Current evidence supports the use of combination therapy in the management of benign prostatic hyperplasia
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Current evidence supports the use of combination therapy in the management of benign prostatic hyperplasia Current evidence supports the use of an a1-adrenergic receptor antagonist in combination with a 5a-reductase inhibitor for the treatment of symptomatic benign prostatic hyperplasia (BPH). The combination of an a1-adrenergic receptor antagonist plus a cholinergic receptor antagonist is an option for the treatment of lower urinary tract symptoms suggestive of BPH.
Very common in older men Benign prostatic hyperplasia (BPH), a very common condition in older men, is caused by unregulated proliferation of smooth muscle and epithelial cells within the transition zone of the prostate.[1] Unregulated cellular proliferation leads to increased stromal smooth muscle tone and prostate volume, which in turn leads to physical compression of the urethra and mechanical obstruction of the bladder outlet. This can result in the following lower urinary tract symptoms (LUTS):[1,2] storage symptoms (e.g. frequency, nocturia, urgency); voiding symptoms (e.g. hesitancy, straining); post-micturition symptoms (e.g. sensation of incomplete emptying). LUTS are also independently associated with diminished health-related quality of life, impaired activities of daily living and falls, with advanced BPH leading to urinary infections, acute urinary retention and renal failure.[1]
a1-Adrenergic receptor antagonists target the dynamic component a1-Adrenergic receptor antagonists relieve the dynamic (smooth muscle) component of BPH.[1] The distribution of the three types of a1-adrenergic receptors (i.e. a1A, a1B and a1D) varies between different organs and tissues. Approximately 70% of a1-adrenergic receptors in the stromal smooth muscle cells of the prostate are of the a1A subtype.[3] a1B-Adrenergic receptors are found in the smooth muscle of arteries and veins, and a1D-adrenergic receptors are found in the bladder and also in the spinal cord, where they appear to play a role in the sympathetic modulation of parasympathetic activity.[1,4] The beneficial effects of a1-adrenergic receptor antagonists are thought to be mediated via a1A- and a1D-adrenergic receptors in the prostate, bladder and spinal cord.[4] By blocking these receptors, a1-adrenergic receptor antagonists relax the smooth muscle of the prostate and bladder neck, thereby improving urine flow and reducing LUTS. However, these agents do not hamper prostate growth, nor do
they appear to reduce the risks of progression to acute urinary retention or the need for surgery.[1] A number of a1-adrenergic receptor antagonists (e.g. alfuzosin, doxazosin, indoramin, naftopidil, prazosin, silodosin, tamsulosin and terazosin)[1,4,5] have been developed, although the availability and approved indications of these agents varies between countries. These drugs differ in their relative selectivity for the a1-adrenergic receptor subtypes (table I). According to recent American Urological Association (AUA)[6] and European Association of Urology (EAU) guidelines,[4] alfuzosin, doxazosin, tamsu
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