Prostatic hyperplasia causes bladder outlet obstruction, which affects the normal function of the urinary system and produces urinary symptoms of varying degrees. Further development of the disease can eventually lead to serious complications: acute urinary retention, urinary tract infection, hematuria, bladder stones, impaired renal function and so on. Surgical treatment methods, although more effective and with a low mortality rate, still bring varying degrees of damage to patients. According to the long-term follow-up of urethral electrolysis of the prostate in the United States, it was found that 20% to 25% of patients had unsatisfactory long-term results. Postoperative still have urinary symptoms, follow-up for more than 10 years, for 15% to 20% of patients to do surgery again, postoperative urinary incontinence occurred 2% to 4%, impotence 5% to 10%, reverse ejaculation up to 70% to 75%, intraoperative blood transfusion may cause serious infection. In recent years, 5α-reductase inhibitors and α1-adrenergic receptor blockers have been used clinically for the treatment of BPH with good results. The latest views generally agree that drug therapy should be the first line of treatment for prostate hyperplasia. However, drug therapy can only be applied to some patients and cannot achieve the results obtained by surgery. The emergence of urinary symptoms and complications in BPH is related to the following 3 lesions: ① forced urethral muscle lesions. ② prostatic dynamics: including the prostate, the prostatic envelope and the smooth muscle of the bladder neck. Increased muscle tone of the smooth muscle will cause varying degrees of lower urinary tract obstruction symptoms. ③ Prostatic factors: urinary frequency, urinary urgency, and urinary incontinence. At present, all prostatic hyperplasia treatments target prostatic power factors and static factors. 1, prostatic hyperplasia drug treatment (1) androgen inhibition therapy: ① 5α reductase inhibitor: the application of 5α reductase inhibitor for the treatment of BPH is inspired by the study of a class of pseudohermaphroditic hereditary diseases. In the Dominican Republic had found 47 patients from 29 families with the clinical phenomenon pseudo vaginal perineal scrotal type of hypospadias. As a child, the penis is small and resembles the clitoris, the scrotum is underdeveloped and resembles the labia, and the testes with incomplete descent can be seen. However, at puberty, the penis grows, the muscles are well developed, and the testes descend, with significant male characteristics, but the prostate gland still cannot be seen; plasma testosterone is mildly increased, while dihydrotestosterone (DHT) decreases significantly, and the testicular biopsy cells and spermatogenesis are normal. These patients confirm that the prostate lacks reductase, which cannot convert T to DHT, causing the prostate to fail to develop normally. The use of 5α reductase inhibitors, blocking the conversion of T to DHT, can be made similar to the model of this disease, to prevent prostate hyperplasia, it is now known that there are two types of 5α reductase in the human body, 5α reductase Ⅰ is located in the skin and liver, while 5α reductase Ⅱ exists in the epididymis, prostate, seminal vesicles and the liver. Finasteride (Finasteride, MK906), now in clinical use, is known by the trade name of Prolixin. It is a synthetic 4-steroidal hormone compound with molecular weight of 373,55 and molecular formula of C23H36N202. It is the first specific type II 5α reductase inhibitor in the clinic. The commonly used dose is 5mg/d, which can inhibit the plasma level of DHT without affecting testosterone. A single administration of 5-40mg of finasteride can reduce the plasma level of DHT by 65%, while the prostate level of DHT can be decreased by 80%-90%, and the prostate level of testosterone can be increased by about 7 times. Since plasma testosterone is not affected, normal sex life and libido are not affected. The failure of plasma and prostate DHT to fall to zero may be related to the uninhibited 5α-reductase inhibitor I. The effect of DHT on the prostate may be due to the fact that the plasma and prostate DHT may not be reduced to zero. The bioavailability of Finasteride (Prolix) is 80% after oral administration and is not affected by dietary factors. It is completely absorbed after 2h of oral administration. Most of the drug is about 93,5% bound to plasma proteins, so the free drug concentration in plasma is very low. The average half-life in people aged 45-60 years is 6 h; in people older than 70 years is 8 h. Dosage adjustment is not necessary in elderly patients, even in patients with renal impairment who have not yet been on dialysis, probably due to an increase in fecal excretion of metabolites equal to the decrease in urinary excretion. Eprileptal is another 5α-reductase inhibitor with similar clinical efficacy. (2) α-receptor antagonists: Tamsulosin (tamsulosin): tamsulosin hydrochloride, HAL is its trade name. Pharmacokinetics: tamsulosin (tamsulosin hydrochloride) 0, 2mg oral, plasma prodrug concentration 3, 7h after the highest value, 8h after the blood concentration is still maintained at a high level. Urinary excretion rate of the original drug 12% ~ 14%, no accumulation in the body. Role and use: α1 receptor can be cloned into α1A, α1B, α1D, 3 subtypes, of which α1A receptor mainly exists in the prostate agent and urethral smooth muscle, α1B mainly exists in vascular smooth muscle. The order of affinity of tamsulosin (tamsulosin) for the various receptor subtypes was α1A > α1D > α1B. This indicates that tamsulosin (tamsulosin) is an α1A receptor blocker, and that its α1A receptor associated with prostatic smooth muscle contraction is 20-fold more selective than the α1B receptor associated with vascular smooth muscle contraction, whereas prazosin and terazosin are not. Tamsulosin is a novel α1A receptor blocker. He can super-selectively block the smooth muscle α1A receptor in the bladder neck, prostate gland and peritoneum, reduce smooth muscle tension, reduce lower urinary tract resistance, improve urination, in order to achieve the purpose of treating prostate hyperplasia. 2, minimally invasive treatment of prostatic hyperplasia In recent years, with the rapid development of science and technology and the continuous application of high technology in the clinic, minimally invasive treatments such as prostate stent, microwave, radiofrequency, tissue ablation, laser and other minimally invasive treatments are more and more applied to the clinical treatment of BPH. (1) Balloon dilatation treatment: ① Indications and contraindications of balloon dilatation treatment of BPH: A. Suitable for high-risk inappropriate for surgical treatment of patients. B, prostate volume generally does not exceed 40g, without prostate stones. C, Prostate urethra length less than 8 cm. D, No obvious hyperplasia in the middle lobe of the prostate. E, No bladder dysfunction, residual urine volume less than 200 ml, and urodynamic examination if necessary. F, Balloon dilatation therapy cannot obtain prostate tissue, preoperative rectal palpation, PSA examination must be carried out, if necessary, transrectal ultrasound-guided prostate biopsy. If prostate cancer is suspected, it is not suitable for treatment. G, Non-compliant bladder (those who have a history of intravesical chemotherapy and radiotherapy), should not be treated with balloon dilatation. H, No urethral stricture or bladder neck contracture. I. No urinary tract infection, no bacterial prostatitis. J, No bladder cancer.