Chronic prostatitis (CP) is one of the most common diseases in urology, and its incidence has been increasing in recent years. In 1995, the National Institutes of Health (NIH) classified prostatitis into four types. Type I: acute bacterial prostatitis; Type II: chronic bacterial prostatitis; Type III: chronic prostatitis/chronic pelvic floor pain syndrome (CP/CPPS), where IIIA is the inflammatory type and IIIB is the non-inflammatory type; and Type V: asymptomatic prostatitis. The type III, CP/CPPS, accounts for about 90% to 95% of prostatitis. Because the etiology and pathogenesis of CP/CPPS are unknown, there is a great deal of confusion and controversy regarding the diagnosis and treatment. The NIH has listed CP, along with congestive heart failure/angina, Cohn disease, and diabetes mellitus, as the four diseases that seriously affect patients’ quality of life, and the progress of research on its etiology and pharmacological treatment is reviewed below. The etiology of the disease is complex, and traditional etiologic research models have focused on the infection and inflammatory process of the prostate and its pathogens, but have encountered difficulties in explaining many problems. The possible etiologies and pathogenesis currently studied are: pathogenic infection, immunological etiology, physical and chemical factors, urinary reflux in the prostate, psychosomatic factors, oxidative stress and the role of zinc, neuroendocrine hormonal imbalance, and altered genetic characteristics. The prostate gland is one of the most susceptible organs in the male reproductive system to infection by bacteria and other pathogenic microorganisms, which can lead to the development of prostatitis. The common factors that cause prostatitis are bacteria, viruses, fungi, mycoplasma, and chlamydia are thought to be related to the development of CP, with bacterial infections being the most common, with the pathogens mainly coming from the urethra and other organs of the reproductive system, caused by retrograde infection of the urinary tract or reflux of infected urine into the prostatic ducts during emptying of the posterior urethra. However, more studies have not confirmed a statistically significant difference in the rate of positive cultures for CP versus asymptomatic controls. A larger urine four-cup test showed bacterial CP in only about 5% of cases. In contrast, the relationship between chlamydia and mycoplasma and CP has not been confirmed.Zdrodowska-stefanow et al. analyzed 46 EPS with CP and showed a 17.4% rate of chlamydial infection and a significant increase in polypoid leukocytes (PMN), polypoid leukocyte protease, and a significant decrease in citrate concentration in EPS, and a significant negative correlation between the decrease in citrate concentration and the increase in PMN and PMN enzyme.Stancik et al. suggested that traditional assays and indicators may not accurately detect evidence of infection in EPS, VB3 and semen of CP patients, and that immune and cytokine factors may be important in the pathogenesis of CP. After 4 weeks of ciprofloxacin treatment in 146 cases of CP, IL-6 in fresh semen and VB3 decreased significantly, suggesting that bacterial infection is associated with the development of CP, and that IL-6 testing can clarify the etiology and determine the efficacy and prognosis. There is no clear evidence of bacterial infection using traditional culture methods and PCR, but there are cytokines of inflammation present in seminal plasma and prostate massage fluid (EPS), such as TNF-α, IL-1β, IL-8, etc. Immunologic etiology: Those with normal systemic immune function may not develop inflammation or have a mild reaction after infection, or have a rapid and obvious reaction, but have a good course and outcome; those with low systemic immune function are prone to infection and inflammation, and the inflammatory reaction is often not obvious, but tends to develop a chronic course. In the past few years, the number of patients with CP has been increasing. The results of the study are not only the results of the study, but also the results of the study. Physical and chemical factors: Researchers have long found that prostate injury may be related to local trauma, long-term pelvic floor muscle compression, chronic and permanent self-stimulation of pelvic contents, such as long-distance cycling or sedentary, external blows to the perineum; also related to mechanical factors (ejaculatory duct obstruction) or chemical stimulation (urinary reflux), frequent sexual intercourse or excessive masturbation, or due to alcohol consumption or consumption of stimulating foods, lack of local warmth, and many other factors. The prostate gland is chronically and chronically congested due to a variety of factors, such as local inattention to warmth. The injury itself does not cause significant clinical symptoms, but the inflammatory response to the injury can release chemokines and cytokines to remove pathogens and aid in the healing process of the body, as well as produce pain and swelling. Urinary reflux in the prostate: functional urinary obstruction may be a part of the pathogenesis of CP. Contractures of the distal urethra and external sphincter cause increased pressure in the prostatic urethra, which allows urine to reflux into the prostatic ducts, thus causing inflammation of the prostatic ducts and surrounding tissues. The systemic reaction and local irritation caused by inflammation further aggravates functional urethral obstruction and contracture of the muscular system in the pelvis, exacerbating abnormalities in voiding function. alterations in urodynamics in patients with CP may contribute to its pathogenesis and may be secondary to pathological changes. Psychosomatic factors: Although the cause of CP may not be related to psychological factors, chronic recurrent pain and other symptoms may further lead to somatization of symptoms, which in turn induce or aggravate psychological factors. There is increasing evidence of a significant decrease in QOL and the prevalence of anxiety and depression in patients with CP, with a clear correlation between these symptoms and the course of the disease and sexual function. The cause-and-effect relationship needs to be further clarified. Patients with CP have obvious psychosomatic disorders, mainly depression, fear and somatic tension. The influence of psychosomatic factors causes systemic autonomic dysfunction, leading to increased excitability of α1 receptors and thus aggravating posterior urethral neuromuscular dysfunction, causing bladder neck dysfunction and increasing urethral pressure in the prostate during urination, making it easy for urine to flow back into the prostate, leading to or aggravating the symptoms of CP. Oxidative stress and the role of zinc: There is biochemical and molecular biological evidence of enhanced oxidative stress within the prostatic fluid of patients with CP, and there is increasing interest in the relationship between reactive oxygen species (ROS) and the development of chronic prostatitis. Several studies have shown that increased levels of ROS can be present in the semen and prostatic fluid of patients with CAP. the antioxidant capacity of patients with CP is significantly reduced compared to normal subjects, and antioxidant therapy aimed at scavenging free radicals has been effective, suggesting that oxygen free radicals play an important role in the pathogenesis and progression of CP. Zinc, as an activator of several enzyme systems, can effectively activate enzymes that are resistant to oxidative stress such as superoxide dismutase and reduce the damage or inflammatory response to prostate tissue caused by excessive oxidative stress in the body. Several studies have shown that zinc levels are decreased in EPS of CP patients, and that prostate resistance to infection is related to zinc levels. Zinc may inhibit the damage to prostate tissue caused by excessive oxidative stress. Zinc preparations may increase the concentration of zinc in the body and relieve prostatitis symptoms. Neuroendocrine hormone imbalance: Chronic or recurrent signals from peripheral tissues and organs that constantly produce sensory injury can be transmitted to and establish chronic functional changes in the central nervous system by direct or indirect means. Peptides released by local sensory injury and norepinephrine and prostaglandins released by efferent sympathetic nerves are important factors in the production of pain and prostatic overproduction in prostatitis. A significant negative correlation was found between total CPSI score, pain score and cortisol, suggesting that corticosteroid imbalance may be the biochemical pathogenesis of CP. The genetic predisposition to prostatitis may also be related to genetic susceptibility, and there is evidence of genetic differences between many CP patients and healthy men. Drug therapy with antibiotics: Although the vast majority of patients with CP have no identifiable pathogen or present only with abnormalities in WBCs, several recent prospective randomized placebo-controlled studies have shown that treatment with fluoroquinolones is effective in nearly 50% of patients. Length of disease and primary treatment are critical to outcome: patients with a longer duration of disease than 4 weeks who have received multiple treatments are as effective as placebo, whereas patients with less than 4 weeks of disease and no treatment have an efficacy of up to 75%. The recommended duration of treatment is 6 weeks. Tetracyclines and macrolides are available for those with evidence of chlamydial and mycoplasma infection, and low-dose maintenance therapy can be tried for possible relapse. The key clinical issue is IIIB, considering that most physicians in China currently may only examine EPS or VB3 and may miss IIIA (false negative for IIIA), which will inevitably affect the efficacy, although of course there is a lack of authoritative or evidence-based medical evidence. In addition, because of the complex relationship between the neighbors of the prostate, once the infection can affect each other, making it difficult to control the infection completely. This is why it is important to pay attention to the treatment of “neighboring” tissues such as the urethra, bladder, epididymis, seminal vesicles, rectum and other infections, especially early treatment, so that they do not spread to the prostate. Alpha-blockers: Alpha-blockers that act selectively on the posterior urethra, bladder neck, and prostate can relieve urethral spasm in the bladder neck and prostate, increase urinary flow rate, promote bladder, reduce urethral closure pressure, and prevent urinary reflux in the prostate, while acting on the sympathetic nerves of the pelvic floor to relieve pelvic floor muscle spasm and relieve perineal and pelvic floor tension. Myalgia. Some randomized, double-blind, placebo-controlled studies have shown that Tamsulosin, Terazosin, and Alfuzosin provide significant symptomatic relief and improvement in CPSI; long-term use (12 weeks to 6 months) is more effective than short-term use (6 weeks), with 6 weeks of use providing only symptomatic relief and improvement in CPSI scores, while more than 12 weeks of use provides relief of pain, voiding symptoms, and significant improvement in QOL and CPSI scores. The Phase III (NIH-CPCRN) study reinforces that α-adrenergic receptor blockers are not suitable for treating patients with long duration of disease (6-8 years), prior overtreatment, and especially those who have taken α-adrenergic receptor blockers before. Adrenergic blockers can also be used in combination with antibiotics, but again, a course of less than 6 weeks is less effective. NSAIDs: The efficacy of anti-inflammatory drugs for CP has been encouraging and is a reasonable option for short-term second-line treatment, with some multicenter randomized, double-blind, placebo-controlled studies demonstrating effectiveness in improving symptoms. Both short-acting NSAIDs and cyclooxygenase-2 inhibitors are increasingly showing benefits in improving prostate inflammation with mild adverse effects. The newer drugs such as Rofecoxib, 50 mg/d, are recommended for a 6-week course. 2.4 Hormones (1) Anti-androgen therapy: Blocking androgens with 5a reductase inhibitors can reduce prostate edema and pressure to reduce symptoms and urinary reflux in the prostate ducts, and reduce the size of prostate tissue to limit inflammation, especially in the presence of BPH. The actual testosterone supplementation can increase libido, improve sexual function, enhance the general resistance of the body to disease and the function of various systems and organs, and also increase the secretion of the accessory gonads, thus accelerating the metabolism in the prostate and improving the internal environment. The company is also able to increase the secretion of the accessory gonads, thus accelerating the metabolism in the prostate, improving the internal environment, promoting drainage and local inflammation. However, evidence from evidence-based and controlled studies is still lacking, and adverse effects need to be considered. Phytopharmaceuticals are mostly pollen or plant extracts, commonly used are: Quercetin, Serenoa Repents (Sabal, Saw Palmetto), Cernilton (Schenectady), etc.. The pharmacological mechanism is not well understood and may be related to non-specific anti-inflammatory, anti-swelling, and smooth muscle relaxation. A few placebo-controlled studies with single-use centers have shown significant efficacy, but the number of cases is small. Although there are published reports of improvement or cure at 6 months with sernitone, the true and reliable efficacy cannot be confirmed because no accepted evaluation metrics were used. The greatest advantages are good compliance, safety, and few adverse effects, and it is widely used in Europe. Tricyclic antidepressants: Blocking the reuptake of norepinephrine and 5-hydroxytryptamine in the central nervous system and suppressing nociceptive receptors may be beneficial in relieving neuropathic pain and mood disorders. In comparison, Nortriptyline is more effective. Anxiolytic and neuromodulatory drugs may be beneficial in patients with CPPS with predominantly painful conditions. Opiate narcotics O-pioids (narcotics) have been used in the treatment of CP and interstitial cystitis and may be carefully considered after evaluation for refractory CP patients with intractable, severe neuropathic pain. Other drugs: Allopurinol has a lowering effect on uric acid in serum and urine , and may be beneficial in patients with intraprostatic urinary reflux. Trace elements, vitamins, immunosuppressants such as rehmannia polysaccharides, and herbal medicines may be effective in some selective patients, but much clinical work has to be done to promote it widely in the clinic. In summary, the etiology of chronic prostatitis is complex and the pathogenesis is not exact. Therefore, there is no one treatment route with particularly good efficacy. The difficulty in its treatment lies in the fact that many drugs cannot penetrate the prostate lipid-like membrane, an anatomical barrier that affects drug absorption, and combination therapy is more suitable than monotherapy for the treatment of patients with CP.