Histologic influence of doxazosin and finasteride in benign prostatic hyperplasia accompanying chronic inflammation.
OBJECTIVE
To evaluate the influence of doxazosin and finasteride on histologic findings in benign prostatic hyperplasia accompanied by prostatitis, and to examine the factors related with prostate carcinogenesis.


METHODS
Prostate tissue from 17 cases of prostatic hyperplasia were divided into three groups; group 1: no medication history, group 2: both doxazosin and finasteride for at least 6 months before surgery; group 3: doxazosin for a minimum of 6 months before transurethral resection. Formalin-fixed, paraffin-embedded sections were stained with hematoxylin and eosin stain and immunohistochemistry for COX-2, CD3, CD68, VEGF, and GSTP (glutathione S-transferase pi).


RESULTS
CD3 showed a tendency toward decreased staining intensity and extent in group 3 (p = 0.026, p = 0.004, respectively). CD68 showed a different staining extent among the three groups (p = 0.020). For VEGF, the staining extent showed different results between groups 2 and 3 (p = 0.044). There was no correlation between COX-2 and VEGF in group 1. However, a positive correlation between COX-2 and GSTP1 was demonstrated in group 2 (p = 0.000).


CONCLUSIONS
Doxazosin-treated prostate tissue showed decreased inflammatory reaction. GSTP1 expression was decreased in combined treatment with doxazosin and finasteride. These findings suggest that finasteride may interfere with the anti-inflammatory reaction. Finasteride also decreases angiogenesis. However, the meaning of our observations is limited by small sample size.
Park
Dong Soo
DS
Department of Urology, Bundang CHA Hospital, Pochon CHA University, Seoul, Korea.
Shim
Jeong Yun
JY
D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D000959:Antihypertensive Agents / Q000009:adverse effects / Q000494:pharmacology; D017252:CD3 Complex / Q000096:biosynthesis; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D017292:Doxazosin / Q000009:adverse effects / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000009:adverse effects / Q000494:pharmacology; D018120:Finasteride / Q000009:adverse effects / Q000494:pharmacology*; D005982:Glutathione Transferase / Q000096:biosynthesis; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D011470:Prostatic Hyperplasia / Q000188:drug therapy*; D011472:Prostatitis / Q000209:etiology; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000959:Antihypertensive Agents; D017252:CD3 Complex; D051546:Cyclooxygenase 2; D017292:Doxazosin; D004791:Enzyme Inhibitors; D018120:Finasteride; D005982:Glutathione Transferase; D042461:Vascular Endothelial Growth Factor A; C067980:CD68 antigen, human; D000097382:CD68 Molecule