Title page
Table of contents
List of figures
List of Abbreviations

1.1       Epidemiology
1.2       Prostate Anatomy
1.2.1    Functions of the prostate
1.2.2    Causes of prostate enlargement
1.2.3    Conversion of testosterone to dihydrotestosterone in the prostate
1.3       Complications of prostate enlargement
1.3.1    Effect of enlarged prostate on the bladder
1.3.2    Effect of enlarged prostate on sexual performance
1.4       Symptoms prostate enlargement
1.5       Diagnoses of BPH
1.5.1    Urinalysis
1.5.2    A urine culture
1.5.3    A prostate specific antigen (PSA) test
1.5.4    Uroflorometry
1.5.5    Pressure-flow urodynamic studies
1.5.6    Ultrasonography
1.5.7    Filling cystometry
1.5.8    Cystoscopy
1.6       Chemotherapeutic agents used in the treatment of BPH
1.6.1    Alpha-1-adrenergic receptor blockers
1.6.2    5-alpha-reductase inhibitors
1.6.3    Antimuscarinics
1.6.4    Phosphodiesterase-5-inhibitors
1.7       Surgical treatment of BPH
1.7.1    Dietary and lifestyle consideration Eating vegetables Weight loss Exercise
1.7.2    Targeted nutritional interventions
1.7.3    Pygeum africanum
1.8       Biochemical markers associated with BPH
1.9       Biomarkers of prostate enlargement
1.9.1    Prostate specific antigen
1.9.2    Metallic prostatic antioxidants (Zinc and selenium)
1.9.3    Renal function test (creatinine and blood urea nitrogen)
1.9.4    Minerals (Potassium, Iron, Magnesium, Calcium, Sodium)
1.10     Aim and Objectives of the Study
1.10.1  Specific Objectives of the Study

2.1       Materials
2.1.1    Sample collection
2.1.2    Chemicals and reagents
2.1.3    Equipment
2.2       Methods
2.2.1    Sample collection
2.2.2    Experimental design
2.2.3    Determination of Prostate Specific Antigen (PSA) Level
2.2.4    Determination of calcium concentration
2.2.5    Determination of magnesium concentration
2.2.6    Determination of sodium concentration
2.2.7    Determination of potassium concentration
2.2.8    Determination of Iron concentration
2.2.9    Determination of selenium concentration
2.2.10  Determination of creatinine concentration
2.2.11  Determination of Blood Urea Nitrogen
2.2.12  Determination of zinc concentration
2.3       Statistical analysis

3.1       Prostate  specific  antigen  (PSA)  level  of  Normal  and  Benign  Prostatic  Hyperplasia subjects attending clinic
3.2       Calcium concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.3       Blood urea nitrogen of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.4       Zinc concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.5       Sodium concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.6       Iron concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.7       Potassium concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.8       Magnesium concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.9       Selenium concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic
3.10     Creatinine concentration of Normal and Benign Prostatic Hyperplasia subjects attending clinic

4.1       Discussion
4.2       Conclusion
4.3       Suggestions for further studies

This study was aimed at investigating biochemical changes associated with benign prostatic hyperplasia in ageing men attending clinic at the university of Nigeria Teaching Hospital, Ituku-Ozalla, Enugu State, Nigeria. The assessment included 50 men with BPH attending clinic in addition to 50 healthy men (control). All samples were divided into 5 groups and with varying age ranges (Group 1: Normal control, Group 2: BPH patients ≤ 60 years, on treatment, Group 3: BPH patients ≤ 60 years, not on treatment, Group 4: BPH patients ≥ 60 years, taking treatment, Group 5: BPH patients ≥ 60 years, not on treatment).PSA levels of BPH positive subjects under treatment increased significantly (p < 0.05) compared with the control. There was a significantly (p < 0.05) high level of calcium in subjects who were ≤60 years of age that are on treatment compared with group 1 (control). Also, the level of blood urea nitrogen (BUN) recorded a high significance (p < 0.05) in comparison to the normal control. In the same study, zinc level decreased non-significantly (p > 0.05) in the groups under investigation and the level of sodium in the blood of positive treated and untreated BPH patients was non-significantly (p > 0.05) high when compared to the healthy subjects. Iron level showed a non-significant (p > 0.05) elevation in subjects ≤ 60 years of age who were on treatment and a significantly level (p < 0.05) in the other groups under investigation. Furthermore, there was a significant (p<0 .05="" 2="" 3="" 4="" 5="" a="" also="" and="" as="" bph="" concentration="" dropped="" elevation="" group="" in="" ion="" level="" levels="" magnesium="" non-significantly="" observed="" of="" p="" patients="" potassium="" result="" showed="" significantly="" study="" the="" this="" though="" untreated="" was=""> 0.05) higher level of selenium in BPH positive patients of all the groups under investigation compared with group 1 (normal control) while creatinine levels showed a significant (p< 0.05) elevation in all the groups being investigated when compared with group 1.

Benign prostatic hyperplasia (BPH) is the nonmalignant enlargement of the prostate gland. It refers to stromal and glandular epithelial hyperplasia that occurs in the periurethral transition zone of the prostate that surrounds the urethra. BPH clinically manifest as lower urinary tract symptoms (LUTS) consisting of irritative (urgency, frequency, nocturia) and obstructive symptoms (hesitancy, a weak and interrupted urinary stream, straining to initiate urination, a sensation of incomplete bladder emptying) (Miller and Tarter, 2009). Prolonged obstructions may eventually lead to acute urinary retention (AUR), recurrent urinary tract infection (UTI), hematuria, bladder calculi, and renal insufficiency (Curtis, 2006). The prevalence of LUTS due to BPH increases with increasing age. Moderate to severe symptoms occur in 40 and 80% of men after the age 60 and by 80 years, respectively. Nearly all men develop microscopic BPH by the age of 90 years (Ogunbiyi and Shittu, 1999). It is also described as quality of life disorder, affecting man’s ability to initiate or terminate urine flow stream (the symptoms interfere with the normal activities), and reduces the feeling of well being. The causes of BPH are not fully known, but the overgrowth of smooth muscle tissue and glandular epithelial tissue is attributed to a number of different causes such as aging, late activation of cell growth, genetic factors, and hormonal changes (Wang and Jicun, 2015).

1.1              Epidemiology

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 (Auffenberg et al., 2009). Prostate tissue is composed of two basic elements: A glandular element composed of secretory ducts and acini; and a stromal element composed primarily of collagen and smooth muscle. In BPH, cellular proliferation leads to increased prostate volume and increased stromal smooth muscle tone. McNeal, (1984) 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......

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Item Type: Postgraduate Material  |  Attribute: 74 pages  |  Chapters: 1-5
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