The Diagnosis of Benign Prostatic Hyperplasia

Several guidelines have been published to aid in the diagnosis of BPH; the most prominent ones are those published by the American Urological Association (AUA)9 and by the European Association of Urology (EAU).29 Both of these guidelines recommend that the diagnosis of BPH is based on a medical history, symptomatic assessment using a validated instrument such as the International Prostate Symptom Score (IPSS), which uses eight items to categorize BPH 'urinary' symptoms as mild (IPSS 0-7), moderate (IPSS 8-19) and severe (IPSS 20-30), and a physical examination consisting of a digital rectal examination (DRE) to evaluate the prostate size. The AUA guidelines have produced a diagnostic algorithm, which is illustrated in Figure 10.

The prostate-specific antigen (PSA) test is used to distinguish between BPH and prostate cancer. PSA, an endogenous serine protease secreted by the epithelium, is a key malignant tumor marker. At present, a number of methods are used to assess PSA (e.g., PSA velocity, PSA density, age-specific PSA, and free/total PSA ratio), which have been developed as a way of enhancing specificity of the measure. More recently, glycosylation of PSA is being examined as a way of further refining the distinction between BPH PSA and prostate cancer PSA. In one study, urinary PSA isoforms were characterized by ion-exchange chromatography and lectin affinity chromatography using immobilized plant lectins in patients with either prostate cancer or BPH. Although PSA recovery from urine was low (up to 60%) the researchers identified two main prostate cancer isoforms and two BPH isoforms, which had different binding affinities to Ulex europaeus agglutinin, Aleuria aurantia agglutinin, Phaseolus vulgaris erythroagglutinin, and P. vulgaris leukoagglutinin.30 Other tumour markers are also being established; for example, telomerase activity in epithelium cells, which is determined by a telomeric repeat amplification protocol assay, was detected in 90% of prostate cancer cases compared with 13% in BPH cases. This measure had a specificity of 76% and a positive predictive value (of cancer) of 87%.31

Animal Models

Figure 10 The AUA diagnostic and treatment algorithm for benign prostatic hyperplasia (BPH): *In patients with clinically significant prostatic bleeding; wpatients with at least a 10-year life expectancy for whom knowledge of the presence of prostate cancer would change management or patients for whom the PSA measurement may change the management of voiding symptoms; DRE, digital rectal examination; IPSS, International Prostate Symptom Score; PE, physical examination; PSA, prostate-specific antigen; PVR, postvoid residue; UTI, urinary tract infection. (Reproduced with kind permission from AUA Practice Guidelines Committee. J. Urol. 2003, 170, 530-547.)

Figure 10 The AUA diagnostic and treatment algorithm for benign prostatic hyperplasia (BPH): *In patients with clinically significant prostatic bleeding; wpatients with at least a 10-year life expectancy for whom knowledge of the presence of prostate cancer would change management or patients for whom the PSA measurement may change the management of voiding symptoms; DRE, digital rectal examination; IPSS, International Prostate Symptom Score; PE, physical examination; PSA, prostate-specific antigen; PVR, postvoid residue; UTI, urinary tract infection. (Reproduced with kind permission from AUA Practice Guidelines Committee. J. Urol. 2003, 170, 530-547.)

A number of optional diagnostic tests are also recommended by the AUA and EAU guidelines. Urinalysis (dipstick testing or microscopic examination of urine sediment) is recommended if hematuria or urinary tract infections (UTIs) are present. To determine the presence of obstruction (i.e., PBOO or BOO) in BPH patients with severe or bothersome LUTS, a number of urine flow and urine pressure assessments can be undertaken; in general, a low urine flow rate and high urine pressure are indicative of obstruction. Urine flow is usually assessed via uroflowmetry, a noninvasive measure that can reveal abnormal voiding. A number of flow-type measures have been developed as a way of improving this measure; for example, the maximum flow rate (Qmax) is a commonly used endpoint in clinical trials, which has a specificity of 78%.32 Pressure-flow studies are used to categorize the severity of obstruction, and usually involve the measurement of both intravesical and intra-abdominal pressure. Postvoid residue (PVR) is a noninvasive measure obtained via transabdominal ultrasonography. Studies have shown that the normal PVR in healthy males is usually less than 5 mL and no more than 12 mL, whereas PVR volumes exceeding 200 mL may indicate that bladder dysfunction or detrusor instability are present.33 Some studies have also reported a correlation between the increase in PVR and a decrease in detrusor contractility. Other diagnostic measures include endoscopy, which can provide additional information on the type and degree of obstruction, and imaging (renal ultrasonography) of the lower urinary tract.

Although these optional diagnostic measures are used to evaluate patients with LUTS suggestive of BOO, there is still few data validating their reliability. In a recent study, 152 men with LUTS and suspected BOO were examined using a number of procedures such as PVR, uroflowmetry, and pressure-flow studies. The researchers found that 45.8% had some form of obstruction, and the degree of obstruction was related to prostate volume, PVR, and Qmax; the severity of BOO was also strongly related to detrusor overactivity, which increased from 16% in the mildly obstructed group to 53.4% in the severely obstructed group.34

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