Benign prostatic hyperplasia (BPH) is one of the main urological diseases with its histological prevalence ranging from 42% in men aged 50 to 59 years to 88% among those over 80 years of age. The clinical manifestations of BPH (LUTS - Lower Urinary Tract Symptoms) may include symptoms of bladder emptying (weak and intermittent stream, hesitancy, terminal abdominal effort and drip), which often result from infravesical obstruction (BOO - Bladder Outlet Obstruction) generated by the prostate, and / or symptoms of bladder storage (pollakiuria, nycturia, urgency and urinary incontinence), usually due to detrusor overactivity (DOA - detrusor overactivity). The mechanisms by which BPH produces LUTS are not fully understood. In clinical practice we observe only a poor correlation between the presence and severity of LUTS and urodynamic and anatomical measures of BOO and benign prostate enlargement (BPE - Benign Prostatic Enlargement). The DOA reaches approximately 16% of men in the United States and Europe and its prevalence increases with age. Previous studies reported that the prevalence of DOA increases from 3% among men between 40 and 44 years old to 42% in those over 75 years old. DOA and BOO usually exist together. Two independent studies found that approximately 50% of men with LUTS and BOO confirmed by urodynamic study had DOA. The response of the detrusor muscle to BOO is increase in muscle mass and proliferation of smooth muscle fibers, resulting in increased bladder weight and size. Because no compensatory vascular proliferation accompanies these changes, there is a relative decrease in bladder blood flow. In animal models, a state of chronic hypoxia resulted in DOA, expression of apoptotic markers in intrinsic neurons of the bladder wall, depletion of antioxidants and formation of oxidative elements, resulting in accumulation of harmful free radicals of oxygen that rapidly interact with nitric oxide and generate products called reactive nitrogen species. These products damage nerve fibers, epithelium and microvasculature. Patients with DOA present bladder denervation, suggesting that periods of ischemia and neuronal death may lead to bladder overactivity. In addition, under ischemic conditions, angiogenesis may occur, initiated by local activation of genes and secretion of angiogenic mediators that activate a cascade of cellular mechanisms which culminate in the growth of new capillaries. Until the present date, no analysis of these markers was performed in patients with a history of detrusor overactivity.
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