Medical treatment of benign prostatic hyperplasia

Medical therapy for the treatment of benign prostatic hyperplasia (BPH) became an accepted standard of care in the 1990s following the reports of randomized, double-blind, placebo-controlled studies showing that finasteride, a 5-α reductase inhibitor, and terazosin, an α-blocker, significantly improved lower urinary tract symptoms and increased peak urinary flow rates in men with BPH. This article reviews novel approaches to the pharmacological treatment of BPH.     

Alpha blockers for the treatment of benign prostatic hyperplasia

The evolution of alpha blocker therapy for benign prostatic hyperplasia (BPH) has focused on improving convenience and tolerability. Indications for treating BPH include reversing signs and symptoms or preventing progression of the disease. The indication that most commonly drives the need for intervention is relief of lower urinary tract symptoms (LUTS) with the intent of improving quality of life. Alpha blockers are the most effective, least costly, and best tolerated of the drugs for relieving LUTS. Four long-acting alpha 1 blockers are approved by the Food and Drug Administration for treatment of symptomatic LUTS/BPH: terazosin, doxazosin, tamsulosin, and alfuzosin. All are well tolerated and have comparable dose-dependent effectiveness. Tamsulosin and alfuzosin SR do not require dose titration. Alfuzosin, terazosin, and doxazosin have all been shown to be effective in relieving LUTS/BPH independent of prostate size.     

The evolution of alpha-blockers for the treatment of benign prostatic hyperplasia

Alpha-blockers have been evaluated for the treatment of benign prostatic hyperplasia (BPH) for 30 years, from early trials with the nonselective alpha-inhibitor phenoxybenzamine to short-acting (prazosin) then long-acting (terazosin, doxazosin, tamsulosin, alfuzosin) selective alpha(1)-antagonists. All of the alpha-blockers evaluated have demonstrated comparable effectiveness, and the evolution of alpha-blocker therapy for BPH has therefore focused primarily on improving convenience and tolerability. Although all of the long-acting alpha(1)-blockers are well tolerated, only tamsulosin and alfuzosin SR are administered without the requirement for dose titration. Alfuzosin has the additional advantage over tamsulosin of a lower incidence of ejaculatory dysfunction. Studies of subtype-selective alpha(1)-antagonists have not demonstrated superior efficacy or improved tolerability over the existing long-acting alpha(1)-blockers.     

Pharmacotherapy for benign prostatic hyperplasia.

Benign prostatic hyperplasia is a benign neoplasm of the prostate seen in men of advancing age. Microscopic evidence of the disorder is seen in about 70% of men by 70 years of age, whereas symptoms requiring some form of surgical intervention occur in 30% of men during their lifetime. Although the exact cause of benign prostatic hyperplasia is not clear, it is well recognized that high levels of intraprostatic androgens are required for the maintenance of prostatic growth. In recent years, extensive surveys of patients undergoing transurethral resection of the prostate reveal an 18% incidence of morbidity that has essentially not changed in the past 30 years. This procedure is also the second highest reimbursed surgical therapy under Medicare. These findings have resulted in an intensive search for alternative therapies for prostatic hyperplasia. An alternative that has now been well defined is the use of alpha-adrenergic blockers to relax the prostatic urethra. This is based on findings that a major component of benign prostatic hyperplasia symptoms is spasm of the prostatic urethra and bladder neck, which is mediated by the alpha-adrenergic nerves. A second approach is to block androgens involved in maintaining prostate growth. Several such drugs are now available for clinical use, and we discuss their side effects and use. We also include the newer recommendations on evaluating benign prostatic hyperplasia that are cost-effective yet comprehensive.     

The role of gonadotropin-releasing hormone antagonists for the treatment of benign prostatic hyperplasia

Medical therapy is the preferred first-line approach in the management of lower urinary tract symptoms in men with benign prostatic hyperplasia. The magnitude of the improvement in lower urinary tract symptoms observed in response to combination therapy (alpha-blocker plus 5-alpha reductase inhibitors) does not approach that achieved with prostatectomy. Various drugs have been under consideration, including BXL628, lonidamine, and phosphodiesterase inhibitors, all of which have had unacceptable side effects. The gonadotropin-releasing hormone antagonist cetrorelix is associated with dose-dependent symptom improvement and reduction of prostate volume. Elucidating the mechanism for cetrorelix-mediated improvement in lower urinary tract symptoms will likely contribute to unraveling the pathophysiology of lower urinary tract symptoms in men.     

Summary of clinical experiences with tamsulosin for the treatment of benign prostatic hyperplasia

Tamsulosin, a uroselective alpha(1A)-adrenergic-receptor antagonist, has been shown to improve lower urinary tract symptoms associated with benign prostatic hyperplasia. It has a better side effect profile than earlier alpha-adrenergic-receptor antagonists, which were initially developed as antihypertensive agents. Clinical trials of 1 year or longer with tamsulosin show high tolerability for the 0.4 mg dose and no significant interaction with other antihypertensive medications.     

Update on the american urological association guidelines for the treatment of benign prostatic hyperplasia

The updated 2003 American Urological Association (AUA) Guidelines for the treatment of benign prostatic hyperplasia (BPH) are the culmination of an exhaustive effort predicated on scientifically accepted methods of reviewing the medical literature. In this second publication of the guidelines, a multidisciplinary panel reviewed a new meta-analysis of outcome data from the BPH literature from before and after 1994. The major differences between the 2 guidelines are the changes in our understanding of the biology of the prostate and the introduction of new therapies. The vast majority of randomized controlled trials, particularly with respect to minimally invasive therapies and progression of BPH, were performed after the release of the 1994 guidelines. Also, the most recent AUA panel carefully reviewed unpublished data to make the guidelines as timely as possible. Studies that were subsequently published included those on the value of combination medical therapy for BPH. The panel agreed on updated recommendations for the treatment of moderate-to-severe lower urinary tract symptoms associated with BPH, and diagnostic algorithms were revised. The durability and utility of the present guidelines should exceed that of its predecessor.     

Clinical evaluation of benign prostatic hyperplasia

Benign prostatic hyperplasia (BPH) is the most common neoplastic condition afflicting men and constitutes a major factor impacting male health. Clinical evaluation to assess the presence and degree of voiding dysfunction and/or the role of BPH in its presence has an increasingly broad spectrum of treatment goals. The goals of the evaluation of such men are to identify the patient's voiding or, more appropriately, urinary tract problems, both symptomatic and physiologic; to establish the etiologic role of BPH in these problems; to evaluate the necessity for and probability of success and risks of various therapeutic approaches; and to present the results of these assessments to the patient so he can make an informed decision about management recommendations and available alternatives.     

Economic impact of surgical intervention in the treatment of benign prostatic hyperplasia

The economic burden of benign prostatic hyperplasia (BPH) on our health care system is significant and likely to continue to grow given the burgeoning elderly population. Coincident with the rising number of annual physician office visits and expenditures for BPH has been a dramatic shift in the disease's management, from surgical to medical care. However, long-term cost data call into question the appropriateness of medical therapy as the initial treatment approach for all men with BPH, particularly those with moderate to severe symptoms. Although there has been a paradigm shift away from traditional BPH surgery, there has been renewed interest in the treatment of BPH with novel surgical techniques and minimally invasive surgeries. The economics of surgical interventions for BPH are discussed.     

Evaluating men with benign prostatic hyperplasia

The clinical manifestations of benign prostatic hyperplasia (BPH) include lower urinary tract symptoms (LUTS), poor bladder emptying, urinary retention, detrusor instability, urinary tract infection, hematuria, and renal insufficiency. However, the majority of men with BPH present with LUTS only. Because LUTS can indicate a variety of conditions, evaluation of symptomatic men must first aim to identify or exclude BPH and, if present, assess its severity. It is important to assess symptom severity at baseline and during follow-up, using the American Urological Association Symptom Index or the International Prostate Symptom Score. Further testing can then be tailored to narrow the diagnosis and guide treatment decisions. Factors such as patient age and concomitant malignancy will also affect management, but the main goal of treatment remains the improvement of quality of life for the patient.     

Role of inflammation in benign prostatic hyperplasia

Inflammation of the prostate may represent a mechanism for hyperplastic changes to occur in the prostate. There are a variety of growth factors and cytokines that may lead to a proinflammatory process within the prostate. There are several proposed mechanisms that lead to both the intrinsic and extrinsic basis of inflammation. Prostatic inflammation may represent an important factor in influencing prostatic growth and progression of symptoms. This article reviews the recent literature on inflammation leading to chronic prostatic diseases, such as benign prostatic hyperplasia.     

A 63 element 1.75 dimensional ultrasound phased array for the treatment of benign prostatic hyperplasia

Background  

Prostate cancer and benign prostatic hyperplasia are very common diseases in older American men, thus having a reliable treatment modality for both diseases is of great importance. The currently used treating options, mainly surgical ones, have numerous complications, which include the many side effects that accompany such procedures, besides the invasive nature of such techniques. Focused ultrasound is a relatively new treating modality that is showing promising results in treating prostate cancer and benign prostatic hyperplasia. Thus this technique is gaining more attention in the past decade as a non-invasive method to treat both diseases.     

Etiological considerations for the growth of stroma in benign prostatic hyperplasia

The finding that human benign prostatic hyperplasia (BPH) consisted primarily of fibromuscular tissue has led to basic research into the hormonal control of the growth of male accessory sex organ smooth muscle. By using the separated epithelium and muscle layers of the guinea pig seminal vesicle, it was determined that the epithelium exhibited only reversible androgen-induced growths, whereas the muscle proved to be a target tissue for both androgen and estrogen, and exhibited irreversible growth responses. It was of particular interest that the normal androgen-dependent pubertal development of the muscle involved an approximate twofold increase in DNA, followed by the development of a complete and relatively selective androgenic insensitivity in this parameter. An understanding of the factors leading to this apparently normal androgen-dependent loss of the proliferative response in muscle may allow for the development of specific hypotheses for the reawakened stromal growth in BPH. Research on other organ systems focusing on the various factors and mechanisms involved in muscle growth regulation is briefly discussed.