学意义(P<0.01)。结论:非那雄胺对前列腺增生组织中CD34、VEGF及bFGF的表达有显著性抑制作用,能减少前列腺增生组织的血管密度,这可能是其缩小前列腺及预防和治疗前列腺出血的主要机制。     

Relationship between prostate specific antigen density, microvessel density and prostatic volume in benign prostatic hyperplasia and advanced prostatic carcinoma

The aim of this study was to investigate the relationship between prostate specific antigen density and prostate volume with microvessel density in patients with benign prostatic hyperplasia and advanced prostatic carcinoma. Sixty-eight patients with benign prostatic hyperplasia and 11 patients with advanced prostatic carcinoma participated in the study. The paraffin blocks of all patients were stained with CD34 by the standard immunohistochemical technique and microvessel density, prostate specific antigen density and prostatic volume were determined. In patients with benign prostatic hyperplasia the mean microvessel density, mean prostate specific antigen density and mean prostatic volume were 74±89±22.73, 0.12±0.10 and 59.97±27.0 ml, respectively. There was no correlation between prostate specific antigen density and mean prostatic volume or microvessel density (r=0.079 and −0.095, respectively). In patients with advanced prostatic carcinoma the mean microvessel density, mean prostate specific antigen density and mean prostatic volume were 147.90±47.55, 0.63±0.41 and 54.00±22.42 ml, respectively. In this group, while there was a good correlation between prostate specific antigen density and microvessel density (r=0.785), no significant correlation was found between prostatic volume and microvessel density (r=−0.07). There was significant statistical difference in patients with advanced prostatic carcinoma compared to patients with benign prostatic hyperplasia in terms of mean microvessel density (p<0.0001). The findings that there was no correlation between prostatic volume and MVD either in benign prostatic hyperplasia or in prostatic carcinoma suggest that microvessel development is not correlated with prostatic volume but may be correlated with morphology.     

Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells

BACKGROUND: This study investigated the effects of finasteride, a 5alpha-reductase inhibitor, clinically used for the treatment of benign prostatic hyperplasia (BPH) on prostate tumor vascularity, apoptosis, and cell adhesion in situ and in vitro. METHODS: Prostate specimens from BPH patients treated with finasteride for 1-12 months (n = 13), or without finasteride treatment (n = 14), were evaluated for apoptosis (TUNEL assay), microvessel density (Factor VIII), and prostate specific antigen (PSA) immunoreactivity. In vitro, the effect of finasteride was investigated in benign prostate cells, BPH-1, and its tumorigenic derivatives, CAFTD-01 and CAFTD-03, using Hoechst staining and cell adhesion assays. RESULTS: A significant increase in the apoptotic index, and reduced microvessel density and PSA expression were detected in prostates from finasteride-treated patients, compared to controls (P < 0.01). In vitro finasteride led to a significant decrease in prostate epithelial cell adhesion (P < 0.05). CONCLUSIONS: Finasteride can induce prostate apoptosis and reduce tissue vascularity by inhibiting epithelial cell adhesion. This evidence supports that finasteride has apoptotic and anti-angiogenic effects against benign and malignant prostate.     

Comparison of microvessel densities in rat prostate tissues treated with finasteride, bicalutamide and surgical castration: A preliminary study

BACKGROUND: A group of anti-androgens with different mechanisms of action and adverse effects have been investigated in patients with gross hematuria related to benign prostate hyperplasia; however, there is not yet any consensus about the standard management of these patients. The present study aims to identify if any one type of the hormonal intervention is superior in terms of the suppression of microvessel formation in the prostate. MATERIALS AND METHODS: A total of 28 mature, healthy male Sprague-Dawley rats (300 +/- 50 g) were used in this study. The rats were randomly assigned to one of four groups (n = 7 per group). The effects of three different hormonal therapies on angiogenesis and microvascularity in rat ventral prostate were compared. Groups 1 and 2 were treated for 28 days with finasteride and bicalutamide, respectively, and rats from Group 3 underwent surgical castration. Following treatment, all rats included in the study underwent dissection of the ventral prostate and immunohistochemical analysis of microvessel density by factor VIII-related antigen. RESULTS: The mean number of microvessels in the finasteride and bicalutamide groups was 24.5 (+/-8.44 SE) and 27 (+/-9.89 SE) respectively. In contrast, the castration and control groups had microvessel numbers of 12.9 (+/-5.35 SE) and 40.3 (+/-5.03 SE) respectively. Differences were statistically significant between all three treatment groups and the controls (P < 0.005); the number of microvessels in rat prostate tissues of the control group was significantly higher than the treatment groups. Mean microvessel densities in the bicalutamide and finasteride groups were significantly higher than microvessel densities in the castration group (P < 0.005). There was no statistically significant difference between mean microvessel number in rat prostate tissue treated with finasteride or bicalutamide (P > 0.05). CONCLUSIONS: Even though finasteride was not as effective as castration in reducing microvessel number, its effect was equal to that of bicalutamide in terms of suppressing the angiogenesis in prostatic tissue. Based on the findings of the present study, finasteride might offer a viable option in the management of macroscopic hematuria by inhibition of microvessel formation within the prostatic tissue. Further clinical studies are warranted.     

Randomized, placebo-controlled trial showing that finasteride reduces prostatic vascularity rapidly within 2 weeks

OBJECTIVE: To measure expression of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in the prostates of men after transurethral resection of the prostate (TURP) following 2 weeks of treatment with finasteride. PATIENTS AND METHODS: Sixty-four men scheduled to undergo TURP were randomized to receive 5 mg of finasteride or placebo daily for 2 weeks before surgery. Sections of prostatic urothelium were stained for VEGF expression and for CD31 to assess MVD. Ten consecutive, non-overlapping high-power fields were analysed in a blinded fashion. RESULTS: In all, 31 men received finasteride and 33 placebo; the groups were similar in patient age, resected prostate weight, preoperative catheterization, prostate-specific antigen level, aspirin use, spinal anaesthesia and postoperative diagnosis of prostate cancer. The mean (95% confidence interval) MVD was significantly lower in the finasteride group (60, 55-65) than in the placebo group (71, 64-78; P < 0.01). Similarly, the mean expression of VEGF was significantly lower in the finasteride group (47, 43-52 vs 61, 54-67; P < 0.001) CONCLUSION: Finasteride inhibits angiogenic growth factors leading to reduced vascularity, and this is the basis of its action in reducing haematuria of prostatic origin. The present study shows that finasteride influences the prostatic microvasculature after only 2 weeks exposure.     

A systematic review of the effects and mechanisms of preoperative 5α-reductase inhibitors on intraoperative haemorrhage during surgery for benign prostatic hyperplasia

5α-reductase inhibitors (5α-RIs), including finasteride and dutasteride, are commonly used medical therapies for benign prostatic hyperplasia (BPH). Many studies reported that preoperative 5α-RI had impact on intraoperative haemorrhage during surgery for BPH, but it was still in controversial. So, we conducted a systematic review of the effects and mechanisms of 5α-RIs on intraoperative bleeding for BPH. MEDLINE, EMBASE, the Cochrane Controlled Trail Register of Controlled Trials and the reference lists of retrieved studies were searched in the analysis. Sixteen publications involving 15 different randomized controlled trials (RCTs) and a total of 1156 patients were used in the analysis, including 10 RCTs for finasteride and five RCTs for dutasteride. We found that preoperative finasteride treatment decreases microvessel density (MVD) in resected prostate specimens. Total blood loss, blood loss per gram of resected prostate tissue and decreases in haemoglobin were all greatly reduced in the finasteride group as compared to controls. Dutasteride appeared to have no effect on bleeding. This meta-analysis shows that preoperative finasteride treatment could decrease intraoperative haemorrhage during surgery for BPH. Preoperative dutasteride had no effect on intraoperative haemorrhage, but further high-quality prospective studies are still needed to confirm this observation.     

非那雄胺对前列腺增生症术中及术后出血的治疗作用

目的：探讨非雄胺（保列治）对前列腺增生症术中和术后出血的疗效及机制。方法：应用免疫组化S－P法检测43例服药组和46例未服药组前列腺组织中CD34、bcl-2、PCNA和VEGF的表达。分析比较二组临床资料及免疫组化指标。结果：服药组术中输血人数、输血量及术后继发性血尿的发生率较对照组均明显减少,两组间差别有显著性意义（P＜0．05）。免疫组化结果显示前列腺组织中血管密度及血管内面积较对照组明显减少,两组差别有非常显著性意义（P＜0．01）。两组前列腺组织中bcl-2、PCNA和VEGF阳性表达率差别有显著性意义（P＜0．01）,表现为服药组较未服药组明显减弱。结论：非那雄胺通过抑制前列腺组织中微血管形成,已形成血管的收缩,促进凋亡,抑制EGF合成和前列腺增殖而防止和减少术中及术后出血。     

Effects of finasteride on the vascular surface density, number of microvessels and vascular endothelial growth factor expression of the rat prostate

Introduction: Finasteride is a 5-alpha-reductase inhibitor used in the medical treatment of benign prostatic hyperplasia (BPH) and appears to be effective in treating prostatic bleeding secondary to BPH. The exact mechanism of this effect is not known. The aim of this study was to evaluate the effects of finasteride on the vascular surface density (VSD), number of microvessels (NVES) and vascular endothelial growth factor (VEGF) expression of the rat prostate. Materials and methods: Nineteen adult male rats were used. Finasteride was given to 14, and there were 5 in the control group. Finasteride 80 mg/kg was administered daily via orogastric tube as a suspension for three months. Rats were sacrificed and vascular structures of the prostates were labelled immunohistochemically using CD31 antibodies. VSD and NVES of the prostates were assessed by means of a peroxidase labeled streptavidin-biotin method. VEGF expression was examined by immunohistochemistry using VEGF monoclonal antibody. Results: Mean prostatic weights were decreased significantly in rats given finasteride (p=0.0001). Although an increase in VSD was detected in the finasteride group it was not significant (p=0.26). NVES was significantly increased in the finasteride group (p=0.033). No significant difference was detected between the two groups in terms of VEGF expression (p=0.48). Conclusion: Finasteride does not seem to decrease VSD, NVES and VEGF expression at the level of the rat prostate. The effect of reduction of bleeding in BPH is likely to be due to its effect on shrinking glandular hyperplasia which might enhance vessel wall stability rather than decreasing overall vascularity.     

非那甾胺对良性前列腺增生继发血尿的防治作用

目的：探讨5-α还原酶抑制剂非那甾胺对良性前列腺增生患者继发血尿的防治作用。方法：良性前列腺增生继发间歇性血尿患者61例，平均年龄76岁。随机分为非那甾胺治疗组(28例)和对照组(33例)，每周尿常规检查观察血尿复发情况及程度。结果：经过12个月的分组观察，对照组31例中出现反复间歇性血尿20例(64％)，3例因血块堵塞需入院进一步处理，2例因反复血尿行耻骨上前列腺切除术；非那甾胺组28例中出现中、轻度间歇性血尿7例(25％)，无需外科治疗。结论：非那甾胺对良性前列腺增生继发性出血有预防及治疗作用。     

良性前列腺增生患者经尿道电切术后再次手术的病理组织学特征分析

目的分析再次TURP患者前列腺组织VEGF、AR的表达,探讨其在再次TURP发生中的作用及意义。方珐选取有再次TURP手术史（再次TURP组）和仅有一次手术史（对照组）的BPH患者各50例。采用免疫组织化学sP法检测前列腺组织中CD34、VEGF、AR的表达,计算MVD值及VEGF、AR指数,并对再次TURP组首次标本和对照组标本、再次TURP组两次手术标本分别进行比较及统计学分析。结果再次TURP组首次标本、再次标本及对照组中MVD值分别为：35．83±20．92、32．16±16．65、20．56±6．99;VEGF指数分别为：7．55±2．72、7．06±2．36、4．28±2．62;AR指数分别为：6．17±1．86、6．99±2．44、4．16±1．34。再次TURP组首次标本MVD值、AR、VEGF指数均高于对照组,两组差别有统计学意义（P〈0．05）;而再次TURP组前后两次手术标本间各指标差别无统计学意义（P〉0．05）。相关分析发现,AR指数和VEGF指数、VEGF指数和MVD值、AR指数和MVD值之间均存在正相关。结论BPH患者前列腺组织中高MVD值及AR、VEGF的高表达是导致其TURP术后复发及再次手术的重要原因之一,可作为判断术后复发的危险因素及采取针对性预防措施的指标。     

非那雄胺剂量对减少经尿道前列腺电切术中出血的影响

目的评价术前服用不同剂量的非那雄胺对经尿道前列腺电切除术（TURP）术中出血量的影响及其作用机理。方法90例拟行TURP术的良性前列腺增生患者,随机分为3组：5 mg组（术前2周每天服用非那雄胺5 mg）、10 mg组（术前2周每天服用非那雄胺10 mg）及未服药组,每组30例。记录各组TURP前列腺切除重量、手术时间、计算术中出血量。免疫组织化学SP法检测各组前列腺组织微血管密度（MVD）及血管内皮生长因子（VEGF）蛋白表达,并进行统计学分析。结果5 mg组、10 mg组及未服药组前列腺组织平均手术切除量分别为（22.3±6.2）g、（22.5±6.5）g和（23.2±5.3）g,差异无统计学意义（P〉0.05）。与未服药组比较,服药组的手术时间、术中平均出血量、前列腺组织MVD值、VEGF阳性计数均显著降低,差异有统计学意义（P〈0.05）,但5 mg组与10 mg组差异无显著性意义（P〉0.05）。结论术前2周每天服用非那雄胺5 mg即可有效抑制前列腺组织中VEGF蛋白表达,抑制前列腺组织血管生成,从而缩短TURP手术时间,减少术中失血量。     

A prospective study of the natural history of hematuria associated with benign prostatic hyperplasia and the effect of finasteride

PURPOSE: We prospectively studied the effect of finasteride on chronic hematuria associated with benign prostatic hyperplasia. MATERIALS AND METHODS: We prospectively evaluated 57 patients with chronic intermittent hematuria who were randomized to a finasteride treated or a control arm. RESULTS: In the untreated control group hematuria recurred in 17 patients (63%) within a year but in only 4 (14%) in the finasteride group, which was a statistically significant difference (p <0.05). Surgery was required for bleeding in 7 controls (26%), while no patient on finasteride required surgery. CONCLUSIONS: Hematuria secondary to prostatic bleeding may be significant if not treated. Finasteride appears to be effective for suppressing hematuria caused by benign prostatic hyperplasia and should be considered as treatment.     

The relationship between angiogenesis and cyclooxygenase-2 expression in prostate cancer

OBJECTIVE: To test the hypothesis that angiogenesis in prostate cancer is associated with tumour invasion and metastasis, and that this is mediated through increased cyclooxygenase-2 (COX-2) expression. PATIENTS AND METHODS: Angiogenesis was assessed in 105 patients with either prostate cancer (79) or benign prostatic hyperplasia (BPH, 26) and these data correlated with levels of COX-2 expression in the same dataset. The mean microvessel density (MVD) was analysed as a marker of angiogenesis, using the endothelial antigen CD34 stained by immunohistochemistry. RESULTS: There was no difference in MVD in progressive tumour stages compared with BPH. There was a negative correlation between MVD and COX-2 expression, but the effect of increased COX-2 expression on MVD was not marked. CONCLUSION: These data suggest that COX-2 drives tumour spread in prostate cancer by means other than the promotion of angiogenesis.     

Haematuria associated with BPH-Natural history and a new treatment option

Bleeding of prostatic origin is usually caused by the friable hypervascularity of the prostate, the vessels of which are easily disrupted by physical activity. The condition is often ignored after the patient has been fully investigated and more serious causes for bleeding excluded and treatment is often withheld unless the bleeding becomes excessive. We analysed the clinical effect of finasteride in the treatment of this condition. We retrospectively reviewed 42 patients diagnosed as having haematuria secondary to bleeding from a benign prostate. Eighteen patients were simply reassured and given no treatment. Twenty-four patients with prostatic bleeding were treated using finasteride. All case notes were reviewed and the patients were contacted by telephone. Of 18 patients who had prostatic bleeding but did not receive treatment the mean age was 70 y and the mean follow-up was 10 months; two had died, nine had no further bleeding, two had a single episode of bleeding requiring no treatment, six had several bleeding episodes of whom one started finasteride, one refused treatment, and three required TURP. In the group treated with finasteride the mean follow up was 9 months, the mean age of the patients was 75 y. Twenty patients had no further bleeding, one patient experienced minor intermittent bleed and required no further treatment. Two patients died of non-urological causes, one patient stopped the treatment because of impotence and one patient had mild gynecomastia. Haematuria secondary to prostatic bleeding can be significant if not treated. Finasteride appears to be effective in suppressing haematuria caused by benign prostatic hyperplasia and should be considered in treating this problem.     

色素上皮衍生因子和血管上皮生长因子在良性前列腺增生组织中的表达及意义

目的:探讨色素上皮衍生因子(PEDF)和血管上皮生长因子(VEGF)在BPH组织中的表达特点和意义.方法:对35例手术切除的BPH组织(BPH组),21例正常前列腺组织(对照组)行免疫组织化学法检测PEDF和VEGF的表达水平和微血管密度(MVD)计数,统计学分析两组标本表达水平的差异以及各因素之间的相关性.结果:BPH组中VEGF和MVD表达明显高于对照组(P＜0.01),PEDF表达明显低于对照组(P＜0.01);MVD与VEGF表达呈显著正相关(P＜0.05),与PEDF表达呈显著负相关(P＜0.05);VEGF与PEDF表达呈显著负相关(P＜0.01).结论:PEDF表达水平降低和VEGF表达水平增加,促进前列腺组织的血管生成作用,导致前列腺组织增生.PEDF和VEGF的不平衡表达可能是BPH组织血管生成的分子基础,是促进BPH发生和发展的因素.     

Pre-surgical finasteride therapy in patients treated endoscopically for benign prostatic hyperplasia

INTRODUCTION: Transurethral resection of the prostate is considered the standard technique for patients with moderate or severe lower urinary tract symptoms related to benign prostatic hyperplasia (BPH). Pathologically BPH is characterized by an increased proliferation of stromal and acinar cells, sustained by increased vascularization (neoangiogenesis). Recent studies have also shown that finasteride reduces angiogenesis and prostatic bleeding associated with BPH. Reducing the volume as a final step in reducing neoangiogenesis could thus represent a fundamental advance in limiting intra- and postoperative bleeding in patients undergoing transurethral resection of the prostate (TURP). MATERIALS AND METHODS: Our study included 60 patients undergoing TURP between January 2001 and January 2002. Of the patients, 30 received pretreatment with finasteride while 30 did not undergo any pretreatment (control group). In all the patients we evaluated the degree of peri-surgical bleeding, intended as a reduction in hemoglobin values in the 24 h following surgery. RESULTS AND CONCLUSIONS: In the group of patients pretreated with finasteride, blood loss, evaluated as a reduction in hemoglobin values, was minimal, and none of the patients required blood transfusion. The average hemoglobin loss in the 24 h following surgery was 0.9%. In the control group (average age 67 years), 4 patients (12%) required blood transfusion. The loss of hemoglobin was 2.36%. Finasteride, therefore, seems to play a fundamental role in the pretreatment of TURP patients, since by reducing dihydrotestosterone synthesis, it interacts with endothelial growth factors, thus reducing angiogenesis and preventing bleeding.     

术前短期大剂量服用非那雄胺减少TURP术中出血的临床研究

目的 评价术前口服非那雄胺(保列治)在经尿道前列腺电切术中的疗效及机制.方法 观察52例服用非那雄胺的(服药组)和52例未服药的(对照组)前列腺增生患者行前列腺电切术中的出血情况,用免疫组化S-P法对患者前列腺切除组织中CD34、bcl-2、增殖细胞核抗原(PCNA)和血管内皮生长因子(VEGF)的表达进行分析,分析比较二组临床资料及免疫组化指标.结果 服药组前列腺电切术中出血量、每分钟出血量和每克组织出血量均较对照组低,差异有显著性(p＜0.05),免疫组化结果显示前列腺组织中血管密度及血管内面积较对照组明显减少,两组差别有非常显著性意义,前列腺组织MVD值分别为60±2.4和123±3.9(p＜0.01),bcl-2、PCNA及VEGF阳性细胞所占面积较对照组少,差异均有统计学意义(p＜0.01).结论 术前短期大剂量服用非那雄胺可抑制前列腺组织微血管生成,从而有效减少TURP术中出血.