ABSTRACT
The pathogenesis of benign prostate hyperplasia (BPH) is still unclear. It is a common disease affecting exclusively humans in its full clinical appearance. There is a broad variety of possible underlying mechanisms which most likely interact in the pathogenesis of the disease: inflammatory processes taking place predominantly in the stroma and inducing proliferation of all tissues within the transitional zone, an imbalance of androgens and estrogens and their receptors, hyperinsulinemia and hypercholesterolemia (metabolic syndrome) as direct promoters of glandular growth and autosomal dominant inheritance. The detrusor muscle responds to the increased outflow resistance with muscular hypertrophy. Decreased compliance of the bladder wall results in voiding difficulties while electric instability of the hypertrophied detrusor muscle and increased recruiting of otherwise silent afferent fibres cause storage symptoms.
