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About this sample
About this sample
Words: 454 |
Page: 1|
3 min read
Published: Dec 5, 2018
Words: 454|Page: 1|3 min read
Published: Dec 5, 2018
Benign Prostatic Hyperplasia (BPH), is an extremely common condition, espically among older man, which refers to the proliferation of smooth muscles and epithelial cells within the prostatic transition zone, resulting in an increase in size of prostate gland.[1] Prostate tissue has two elements: a glandular element which is composed of secretory ducts and acini; and a stromal element which is composed primarily of collagen and smooth muscle. BPH progression has two phases in which first phase include increase in BPH nodules in the periurethral zone and second phase include significant increase in size of glandular nodules.[2,3]
BPH results in the compression of urethra and may present as Lower Urinary Tract Symptoms (LUTS).[4] LUTS include urinary frequency, urgency, weak stream and nocturia and often have negative impact on Quality Of Life (QOL), commonly in elderly man. [5]. In severe cases patients may develop urinary retention, kidney blockage (hydronephrosis), or renal failure.[6].The excat etiology for BPH is not known, but the hypothesis has been proposed that BPH may be caused from a “reawakening” of embryonic induction processes in adulthood because of the similarity between BPH and the embryonic morphogenesis of prostate. [1,7]
According to the analysis of prostate needle biopsy, the most common benign lesions observed was BPH which is followed by BPH with chronic prostatitis and chronic prostatitis alone. Most of the benign lesions was seen between the age of 60-79 years, and malignant lesions between the age of 70-79 years. [8,9,10,11] The prevalence of BPH increases with age. The histological prevalence of BPH has been observed as 8%, 50% and 80% in 4th, 6th and 9th decades of life, respectively.[12]
Prostatic Hyperplasia is associated with numbers of genetic factors. The growth of prostate gland is controlled by circulating androgens and intacellular steroid signaling pathways mediated through Androgen Receptor (AR). Testosterone (major androgen in males) is converted to Dihydrotestosterone (DHT) by hormone 5-a reductase in Prostatic cells. DHT is a potent stimulator of prostate growth, and plays a central role in pathogenesis of BPH.[13, 14,15] There is no variation in incidence of histological BPH (diagnosed via biopsy or autopsy) across all racial groups, but the incidence of clinical BPH (diagnosed via symptoms and clinical examinations) is found higher among African and Americans than in Asian.
Diet is a potential modifiable risk factor. Asian populations are associated with soya-rich diets, which are high in phyto-estrogens (eg: genistenin), which have an inhibitory effect on BPH. Increased total energy intake, milk and dairy products, red meat, cereals, bread, starch increases the risk for BPH whereas fruits, vegetables (particularly carotenoids), Vitamin D and Vitamin A decreases the risk.[16,17] Other modifiable risk factors may include HTN, serum lipids and lipoproteins, and smoking.[18]
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