The etiology of benign prostatic hypertrophy.
Benign prostatic hypertrophy (BPH) is a hyperplasia and not a hypertrophy. No cogent total explanation for the etiology of this ubiquitous disease has ever been given. There is such a vast cascade of incongruities in respect of hormonal influences, on the one hand, and the degree, variation, timing and rate of development of the condition, on the other hand, that a 'missing link' has constantly been envisaged in its etiology. In the search for this, two simple facts stand out: (a) BPH starts at some time after involution commences; (b) it is the transitional zone that is affected in the major extent. This hypothesis proposes that, owing to dynamic embryological differences between the transitional and the other zones, its secretions are differently affected by involution, resulting in stimulatory factors affecting known hormonal influences upon prostatic growth, further resulting in the development of BPH. These stimulatory factors are considered to be the 'missing link' in the etiology of BPH. It is further suggested that one of these stimulatory factors may be E. coli endotoxin, repeatedly released within a contained prostatic environment. This is considered secondary to intermittent colonization of the transitional zone acini and/or ducts by E. coli, followed by the destruction of these E. coli. This colonization is considered mandatory, if the known 95% occurrence of invasive infection of BPH is to be explained.
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D000818:Animals; D001424:Bacterial Infections / Q000150:complications; D005260:Female; D006801:Humans; D006965:Hyperplasia; D015994:Incidence; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D011467:Prostate / Q000196:embryology / Q000254:growth & development / Q000473:pathology; D011469:Prostatic Diseases / Q000150:complications; D011470:Prostatic Hyperplasia / Q000453:epidemiology / Q000209:etiology* / Q000473:pathology