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Transition zone ratio and prostate‐specific antigen density as predictors of the response of benign prostatic hypertrophy to alpha blocker and anti‐androgen therapy
Author(s) -
KURITA Y.,
MASUDA H.,
SUZUKI K.,
FUJITA K.,
KAWABE K.
Publication year - 1997
Publication title -
british journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 0007-1331
DOI - 10.1046/j.1464-410x.1997.00232.x
Subject(s) - tamsulosin , urology , medicine , prostate , prostate specific antigen , androgen , muscle hypertrophy , hormone , cancer , hyperplasia
Objective To determine whether transrectal ultrasonography (TRUS) can predict the clinical response of patients with benign prostatic hypertrophy (BPH) to α1‐blocker and anti‐androgen therapy. Patients and methods From April 1994 to July 1995, 128 patients with BPH were randomized to treatment for 6 months with either tamsulosin (a long‐acting selective α1‐blocker) or allylestrenol (an anti‐androgen), with 64 patients receiving tamsulosin (0.2 mg/day) and 64 receiving allylestrenol (50 mg/day). The results of TRUS, uroflowmetry and the American Urologic Association (AUA) symptom score were compared before and after treatment. TRUS was used to calculate the transition zone (TZ) volume, transition zone ratio (TZ ratio=TZ volume/total prostate volume), total prostate volume and prostate‐specific antigen density (PSAD). Results Both groups showed a statistically significant improvement in the AUA symptom score, quality‐of‐life (QOL) score and peak urinary flow rate (Q max ) at 6 months ( P <0.001). In the tamsulosin group, there was a significant negative correlation between the pretreatment PSAD and the percentage change in Q max ( r =−0.640, P <0.001), while there was a positive correlation between PSAD and the percentage change in the AUA symptom score ( r =0.589, P <0.001). On the other hand, the allylestrenol group showed a significant positive correlation between PSAD and the percentage change in Q max ( r =0.397, P <0.01) and a negative correlation between PSAD and the AUA symptom score ( r =−0.313, P <0.01). Conclusion Patients with a high pretreatment PSAD responded well to anti‐androgen therapy, while those with a low PSAD responded better to α1‐blocker therapy.