Benign prostatic hyperplasia is one of the most common benign diseases causing urinary disorders in middle-aged and elderly men. The main manifestations are histological hyperplasia of the interstitial and glandular components of the prostate, anatomical enlargement of the prostate, urodynamic obstruction of the bladder outlet and clinical symptoms mainly in the lower urinary tract, there is no obvious correlation between them, and generally patients with prostatic hyperplasia do not have both of these features.
I. Etiology and epidemiology
At present, the etiology of prostatic hyperplasia is still not well understood. The occurrence of prostatic hyperplasia must be accompanied by both advancing age and functioning testes. Domestic scholars investigated 26 elderly eunuchs of the Qing Dynasty and found that the prostate glands of 21 people had become completely inaccessible or significantly atrophied, suggesting that the secretion of androgens from the testes plays an important role in maintaining the growth, structure and functional integrity of the prostate.
Prostate enlargement is closely related to the imbalance of androgens and estrogens in the body. Testosterone is the main male androgen, and current research has found that testosterone is converted into dihydrotestosterone through the action of 5-reductase and then has an effect on the prostate gland. Dihydrotestosterone is the active hormone that androgens stimulate prostate hyperplasia, and studies have found that the content of dihydrotestosterone in hyperplastic prostate tissue is significantly higher than in normal prostate tissue. However, the mechanism of androgen-induced prostate hyperplasia is still unclear, and most scholars believe that it is related to the disruption of the balance between proliferation and apoptosis of mesenchymal and epithelial cells. Estrogen, growth factors, inflammatory mediators, neurotransmitters and genetics also have an impact on prostate hyperplasia.
There is little regional variation in the ethnicity of histological prostate enlargement found at autopsy, but there is a large regional variation in the epidemiology of clinical prostate enlargement, with some studies suggesting that Asians are more likely than Americans to have symptoms associated with moderate-to-severe prostate enlargement. Data suggest that the incidence of enlarged prostate volume in older adults increases with age, usually initially occurring after age 40, accounting for 50% of those older than 60 years, and reaching more than 80% by age 80. However, these individuals do not always have clinical manifestations. It is now considered that an enlarged prostate with prostatic hyperplasia, along with lower urinary tract symptoms, difficulty urinating and/or a maximum urinary flow rate <15 ml/s is the clinical meaning of prostatic hyperplasia.
II. Pathology
McNeal divides the prostate into periurethral glandular, peripheral, central and migratory zones depending on its embryologic origin. All prostatic hyperplastic nodules occur in the prostatic migratory zone and the periurethral glandular zone. Stromal hyperplasia is the main pathological feature of prostatic hyperplasia. The enlarged nodules compress the rest of the gland to form what is called a “surgical envelope”, which is clearly delineated and is removed during prostatectomy to remove the enlarged tissue on the inside of the envelope. In addition, prostate enlargement is not a pre-prostate cancer, but in about 10% of cases, prostate cancer can be seen in the peripheral area.
Prostate enlargement can cause bladder outlet obstruction, but the degree of obstruction is not proportional to the volume of the prostate, but is directly related to the location and shape of the prostate enlargement. A large number of a receptors exist in the prostate and bladder neck orifice. a1 receptor activation can significantly increase prostatic urethral resistance after activation.
Prostatic hyperplasia can cause lower urinary tract obstruction and produce a series of pathophysiological changes. The first is that the bladder is affected by the extension of the interureteral ridge to both sides, the ureteral orifice moves to the posterior, the compensatory hypertrophy of the forced ureteral muscle occurs due to the elevated resistance to overcome the urethra, and trabecular chambers and even pseudo-diverticulae form. If the obstruction is not lifted for a long time, the forced urinary muscle gradually becomes decompensated, the bladder wall becomes thinner and the contraction force is reduced. The thickening of the bladder forceps can make the ureteral bladder wall segment lengthen and stiffen, leading to ureteral obstruction, and after the bladder loss of compensation, the ureteral bladder wall segment can be shortened again, and under the effect of increased pressure in the bladder caused by obstruction, there will be vesicoureteral reflux, eventually leading to hydronephrosis and renal failure.
Third, clinical manifestations
The symptoms of prostate hyperplasia appear gradually with pathological changes, and patients mostly develop symptoms above the age of 50. The severity of the symptoms is not proportional to the size of the prostate but is related to the degree of obstruction and the presence of infection.
The main manifestations are lower urinary tract symptoms and comorbidities.
1. The clinical manifestations of LUTS include
The symptoms of the urinary storage phase include urinary frequency, urinary urgency, urinary incontinence and increased nocturia; the symptoms of the urinary storage phase include urinary hesitation, difficult urination and intermittent urination; the symptoms of the urinary storage phase include incomplete urination and dribbling after urination.
2.Complications
(1) Hematuria: Prostatic hyperplasia causes varicose veins on the surface of the prostate, which is one of the most common causes of hematuria in elderly men.
(2) Urinary tract infection: prostatic hyperplasia causing lower urinary tract obstruction is very likely to cause urinary tract infection, especially when residual urine appears, the chance of infection is higher.
(3) Bladder stones: long-term lower urinary tract obstruction, especially the increase in residual urine, the accumulation of crystals in the urine in the bladder, coupled with the frequent complications of urinary tract infections and other factors contribute to the formation of bladder stones.
(4) Kidney function damage: mostly late symptoms of prostate enlargement, manifested as loss of appetite, anemia, swelling, etc. Therefore, elderly men with unexplained symptoms of renal insufficiency should first exclude prostatic hyperplasia.
IV. Diagnosis and differential diagnosis
1. Diagnosis Male patients over 50 years old with LUTS as the main complaint should first consider the possibility of PPH. Therefore, it is not difficult to diagnose prostatic hyperplasia clinically based on the patient’s symptoms, which generally requires the following tests.
(1) Rectal palpation: It is a simple and important diagnostic method, and every patient needs to undergo this examination. It is important to check the anal sphincter tone (to distinguish neurogenic bladder dysfunction) and the prostate, noting the size, shape, texture, presence of nodules and pressure pain of the prostate. In the case of prostate enlargement, the first manifestation is the shallowing or disappearance of the central sulcus of the prostate. This is a good way to make a preliminary diagnosis of prostate enlargement. If a suspicious nodule or hard texture of the prostate is found, a systematic biopsy under ultrasound guidance should be performed to exclude prostate cancer.
(2) Ultrasound: Ultrasound can understand the morphology and structure of the prostate, determine the volume of the prostate, and the volume of residual urine. It can also detect early prostate cancer and perform ultrasound-guided systematic biopsy of the prostate. Transrectal ultrasound is more accurate than the transabdominal route in determining prostate volume or internal structure and is now commonly used.
(3) Urine flow rate: The results are more accurate when the patient’s urine volume is 150-200 ml. The most important parameter is the maximum urine flow rate (Qmax), with Qmax ≥ 15 ml/s being normal. The urine flow rate is also one of the best evaluation parameters to compare the efficacy of treatment before and after prostate enlargement patients.
(4) Urodynamics: This test analyzes the function of the detrusor muscle through the pressure flow rate curve and determines the presence of bladder neck obstruction. This test is important to identify whether the difficulty in urination is caused by bladder neck obstruction or neurogenic bladder dysfunction. This test is especially important for patients who are considering surgical treatment.
(5) Cystoscopy: Cystoscopy is not a necessary test for the diagnosis of patients with prostatic hyperplasia, but it is recommended when there is suspicion of combined urethral stricture or intravesical occupational lesions.
(6) Serum prostate-specific antigen (PSA): It is an important screening indicator for prostate cancer. Patients with PSA >4.0ng/ml should be considered for prostate cancer, but there are many factors affecting PSA, such as prostate enlargement, urinary tract infection, prostate puncture and indwelling catheterization can also lead to elevated PSA.
(7) Blood creatinine (creatinine): Bladder outlet obstruction due to BPH can cause impairment of renal function. In patients with hydronephrosis and ureteral dilatation, this test can be performed to understand the status of renal function.
(8) Other: routine urinalysis can be used to understand the presence of urinary tract infection. Urodynamic examination can be used to assess the efficacy of surgery and as a means of differentiation from certain neurogenic urinary disorders.
2.Differential diagnosis
(1) Neurogenic bladder dysfunction: the clinical manifestations are very similar to prostatic hyperplasia, mainly manifesting as difficulty in urination, increased residual urine, hydronephrosis, and decreased renal function, but the patient’s prostate is generally not large, and the patient often has a history of central or peripheral nervous system damage, and urodynamic examination can clarify the diagnosis.
(2) Prostate cancer: patients with prostate enlargement have the possibility of complicating prostate cancer. Therefore, clinical screening tests for prostate cancer in BPH patients are necessary. If a hard node is palpated on rectal examination of the prostate, or if the serum PSA is elevated, or if a suspicious hypoechoic lesion is found in the prostate by transrectal ultrasound, transrectal prostate biopsy should be performed.
(3) Bladder neck obstruction: The age of onset is young, usually in the 40s to 50s. The presence of bladder outlet obstruction on urodynamic examination, but no prostate enlargement on rectal palpation or ultrasound, is usually caused by chronic inflammatory lesions and can be identified by cystoscopy.