Early treatment of benign prostatic hyperplasia: implications for reducing the risk of permanent bladder damage.

A significant change has occurred in the management of symptomatic benign prostatic hyperplasia (BPH) since effective pharmacological treatment became available and led to a significant decrease in the number of surgical procedures in many Western countries. The hypothesis of a causative role of benign prostatic enlargement and bladder outflow obstruction (BOO) in lower urinary tract symptoms (LUTS) was based on the association between prostate growth and symptoms of prostatism in elderly men and on the dramatic reduction of LUTS upon relief of obstruction. Careful investigation into the epidemiology of LUTS and BPH failed to confirm such an association and opened new perspectives in the pathophysiology of lower urinary tract dysfunction and symptoms. The observation that LUTS were equally distributed in male and female cohorts, when matched for age, moved attention away from the prostate and towards the urinary bladder and its aging-related disorders. When BPH surgery was developed, the management of the disease was aimed at preventing death from chronic renal failure, but the picture has changed and modern medical treatment is now aimed at improving the patient's quality of life. The increasing size of elderly populations in the Western world and the consequent financial constraints of national healthcare systems have raised the question of when pharmacological treatment of symptomatic BPH should be initiated. Retrospective and prospective analysis of various BPH populations and clinical studies has clearly defined the capacity of pharmacological treatment to reduce the incidence of complications of BPH, such as acute urinary retention and the need for surgery, but the cost/benefit ratio is unclear. Notwithstanding the limitations inherent in the experimental models, there is evidence from various animal models, investigating the pathophysiology of the urinary bladder in the presence of outflow obstruction, to indicate that a cause and effect relationship between BOO and bladder decompensation has been established and to support the hypothesis that permanent bladder damage may occur when the obstruction is not relieved early enough. Preliminary experimental evidence also suggests that alpha(1)-adrenoceptor antagonists may have a role in reducing the damaging effects of BOO on the urinary bladder. At present, there is no evidence to support the need for early pharmacological treatment of symptomatic BPH with no BOO beyond the obvious target of improving the patient's quality of life. The evidence for early treatment of BOO and the need to preserve bladder function is clear. Further experimental and clinical research is required to identify markers of early bladder damage and decompensation which can be used to select patients for early pharmacological treatment of BPH.