Benign prostatic hyperplasia (BPH), referred to as benign prostatic hyperplasia or prostatic hyperplasia, is one of the most common urological conditions in older men. This is a pathological diagnosis of benign prostatic hyperplasia, which is mainly a hyperplasia of the prostate gland epithelium or stroma, not cellular hypertrophy, so it is inaccurate to call it prostate hypertrophy in the past. As benign prostatic enlargement can lead to benign prostatic enlargement (BPE), the obstruction of the bladder outlet caused by benign prostatic enlargement can cause a series of urinary symptoms. In recent years, many scholars have found that the so-called prostatic enlargement symptoms in elderly men are not exclusively related to bladder outlet obstruction due to prostate enlargement, but that alterations in the function of the forceps muscle in the elderly can also produce similar symptoms, either due to long-term bladder outlet obstruction or due to aging of the forceps muscle. The term “lower urinary tract symptoms” (LUTS) is used internationally to describe a range of urinary symptoms in older men. Therefore, having BPH is not necessarily associated with BPH, and BPH is not necessarily associated with bladder outlet obstruction. The symptoms of BPH usually refer to a series of lower urinary tract symptoms caused by the enlargement of the prostate gland due to BPH, which results in bladder outlet obstruction. The etiology and pathogenesis is still unclear. The production of testosterone by old age and functional testes is changed to dihydrotestosterone (DHT) by 5α-reductase and is the basis for the occurrence of hyperplasia. In human prostate androgens as DHT account for 90% of the production from the testes. The adrenal glands produce only 10% of the androgens. Androgens are not only necessary for normal cell proliferation and differentiation in the prostate, but they also inhibit cell death, and it is thought that reducing death may be more important. Eunuchs who have their testes removed before puberty have a lifelong undeveloped prostate, and even in old age, the prostate does not develop because of the lack of androgens. Those congenitally deficient in 5α-reductase have a non-developing prostate. 5α-reductase is also clinically applied to treat benign prostatic hyperplasia, causing it to shrink. Testosterone and dihydrotestosterone bind to the same receptor in the prostate, but dihydrotestosterone has a five-fold stronger affinity than testosterone and is also more stable. In contrast to the prostate, which responds to androgen receptors throughout life and remains at high levels even in old age, penile development is controlled by androgen receptors but stops growing after adulthood without control. Nuclear androgen receptors are higher in prostate hyperplastic tissue than in normal tissue. The role of estrogen in the pathogenesis of BPH has been demonstrated experimentally in dogs, but is not yet known in humans. Estrogen plasma levels in older men are elevated both in their absolute values and in their ratio to testosterone, while estrogen is also increased within BPH and estradiol levels in peripheral blood are higher in patients with bulky prostates. Regulation of programmed cell death (apoptosis) is important for maintaining prostate volume, testosterone and dihydrotestosterone inhibit apoptosis, and orchiectomy increases apoptosis in the epithelium of the gland lumen and the distal portion of the glandular ducts. An imbalance between cell proliferation and apoptosis is responsible for the development of prostatic hyperplasia. Numerous growth factors are involved in the proliferative and apoptotic processes. Cell proliferation and BEGF, EGF, KGF, IGF interact with each other and are regulated by dihydrotestosterone. tgeβ inhibits epithelial proliferation. The stromal and epithelial theory, after a lot of experiments, proved that the interaction between prostate epithelium and stroma, stromal cells can regulate the growth of epithelium and other stroma through paracrine or autocrine mechanisms, and a variety of growth factors are involved in the role. Stem cell theory, aged stem cells block their maturation process and prevent their apoptosis. Family genetics, first-degree family members with BPH surgery have a 4.2-fold higher chance of developing BPH than controls; 50% of patients who had surgery before age 60 may be genetically related, while only 9% of patients who had surgery over age 60 were genetically related. The volume of domestic BPH was also greater than that of disseminated, 82.7 ml and 55.5 ml, respectively. Pathology Prostatic hyperplasia begins in the gland surrounding the urethral mons (the migratory zone), which accounts for 5% of the prostate tissue, with the remaining 95% consisting of 3/4 of the peripheral zone and 1/4 of the central zone. The peripheral zone is the starting site of prostate cancer, which is compressed into a pseudo-envelope during prostate enlargement, while the central zone is the site through which the ejaculatory ducts pass. Atypical hyperplasia in the prostate tissue may be a precancerous state. The enlarged prostate gland may compress the peripheral gland to form a pseudo-envelope that is clearly delineated from the enlarged gland. The hyperplastic gland may develop in all directions and have become lobulated, causing the urethra of the prostate segment to bend and elongate, the urethra to be compressed, and the seminal caruncle to move down close to the external sphincter. In the early years, prostatic hyperplasia was divided into several types, which are still useful for reference: ① 30% enlargement of the middle lobe alone, ② 14% enlargement of both lobes alone, ③ 22% increase in both lobes and middle lobe, ④ posterior joint hyperplasia, where the glandular hyperplasia causes a wide block to form on the posterior lip of the bladder neck for 14%, ⑤ 17% hyperplasia of both lobes and posterior joint. These different sites of prostatic hyperplasia cause varying degrees of urethral obstruction, so the size of the prostate and the degree of obstruction are not closely related. Sometimes a prostate located at the bladder outlet of less than 10 g can cause severe obstruction and difficulty in urination, while bilateral lobar enlargement several times larger does not affect urination. The onset of prostatic hyperplasia is slow, and the obstruction to urination causes thickening of the bladder forcing muscles, the appearance of trabeculae on the mucosal surface, and in severe cases, the formation of pseudodiverticulae. Hypertrophy of the interureteral crest can aggravate the difficulty in urination. Long-term difficulty in urination makes the bladder highly distended, the internal pressure rises, the end of the ureter loses its valve, vesicoureteral reflux occurs, causing hydronephrosis and renal insufficiency, and obstruction causes urinary retention prone to infection and stone formation. The symptoms of prostate enlargement usually appear after the age of 50. The severity of symptoms depends on the degree of obstruction, irritation, the functional status of the forced urinary muscles, the presence of complications such as infection and stones, and not on the size of the prostate. The clinical symptoms can be mild or severe. The symptoms of prostatic hyperplasia can be divided into two main categories: Obstruction: hesitant urination, intermittent urine line, terminal drip, thin and weak urine line, prolonged urination time, incomplete urination, filling incontinence, etc. Stimulation: urinary frequency, urinary urgency, increased nocturia, low urine volume, urge incontinence. In recent years, with the development of urodynamics, it has been found that 50% to 80% of patients with prostatic hyperplasia have an unstable bladder. And those who are routinely examined for prostatic hyperplasia are found to have no bladder outlet obstruction by urodynamic examination in about 1/4 of the patients, which means that these patients, whether they have difficulty urinating or have irritative symptoms, are not due to bladder outlet obstruction caused by prostatic hyperplasia, but are related to changes in the function of the forced urinary muscle. Therefore, while understanding the patient’s symptoms, attention should also be paid to the presence of corresponding diseases that may cause dysfunction of the forceps urinaryis muscle, such as diabetes mellitus and cerebrovascular accidents, etc. If further determination of the cause of their symptoms is needed, urodynamic testing is required. Among the symptoms of obstruction, thinning and weakness of the urinary line is due to compression of the urethra by the enlarged prostate, which can appear in the early stages of prostate enlargement. Hesitation of urination is the prolongation of the time required for the contraction of the forceps to begin to cause the intravesical pressure to exceed the urethral resistance. The urinary line is interrupted because the forceps cannot maintain its pressure until the end of urination. Sometimes urine dribbling continues at the end of urination. Patients often have a sense of incomplete urination, and in severe cases, urinary retention, inability to empty the bladder, residual urine, frequent filling of the bladder, reduced effective capacity, and shorter intervals between urination. The enlarged prostate makes the bladder forceps respond more frequently to urination. If the prostate is large and protrudes into the bladder, the bladder capacity is reduced and the frequency of urination is more pronounced. The frequency of urination and the increase in the number of nighttime urination are irritating symptoms of urination and are also symptoms that appear in the early stages of prostate enlargement. More than 8 times a day can be considered frequent urination. In addition to the above-mentioned incomplete emptying due to obstruction and enlarged prostate to reduce bladder capacity, prostate congestion and unstable bladder can also cause urinary frequency. Increased nocturia is a result of decreased cortical inhibition during sleep and decreased urethral and urethral sphincter tone, which increases the frequency of nocturia. Urinary urgency and painful urination among the irritation symptoms are uncommon in prostate enlargement and may be caused by co-infections and/or urinary stone formation, etc. If prostate enlargement is dominated by irritation symptoms and prostate enlargement is not obvious, one should think that there may be other causes of urinary disturbance. Urinary retention and filling incontinence, as well as impaired renal function, are late symptoms of prostatic hyperplasia. The more severe the obstruction, the more residual urine in the bladder appears, the greater the amount of residual urine, the gradual loss of contraction of the detrusor muscle, and incontinence can occur. Overfilling of the bladder causes urine to overflow from the urethra, called filling incontinence. In the case of filling incontinence, due to increased pressure within the bladder, it can lead to fluid accumulation in the ureters and kidneys, which can impair kidney function. Hematuria is not uncommon in prostate enlargement and may be caused by local congestion or, if combined with infection and urinary stones, hematuria with bladder irritation. Prostate enlargement can sometimes be associated with abdominal pain, especially lower abdominal distension. In case of renal insufficiency, there is loss of appetite, nausea and vomiting, pallor and drowsiness. Chronic difficulty in urination and increased abdominal pressure can lead to inguinal hernia, prolapse and hemorrhoids. The diagnosis should include the following aspects: 1. Medical history: Prostatic hyperplasia is a disease of the elderly, if the patient has similar symptoms before the age of 50, the possibility of other diseases should be thought of. History of genitourinary system, history of surgery, history of injury, presence of neurological disorders, history of diabetes mellitus, certain medications that may affect urinary function, especially psychiatric treatment medications. 2. Symptom assessment: Currently, the symptoms of prostate enlargement are quantified and the international prostate symptom score (I-PSS) and quality of life index (QOL) are more widely used (see Table 1). The quality of life index is advocated to include sexual function in addition to urinary symptoms. Symptom assessment may be used not only to assess the severity of symptoms, but also to judge the efficacy of treatments.