ABSTRACT
Benign prostatic hyperplasia therapy has evolved over the last two decades from a simple choice between watchful waiting and transurethral resection of the prostate to more complex treatment decisions between various medical therapies and an expanding range of minimally invasive treatment options. Most patients who suffer some degree of bother from their benign prostatic hyperplasia-associated symptoms will now opt for medical therapy in the first instance. Plant extracts from a variety of sources (Figure 122) are popular, especially in continental Europe, but there is little hard evidence from randomized trials of their efficacy and safety. α-Blockers, such as doxazosin, tamsulosin and alfuzosin, can all be administered once per day and produce rapid and sustainable improvement of lower urinary tract symptoms and uroflow (Figure 123)55. It has been argued that tamsulosin, which has selec tivity for the α1A and α1D adrenoceptor subtypes, and alfuzosin, which is also relatively ‘uroselective’ (i.e. has more impact on
prostate obstruction than blood pressure) have some advantages over doxazosin and terazosin, which have a balanced effect on all three receptor subtypes. However, doxazosin reduces the blood pressure in hypertensive men but has little or no impact on the blood pressure of normotensive individuals56. Doxazosin also reduces platelet adhesiveness and reduces LDL cholesterol, and thus may offer some cardiovascular protection in addition to improvement of lower urinary tract symptoms and uroflow57. Both doxazosin and terazosin, but not tamsulosin or alfuzosin, have been shown to cause apoptosis within the prostate, and it has been argued that this may rebalance the proliferative processes that underlie the condition (Figure 124). However, the clinical utility of this is still unproven.
