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Effects of finasteride on vascular endothelial growth factor.
Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
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2002 (Engelska)Ingår i: Scandinavian Journal of Urology and Nephrology, ISSN 0036-5599, E-ISSN 1651-2065, Vol. 36, nr 3, s. 182-7Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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.

Ort, förlag, år, upplaga, sidor
2002. Vol. 36, nr 3, s. 182-7
Nationell ämneskategori
Cancer och onkologi
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URN: urn:nbn:se:umu:diva-94366DOI: 10.1080/003655902320131848PubMedID: 12201932OAI: oai:DiVA.org:umu-94366DiVA, id: diva2:753529
Tillgänglig från: 2014-10-08 Skapad: 2014-10-08 Senast uppdaterad: 2017-12-05

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