Epidemiology and etiology of benign prostatic hyperplasia and bladder outlet obstruction Patel ND, Parsons J K. SYMPOSIUMYear : 2. BPH may compress the urethra and result in anatomic bladder outlet obstruction (BOO); BOO may present as lower urinary tract symptoms (LUTS), infections, retention and other adverse events. BPH and BOO have a significant impact on the health of older men and health- care costs. As the world population ages, the incidence and prevalence of BPH and LUTS have increased rapidly. This article has a correction. Please see: “Differential diagnosis of usual interstitial pneumonia: when is it truly idiopathic?” Wim A. Wuyts, Alberto Cavazza. Hypertension affects approximately 75 million adults in the United States and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic. Although non- modifiable risk factors - including age, genetics and geography - play significant roles in the etiology of BPH and BOO, recent data have revealed modifiable risk factors that present new opportunities for treatment and prevention, including sex steroid hormones, the metabolic syndrome and cardiovascular disease, obesity, diabetes, diet, physical activity and inflammation. We review the natural history, definitions and key risk factors of BPH and BOO in epidemiological studies. Keywords: Etiology, benign prostatic hyperplasia, bladder outflow obstruction, epidemiology, genetics, public health. How to cite this article: Patel ND, Parsons J K. Benign prostatic hyperplasia (BPH) is a histological diagnosis associated with unregulated proliferation of connective tissue, smooth muscle and glandular epithelium. How to cite this URL: Joshi VM, Wadhwa V, Mukherji SK. Imaging in laryngeal cancers. Indian J Radiol Imaging IgG4-related disease is a newly recognized fibroinflammatory condition characterized by tumefactive lesions, a dense lymphoplasmacytic infiltrate rich in IgG4. Epidemiology and etiology of benign prostatic hyperplasia and bladder outlet obstruction. Indian J Urol 2. 01. Benign prostatic hyperplasia (BPH) is a histological diagnosis associated with unregulated proliferation of connective tissue, smooth muscle and glandular epithelium within the prostatic transition zone. In BPH, cellular proliferation leads to increased prostate volume and increased stromal smooth muscle tone. Mc. Neal describes two phases of BPH progression.
The first phase consists of an increase in BPH nodules in the periurethral zone and the second a significant increase in size of glandular nodules. Although age and genetics play important roles in the etiology of BPH and BOO, recent data have revealed novel, modifiable risk factors that present new opportunities for treatment and prevention. These risk factors appear to potentially influence the natural history of BPH and BOO throughout the different stages of clinical progression . Herein, we review current concepts in the epidemiology and etiology of BPH and BOO. Figure 1: Natural history of benign prostatic hyperplasia and bladder outlet obstruction. Click here to view. A persistent challenge in the interpretation of data from population based studies of BPH and BOO is the heterogeneity of the case definitions in the literature. Investigators have utilized many different definitions for BPH, including histological analysis of prostate tissue, radiologic benign prostate enlargement (BPE), decreased urinary flow rates, urodynamic studies consistent with BOO, need for BPH surgery, AUR, and physician- diagnosed BPH and LUTS. LUTS describes a distinct phenotype of a group of disorders affecting the prostate and bladder that share a common clinical manifestation. In recent years, LUTS has become the preferred term for studying urinary symptoms in male populations . The most commonly used measures of LUTS in epidemiologic studies are the American Urological Association Symptom Index (the AUA- SI) and its internationally validated counterpart, the International Prostate Symptom Score (I- PSS). The AUA- SI and I- PSS are robust and reliable metrics for measuring male LUTS. The AUA, European Association of Urology and the World Health Organization International Consultation on Urologic Disease recommend the routine use of the I- PSS in the clinical evaluation of patients with suspected BPH and BOO. However, prior epidemiological studies have not consistently utilized the term . Despite widespread use of medical therapy, BPH remains, on a population level, associated with a substantial incidence of BOO- associated adverse events, including LUTS, urinary infections, bladder calculi, urinary retention and acute renal failure. In a study of 3. 7 million US men presenting to emergency rooms in the state of California, for example, the incidence of urinary retention increased 2. In 2. 00. 0, BPH accounted for $1. US estimated annual costs of BPH treatment in the US total at least $3. Autopsy studies have observed a histological prevalence of 8%, 5. In the osteoporotic fractures in men study cohort, a prospective study of 6. US, 2. 9% of those without LUTS at baseline developed clinically significant LUTS within 2 years of follow- up; among those . By 2. 03. 0, for example, 2. US population will be 6. Significantly, the fastest growing segment of the elderly population is the oldest age group: Those over age 8. Current estimates are that the number of individuals 8. US will rise from 9. Significantly lower prostate volumes have been observed in men from Southeast Asia compared to western populations. One case control analysis, in which cases were men less than 6. BPH, noted 4- fold and 6- fold increase in the age- specific risks of BPH surgery among all male relatives and brothers, respectively, of cases. These investigators further estimated that 5. BPH less than 6. 0 years of age had an inheritable form of the disease. In a study of 1. 60 North Indian men with LUTS, deletions of Glutathone S- transferase enzyme genes, thought to confer cellular resistance to oxidative stress, were significantly associated with an increased risk of symptomatic BPH. Multiple studies have explored associations of endogenous sex steroid hormones - namely testosterone, DHT and estrogen - with BPH and LUTS. At least 7 observational studies have reported no associations and 5 inverse associations of serum testosterone (total, bioavailable, or free) with BPH or LUTS. Furthermore, data from a subset of men in the Proscar long- term efficacy and Safety trial demonstrate low testosterone (< 3. BPH. In one prospective study of community men, those with the highest midlife levels of DHT had nearly 3 times the risk of subsequent BPH compared with those with the lowest levels. These metabolites are surrogate markers for DHT activity, with higher concentrations indicating increased and lower concentrations decreased levels of DHT. Two cross- sectional and one prospective study have shown direct associations of these DHT metabolites with BPH or LUTS. Prior studies have reported positive, negative and null associations of endogenous estrogens with BPH and LUTS. Accumulating data suggest that many of the same metabolic disturbances associated with cardiovascular disease - and the life- style factors that alter these disturbances - influence the risk of BPH and LUTS. These observations are important because they suggest novel targets for prevention and treatment. The metabolic syndrome is a collection of metabolic abnormalities - obesity, glucose intolerance, dyslipidemia and hypertension - that increases the risk of cardiovascular disease and results primarily from dietary and other life- style practices endemic to Westernized societies. Other studies have shown that men with heart disease are at significantly increased risk of both BPH and LUTS. Body weight, body mass index (BMI) and waist circumference have all been positively associated with prostate volume in multiple different study populations. Moreover, obese (BMI . Higher serum concentrations of IGF- 1 and insulin- like growth factor binding protein 3 have been associated with increased risk of clinical BPH and BPH surgery. For macronutrients, increased total energy intake, energy- adjusted total protein intake, red meat, fat, milk and dairy products, cereals, bread, poultry and starch potentially increase the risks of symptomatic BPH and BPH surgery; vegetables (particularly carotenoids), fruits, polyunsaturated fatty acids, linoleic acid, Vitamin A and Vitamin D potentially decrease the risks of symptomatic BPH and LUTS. The mechanisms underlying this relationship are unclear. One potential explanation is that the metabolic syndrome, which promotes systemic inflammation and oxidative stress, mediates the connection. Inflammation has been implicated as a primary stimulus for prostate carcinogenesis and it is possible that BPH represents a non- malignant proliferative pathway promoted by oxidative stress and inflammatory mediators. In one community cohort, men who reported daily non- steroidal anti- inflammatory (NSAID) use experienced significantly decreased risks of LUTS, low urinary flow rate, increased prostate volume and elevated PSA. Current disease trends in the US, Europe and other regions suggest that the incidence and prevalence of these conditions will increase in the near future due to aging of the world population and the increased prevalence of the metabolic syndrome and its components, thereby placing even greater burdens on finite resources. While age and genetic factors play a role in the development of BPH and BOO, many modifiable variables contribute as well - factors that potentially may be altered in order to delay onset, prevent progression or diminish symptoms. Potential strategies include inhibition of DHT synthesis with five- alpha reductase inhibitors, modulation of metabolic risk factors with comprehensive life- style interventions incorporating diet change and physical activity and suppression of inflammatory pathways with NSAIDs. Auffenberg GB, Helfand BT, Mc. Vary KT. Established medical therapy for benign prostatic hyperplasia. Urol Clin North Am 2. Mc. Neal J. Pathology of benign prostatic hyperplasia. Insight into etiology. Urol Clin North Am 1. Update on AUA guideline on the management of benign prostatic hyperplasia. J Urol 2. 01. 1; 1. Trends in adverse events of benign prostatic hyperplasia (BPH) in the USA, 1. BJU Int 2. 01. 2; 1. Prevalence, severity, and health correlates of lower urinary tract symptoms among older men: The Mr. OS study. Urology 2. Lower urinary tract symptoms increase the risk of falls in older men. BJU Int 2. 00. 9; 1. Prevalence and characteristics of lower urinary tract symptoms in men aged> or=8. Urology 2. 00. 8; 7. EAU Guidelines on benign prostatic hyperplasia (BPH). Eur Urol 2. 00. 1; 4.
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August 2017
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