Bosch R J
Department of Urology, Erasmus University Hospital, Rotterdam, The Netherlands.
Eur Urol. 1991;20 Suppl 1:27-30. doi: 10.1159/000471742.
The pathogenesis of benign prostatic hyperplasia (BPH) remains largely unresolved. Three major theories have evolved over the years, each emphasizing a possible causative mechanism. The first theory, the dihydrotestosterone hypothesis, is based on the failure of BPH to develop in men castrated prior to puberty. The second, the embryonic reawakening theory, assumes a reawakening of the embryonic induction potential of prostatic stroma. The third, or stem cell theory, postulates the development of BPH through an increase in the number of stem cells or through an abnormal increase in clonal expansion of amplifying or transit cells. These mechanisms may act in concert.
良性前列腺增生（BPH）的发病机制在很大程度上仍未得到解决。多年来已形成了三种主要理论，每种理论都强调一种可能的致病机制。第一种理论是双氢睾酮假说，其依据是青春期前被阉割的男性不会发生BPH。第二种理论是胚胎再唤醒理论，该理论假定前列腺基质的胚胎诱导潜能被重新唤醒。第三种理论即干细胞理论，推测BPH是通过干细胞数量的增加或通过扩增细胞或过渡细胞克隆扩增的异常增加而发生的。这些机制可能共同起作用。
