[Benign prostatic hyperplasia and growth factors: mechanisms and hypotheses]

The aetiology and pathogenesis of benign prostate hyperplasia (BPH) are still unresolved questions, although a number of hypotheses have been developed, most of which have still not been confirmed by experimentation. BPH has been regarded as a kind of adenoma, as a stromal disease, as the result of either hormonal imbalance (altered oestrogen/testosterone ratio) or testosterone or dihydrotestosterone stimulation, and finally as the result of oestrogen stimulation, perinatally or involutionally. More recently, scientific interest has focused on the presence and possible function of growth factors and their receptors in the human prostate and their autocrine or paracrine stimulatory effects in BPH development. Hypotheses on their hormonal regulation as well as their interplay during epithelial-stromal interaction have been developed. The intact human prostate produces epithelial (EGF) and basic fibroblast (bFGF) growth factors. Normally, they do not appear to have autocrine or paracrine effects. In androgen deficiency, however, as shown experimentally in castrated rats, the stromal cells express increased amounts of TGF beta, of TGF beta receptor, and of bFGF. Platelet-derived growth factor (PDGF), but not the corresponding receptor, has been shown in prostate. The growth factor receptor-associated tyrosine protein kinase is present in the human prostate in two different forms, but its functional significance in BPH development has not yet been elucidated. A more significant role may be attributed to the recently described growth factors in cultured human stromal cells, which exert multifarious mitogenic and non-mitogenic effects on prostatic epithelium as well as neuronal and non-neuronal cells.(ABSTRACT TRUNCATED AT 250 WORDS)