Pareek Gyan, Shevchuk Maria, Armenakas Noel A, Vasovic Ljiljana, Hochberg David A, Basillote Jay B, Fracchia John A
Department of Surgery, Division of Urology, Lenox Hill Hospital, 44 East End Avenue #2E, New York, NY 10028, USA.
J Urol. 2003 Jan;169(1):20-3. doi: 10.1016/S0022-5347(05)64025-6.
Several studies have confirmed the benefit of finasteride in limiting hematuria from benign prostatic hyperplasia. Vascular endothelial growth factor (VEGF), a potent stimulator of angiogenesis, and microvessel density have been independently evaluated in the mechanism of decreased bleeding observed in patients treated with finasteride. We evaluated the expression of VEGF and suburethral prostatic microvessel density in patients with benign prostatic hyperplasia treated with finasteride.
The study included 24 patients undergoing prostatic surgery for benign disease, of whom 12 were given finasteride for a minimum of 6 weeks before surgery and the remaining 12 served as controls. Sections from the prostatic urothelium and hyperplastic prostate were individually stained for CD34 specific for nascent blood vessels and VEGF. Analysis of each specimen was performed in a blinded fashion. Microvessel density was calculated by counting the number of positively stained blood vessels on 10 consecutive, nonoverlapping, high power fields within the suburethral and hyperplastic prostate compartments. VEGF expression was examined by immunohistochemistry. Statistical analysis of the results was performed using Student's t test.
Prostatic suburethral VEGF expression and microvessel density were significantly lower in the finasteride group compared to controls (p <0.05). Differences in VEGF expression and microvessel density at the level of the hyperplastic prostate were not found to be significantly different between the 2 groups. CONCLUSIONS Decreased expression of VEGF by finasteride inhibits angiogenesis and significantly decreases microvessel density in prostatic suburethral tissue. This sequential relationship provides histochemical insight into the mechanism by which finasteride reduces prostatic urethral bleeding.
多项研究已证实非那雄胺在限制良性前列腺增生引起的血尿方面的益处。血管内皮生长因子（VEGF）是一种强大的血管生成刺激因子，已对非那雄胺治疗患者中观察到的出血减少机制独立评估了微血管密度。我们评估了非那雄胺治疗的良性前列腺增生患者中VEGF的表达及尿道下前列腺微血管密度。
该研究纳入24例因良性疾病接受前列腺手术的患者，其中12例在手术前至少6周服用非那雄胺，其余12例作为对照。对前列腺尿路上皮和增生前列腺的切片分别进行新生血管特异性的CD34和VEGF染色。对每个标本的分析采用盲法进行。通过计数尿道下和增生前列腺区域内10个连续、不重叠的高倍视野中阳性染色血管的数量来计算微血管密度。通过免疫组织化学检查VEGF表达。使用学生t检验对结果进行统计学分析。
与对照组相比，非那雄胺组前列腺尿道下VEGF表达和微血管密度显著降低（p<0.05）。未发现两组在增生前列腺水平的VEGF表达和微血管密度差异有统计学意义。结论：非那雄胺使VEGF表达降低抑制血管生成，并显著降低前列腺尿道下组织的微血管密度。这种先后顺序关系为非那雄胺减少前列腺尿道出血的机制提供了组织化学方面的见解。
