医学
前列腺
睾酮(贴片)
内科学
炎症
下尿路症状
雌激素
内分泌学
泌尿科
催乳素
泌尿系统
激素
癌症
作者
Jenni Bernoulli,Emrah Yatkin,Yvonne Konkol,Eva‐Maria Talvitie,Risto Santti,Tomi Streng
出处
期刊:The Prostate
[Wiley]
日期:2008-05-23
卷期号:68 (12): 1296-1306
被引量:59
摘要
Abstract BACKGROUND The age‐related decline of the testosterone to estradiol (T‐to‐E 2 ) ratio in serum is associated with the increased prevalence of prostatic inflammation and lower urinary tract symptoms suggesting obstructive voiding. The impact of the T‐to‐E 2 ratio on the development and reversal of non‐bacterial prostatic inflammation and obstructive voiding was tested in adult Noble rats. METHODS Adult male Noble rats (n = 16) were treated with estradiol (83 µg/day) and two different doses (280 and 830 µg/day) of testosterone to cause hypoandrogenic and hyperandrogenic states with elevated estrogen. After the 13‐week hormonal treatment, urodynamical measurements and electrical activity recording of the rhabdosphincter muscle were performed under anesthesia. Testosterone, estradiol, and prolactin concentrations in serum were measured and inflammatory changes in the dorsolateral prostate were classified and counted. RESULTS Histopathological and urodynamical analyses indicated that the hypoandrogenic animals with a decreased T‐to‐E 2 ratio (10 versus > 300 in control) developed prostatic inflammation and non‐obstructive voiding. The hyperandrogenic state with decreased T‐to‐E 2 ratio of 50 decreased the aggressiveness of the inflammation and the number of inflamed acini in the prostate and caused urethral obstruction associated with rhabdosphincter dysfunction. CONCLUSIONS Different responses of the prostatic inflammation and voiding function to the change in T‐to‐E 2 ratio imply that non‐bacterial prostatic inflammation is not a sufficient condition for the development of obstructive voiding. The present study finds no support for the idea that age‐ and/or obesity‐related hypoandrogenic state with a decreased ratio of T‐to‐E 2 would cause urethral obstruction. Prostate 68:1296–1306, 2008. © 2008 Wiley‐Liss, Inc.
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