The effect of finasteride on the expression of vascular endothelial growth factor and microvessel density: a possible mechanism for decreased prostatic bleeding in treated patients.
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.
Pareek
Gyan
G
Department of Surgery, Division of Urology, Lenox Hill Hospital, 44 East End Avenue #2E, New York, NY 10028, USA.
Shevchuk
Maria
M
Armenakas
Noel A
NA
Vasovic
Ljiljana
L
Hochberg
David A
DA
Basillote
Jay B
JB
Fracchia
John A
JA
D000368:Aged; D018952:Antigens, CD34 / Q000032:analysis; D016228:Endothelial Growth Factors / Q000378:metabolism*; D018120:Finasteride / Q000494:pharmacology* / Q000627:therapeutic use; D006417:Hematuria / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D008222:Lymphokines / Q000378:metabolism*; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000503:physiopathology; D011446:Prospective Studies; D011467:Prostate / Q000098:blood supply* / Q000378:metabolism; D011470:Prostatic Hyperplasia / Q000150:complications / Q000473:pathology* / Q000601:surgery; D014521:Urethra / Q000098:blood supply / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D018952:Antigens, CD34; D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D018120:Finasteride