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Hyun, Cho, Han, Kim, and Chang: The Effect of Finasteride on Microvessel Density and Expression of Vascular Endothelial Growth Factor and 5α-Reductase in Prostatic Hyperplasia
Original Article
Urological Oncology
Korean Journal of Urology

Korean Journal of Urology 2009; 50(10): 947-954.

Published online: 22 October 2009

DOI: https://doi.org/10.4111/kju.2009.50.10.947

The Effect of Finasteride on Microvessel Density and Expression of Vascular Endothelial Growth Factor and 5α-Reductase in Prostatic Hyperplasia

Jae-Ho Hyun, Kun-Hyun Cho, Dong-Seok Han, Jin-Bum Kim, Young-seop Chang

Department of Urology, College of Medicine, Konyang University, Daejeon, Korea.

Correspondence to: Young-seop Chang. Department of Urology, College of Medicine, Konyang University, 685, Gasuwon-dong, Seo-gu, Daejeon 302-718, Korea. TEL: 042-600-9225, FAX: 042-542-3790, ovalboy@hanmail.net

Received 2 June 2009       Accepted 8 September 2009

Copyright © The Korean Urological Association, 2009

Abstract

Purpose

Vascular endothelial growth factor (VEGF), a potent stimulator of angiogenesis and microvessel density (MVD), which is an important indicator of neoangiogenesis, were independently evaluated to elucidate the mechanism of decreased bleeding observed in patients treated with finasteride, an inhibitor of 5α-reductase (5AR). We evaluated MVD and the expression of VEGF and 5AR type II in patients with benign prostatic hyperplasia (BPH) treated with finasteride.

Materials and Methods

The study included 61 patients undergoing transurethral prostatectomy (TURP) for BPH. Among these patients, 29 had well-preserved paraffin blocks, 13 of whom were given finasteride for a minimum of 3 weeks before surgery; the remaining 16 patients served as controls. MVD was calculated by counting the number of positively stained blood vessels on 5 random, high-power fields within the prostatic section. Expressions of VEGF and 5AR type II were analyzed with a confocal laser scanning microscope and an image analyzer.

Results

Prostatic MVD was significantly lower in the finasteride-treated group (p<0.05). The expression of VEGF and 5AR type II at the level of the prostatic glandular epithelium and stroma was not significantly different between the 2 groups. VEGF and 5AR type II were more strongly expressed in the epithelium of both groups than in stromal smooth cells (p<0.05).

Conclusions

Finasteride treatment had no clear effect on the expression of VEGF or 5AR type II. It is possible, however, that finasteride improves blood loss after TURP and BPH-induced hematuria by reducing MVD. Further study on the mechanism of MVD reduction is needed.

Keywords: Vascular endothelial growth factor A, Steroid-5alpha-reductase type 2, Prostatic hyperplasia, Finasteride

Figures and Tables

Fig. 1
Immunohistochemistry of CD34-stained sections showing microvessel density in the finasteride-treated (A) and control (B) groups. CD34-stained microvessels were less in the finasteride-treated group than in the control group. Reduced from ×200.
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Fig. 2
Microvessel density in the finasteride-treated and control groups. Microvessel density was lower in the finasteride-treated group than in the control group (p<0.05). Bars are Mean±SD. MVD: microvessel density.
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Fig. 3
Immunofluorescent staining of VEGF and 5AR in the finasteride-treated and control groups. (A, E): DAPI staining of the nucleus in BPH specimens. (B, C, F, G): There were no differences in expression of 5AR and VEGF between the finasteride-treated and control groups. Luminal epithelium (arrow) shows stronger 5AR and VEGF immunoreactivity than does the stroma (arrowhead) in both groups. (D, H): Merged image of 5AR and VEGF (A-D: finasteride-treated group; E-H: control group). Reduced from ×400. VEGF: vascular endothelial growth factor, 5AR: 5-α reductase.
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Fig. 4
Expression of VEGF and 5AR in the finasteride-treated and control groups. No difference in expression is shown between the finasteride-treated and control groups according to regional distribution. However, the luminal epithelium shows stronger expression than the stroma in both the finasteride-treated and control groups (p<0.05). Bars are Mean±SD. VEGF: vascular endothelial growth factor, 5AR: 5-α reductase. a,b: p<0.05 compared with stromal VEGF, c,d: p<0.05 compared with stromal 5AR.
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Table 1
Comparison of the characteristics of the patients according to finasteride medication
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Table 2
MVD and expression of VEGF and 5AR in both groups
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MVD: microvessle density, VEGF: vascular endothelial growth factor, 5AR: 5-α reductase, E: luminal epithelium, S: stroma

Notes

This work was supported by the research grant of the Myung-Gok Konyang university in 2005.

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