Etiology and Pathogenesis of Prostatitis
Etiology.
The etiology of prostatitis is varied and varies from one type of prostatitis to another. Infectious factors predominate in the development of bacterial prostatitis, and in the development of non-bacterial prostate and prostate pain, infectious factors may be a precipitating or initial acting factor, while non-infectious factors may play a dominant role.
The factors that may play a role in the development of prostatitis are the following.
Infectious factors
Bacteria: The pathogenic microorganisms in bacterial prostatitis are similar to those that cause genitourinary tract infections. The common pathogenic bacteria are Escherichia coli (E. coli), a few are Aspergillus, Klebsiella, Enterococcus, etc.; Gram-positive bacteria do not have much chance of causing infection. Absolute anaerobic bacteria rarely cause prostate infections. The role of gram-positive bacteria in the etiology is debated, and most researchers agree that enterococci cause chronic prostatitis. However, the pathogenic role of other gram-positive bacteria such as Staphylococcus spp., Streptococcus spp., Clostridium perfringens, and Diphtheria spp. on prostatitis is still questioned by many scholars. Some researchers recently concluded that Gram-positive bacteria, with the exception of enterococci, rarely cause significant prostatitis. In China, Staphylococcus aureus is still a common bacterium in patients’ prostate fluid cultures. Whether the strain differs from the situation abroad or is a contamination of urethral bacteria needs to be further elucidated. Most prostate infections are caused by a single pathogenic bacterium, however, it is not uncommon for two or more strains or types of bacteria to cause them.
Bacterial prostatitis may be due to retrograde or reflux infection of urine following bacterial infection. Infected urine may invade through the prostatic ducts that open into the posterior urethra. Urine flow into the prostate is relatively common and certainly plays an important role in the causative agent of bacterial prostatitis. Some investigators have analyzed prostate stones by crystallographic morphology and found that many components of the stones do not occur in normal prostate fluid but only in urine.
Other possibilities include the spread of bacteria in the rectum through direct diffusion or lymphatic diffusion and hematogenous infection.
Some researchers have found that the prostatic fluid of some patients with chronic bacterial prostatitis and the vaginal secretions of their female sexual partners have the same pathogenic bacteria, suggesting that bacterial prostatitis may be the result of retrograde infection of bacteria through the external urethra during sexual intercourse. Patients with Neisseria gonorrhoeae (gonococcus) or non-gonococcal urethritis combined with Neisseria gonorrhoeae prostatitis as a sexual contact disease. Anorectal intercourse without condom protection may cause urethritis, genitourinary tract infection or epididymitis due to intestinal bacterial infection, and can likewise cause bacterial prostatitis.
Many bacterial prostatitis are the result of transurethral catheterization complicated by urethral infection.
The routes of infection for non-bacterial prostatitis and bacterial prostatitis may be.
1. upstream urethral infection ;
2. retrograde flow of infected urine into the prostatic canal from the posterior urethra;
3, direct diffusion of rectal bacteria or invasion of the prostate through the lymphatic vessels;
4, blood-borne infections.
Many scholars believe that ureaplasma urealyticum may be the causative agent of this prostatitis and may also be a saprophyte (saprophytes). Whether Chlamydia trachomatis is a causative factor in prostatitis is debated. Forty percent of men with non-gonococcal urethritis and most acute epididymitis under 35 years of age are caused by Chlamydia trachomatis sense chlamydial infection, while about 1/3 of patients with non-bacterial prostatitis have urethritis. Therefore, it is possible that it could be the cause of non-bacterial prostatitis, but a number of studies have proven that it is not an important factor, if at all.
Fungi and parasites: fungal causes of prostate infection are mainly seen in patients with AIDS. The patient suffers a severe loss of resistance and develops fungal prostatitis. The main parasites that cause prostatitis are Trichomonas vaginalis and Schistosoma haematobium.
Chemical factors: The cause and causative agent of non-bacterial prostatitis is still unclear. The causative agent may be a pathogenic microorganism that cannot be identified. In recent years, clinical studies have found that Chlamydia and Mycoplasma may be the main causative agents of chronic prostatitis. The actual fact is that it is possible to get a lot more than just a few of these.
In recent years, studies have found that patients with chronic prostatitis have urinary reflux in the prostate, which may be important for the development of all types of prostatitis. In addition, many adult men are found to have stones in the prostate by ultrasound, but they cannot be detected on X-ray. The stones were found to be in the urine and not in the prostate fluid. Therefore, it is presumed that the formation of prostate stones is related to urinary reflux. Infected stones can remain in the gland for a long time and are not easily eliminated as infected lesions. It has been studied that the charcoal powder solution was injected into the patient’s bladder before prostatectomy, and later charcoal ends were found in the gland and duct in the resected prostate specimen; the charcoal powder solution was first injected into the bladder of patients with non-bacterial prostatitis, and then prostate massage was performed 3 days later, and many macrophages containing carbon particles were seen in the prostate fluid; when cystourethrography was performed in patients with non-bacterial prostatitis and prostatodynia during the urination period, it was found that The urine reflux is very serious and is visible in the prostate and ejaculatory ducts. Therefore, it is believed that chemical factors caused by urinary reflux in the prostate may be important in the development of non-bacterial prostatitis.
It has been suggested that urine reflux into the prostate is an important factor that causes prostatitis by affecting the metabolism of pyrimidines and purines and increasing the concentration of uric acid, and that the development of non-bacterial prostate and the level of uric acid in the prostatic secretions are related. According to the above theory, the use of allopurinol has a therapeutic effect on non-bacterial prostatitis. However, there are studies that have come to the opposite conclusion of these results.
Immunological factors: Immunological studies on prostatitis can be traced back to the original discovery of antibody-coated bacteria through the study of immunoglobulins in prostatic fluid and the presence of anti-prostate antibodies. Recently animal models have been applied to successfully simulate prostatitis as a process of autoimmune response. It is encouraging to find that bacterial products in the pathogenesis of prostatitis provide the initial antigenic stimulus that elicits the subsequent immune response process.
Immunoglobulin-coated bacteria: In 1979, Thomas published an article describing how pyelonephritis could be distinguished from cystitis by detecting antibody-coated bacteria in the urine, and antibody-coated bacteria could be detected in 34 of 35 patients with lateral pyelonephritis. In contrast, only one case of antibody-coated bacteria was detected in 20 patients with cystitis. By this method it was possible to distinguish upper urinary tract from lower urinary tract infections. Subsequent studies of semen from 14 normal subjects and 51 patients with prostatitis revealed that antibody-coated bacteria were detectable in 25 prostate patients. IgA antibodies were found in 24 of the 25 cases and IgG antibodies were found in 10 cases. Antibodies to encapsulated bacteria were not found in the semen of the normal population.
Bacteria-specific antibodies in plasma: A later study evaluated the titer of anti-Escherichia coli (E. coli) antibodies in the plasma of patients with prostatitis.Meares et al. studied 25 patients with prostatitis caused by E. coli (E. coli) with significantly higher titers of plasma agglutinating antibodies than the control group. In this study the dilution titer of the control group was used as a non-response. The next study found that in patients with prostatitis, those who were effectively treated had a gradual decrease in antibody titers to normal. In those who were not treated, antibody titers remained high.
Immunoglobulins in prostate fluid: A number of research groups have studied immunoglobulins in prostate fluid. The initial studies began in 1963 when Chodirker and Tomasi first confirmed and qualitatively determined IgG and IgA in normal human prostatic fluid, and subsequent investigators, using different techniques, confirmed the presence of systemic and local immune responses in bacterial prostatitis.
Shortliffe et al. applied a solid-phase radioimmunoassay (RIA) to study the immune response in humans with acute and chronic prostatitis. They found a well-defined local antibody response in prostatic fluid, mainly secretory IgA, which was independent of the plasma response and showed antigenic specificity against the infectious agent. Antigen-specific IgG is elevated in plasma and prostatic fluid at the beginning of acute prostate infection and slowly decreases after drug treatment, continuing for 6 to 12 months. Antigen-specific IgA levels in prostatic fluid increase immediately after infection and slowly decrease only after 12 months of treatment; however, plasma IgA levels that are elevated at the beginning of infection decrease after only 1 month. In chronic bacterial prostatitis, although both antigen-specific IgA and IgG are elevated in the prostatic fluid, there is no definite immunoglobulin in the plasma. In chronic bacterial prostatitis treated with medication, IgA in prostatic fluid remained elevated for 1 year, while IgG persisted for 6 months. In patients with untreated chronic bacterial prostatitis, prostatic fluid antigen-specific IgG was maintained at elevated levels. Measurement of antigen-specific IgA and IgG levels in prostatic fluid is useful not only to help diagnose prostatitis, but also to clarify the effectiveness of treatment.
Once it is clear that total immunoglobulins are elevated, the next step is to study changes in bacterial-specific antibodies.
Early studies used bacterial profiles and found elevated bacterial-specific antibodies in the prostate fluid. Studies found moderately elevated immunoglobulins (both IgA and IgG) in prostate fluid from patients with non-bacterial prostatitis, but failed to detect bacterial-specific antibodies.
To determine the true specificity of antimicrobial immunoglobulins, one study used patients’ own infected bacteria to detect antibody specificity. The investigators determined bacterial immunoglobulins by testing for secretory immunoglobulins. This included detecting immunoglobulins in urine after mid-stage urine and prostate massage. The study population consisted of 14 cases of bacterial prostatitis, 8 cases of non-bacterial prostatitis, and 11 cases in the uninfected population. In all groups, IgA and IgG were elevated after prostate massage; however, after detection of specific antibacterial immunoglobulins, it was found that this immunoglobulin, mainly IgG, was slightly elevated in the normal population and in patients with nonbacterial prostatitis, whereas in patients with bacterial prostatitis, this immunoglobulin, including both IgA and IgG, was significantly elevated.
Histological localization of immunoglobulins: One study on the localization of immunoglobulins in the prostate was performed between normal controls and benign prostatic hypertrophy. IgG was found to be mainly in the cytoplasmic basal portion of the glandular cells and in the secretory granules of the ductal lumen; IgA was found only in the differentiated granules of the ductal lumen. In the later studies conducted on immunoglobulins in prostatitis, unlike previous studies, immunoglobulins were detected in only 1 of 21 normal controls. immunoglobulins were detected in prostate tissue in 57% of patients with prostatitis. IgM was the main immunoglobulin, accounting for 85% of the total, with the main sites of deposition being the periglandular cells, the vascular wall and the glandular cells, in decreasing order. IgA was detectable in 35% of the patients, while C4 was detected in 44% of them. none of them could detect IgG.
Other characteristics of the altered immune status: prostate infection is considered to be a fatal factor in male infertility. huleihel M et al. recently studied the levels of cytokines and cytokine receptors in the seminal plasma of fertile men and infertile men with a history of germ line infection. The study examined the levels of IL-1, IL-6, INF-α and their receptors in semen. These factors are mainly produced by macrophages in response to foreign antigens and appear in chronic inflammatory responses as a result of the activation of immunoglobulins. These immune responses can be controlled by soluble cytokine receptors (including TNF receptors and IL-2 receptor antagonists). The authors did not detect changes in IL-1, IL-6 and TNFα levels. However, testing of TNFα-1 receptors and IL-1 receptor antagonists revealed a decreased presence of TNF-1 receptors in patients with a history of infection, while IL-1 receptor antagonist concentrations were significantly higher. Soluble TNF-1 receptors tend to be elevated in the immune response, which leads to the assumption that prostatitis is an altered immune response process. Other studies have found significantly elevated IL-8 in semen and prostate fluid in patients with oligospermic infertility.
Autoimmune response: The presence of anti-prostate antigen antibodies found through studies may be considered as an evidence that NBPH is an autoimmune disease. Studies have found that prostate specific antigen (PSA) antibodies are indeed present in the prostate tissue of BPH patients.
Animal model: In 1984, Pacheco-Rupil administered spleen cells from Winstar rats that had been immunized with prostate extracts 30 days before by infusion. It was demonstrated that T lymphocytes are required in the development of prostatitis. The next study confirmed that prostatitis is not initiated by immunization with antibodies against prostate extracts. Using the same model, activation and degranulation of mast cells were found to be present during the inflammatory response. In spontaneous prostatitis in Winstar rats, prostate nerve fiber density, mast cell density and inflammatory response were found to increase with age, and degranulation of nerve fibers adjacent to mast cells was particularly pronounced, whereas this did not occur when mast cells were distant from nerve fibers, a phenomenon suggesting a process of neuroimmune regulation.
PSA is a tissue-specific antigen, and the interaction between tissue-specific antigen and thymic T lymphocytes is mainly due to the absence or unresponsiveness of the relevant clone. Using this concept, Tagneli et al. excised the thymus of mice at birth, 3 days postnatal survival, and 7 days postnatal survival, respectively. Only those rats whose thymus was removed 3 days after birth developed prostatitis. And these corresponding mice produced anti-prostate IgG antibodies. Therefore, the initial immune process was mediated by T lymphocytes and followed by antibody production. Further studies revealed that giving back CD4+ T spleen cells from normal adult mice to these mice 3 days after birth prevented the development of prostatitis. However, splenocytes from adolescent male mice did not have this effect.
Influence of immune factors on treatment: Using animal models that form a phantom of the autoimmune response, steroid techniques and androgens can be successfully used in a model of recurrent prostatitis (Lewis rats) to reduce the extent of the inflammatory response.
As the role of mast cell granulation and histamine release in the pathogenesis of prostatitis has been noted, a small amount of spermidine preparation (hydrosysin) can be used in the treatment.
Other associated factors: Previous studies have identified sex hormone nutrition, past history of urinary tract infections, stress levels, psychological factors, allergies and sexuality, among others, as potential factors in the development of prostatitis. In the following studies of related factors, there are more studies in Europe and the United States, while there is a lack of systematic studies in China.
The age: Many studies have found that the incidence of prostatitis is higher in younger men than in older men. Recently, it has been found that prostatitis is seen in teenagers before the age of 20. However, some studies have also found that more senior patients than younger ones are likely to be misdiagnosed due to the similarity of symptoms between the two because of the presence of prostatic hypertrophy in the older ones.
Race: There was no statistically significant difference in the incidence of prostatitis between whites and blacks in the United States.
Region: A U.S. statistic from 1990 to 1994 found that the incidence of prostatitis was twice as high in the southern United States as in the northeast. Is this due to climatic or sexual activity factors? Because of the inconsistency in all aspects of the definition and treatment of prostatitis, the differences in incidence between regions cannot be satisfactorily explained.
Sexual activity: Some studies have found that patients with chronic prostatitis have longer sexual intervals and less frequent sexual intercourse compared to controls. More studies have shown that impure sex is an important factor. However, there are also studies. A questionnaire survey through the Internet found that sexual intercourse was not an influential factor in causing prostatitis.
Prostate biopsy: Infection of the prostate is a complication of prostate biopsy. A current study found that prophylactic antibiotics administered 2 times/d for 1 week were significantly better than 1 time/d for the same course in 491 patients who underwent transrectal biopsy. Indwelling catheters and diabetic complications are risk factors for prostate infection after prostate biopsy.
Prostate congestion: Prostate congestion due to various different causes, especially passive congestion, is an important pathogenic factor. Non-infectious, non-microbial prolonged congestion can create a non-specific inflammatory response, and congestion is commonly seen in the following situations.
An abnormal sex life, too frequent sex, forced interruption of intercourse, or too much masturbation can cause abnormal congestion of the prostate. However, excessive inhibition of sexual life can also produce prolonged suppressed arousal, causing passive congestion.
The actual pressure on the perineum, bicycling, horseback riding, and prolonged sitting can make the prostate congested, especially when bicycling.
The actual fact is that you can get a lot more than just a few of the most popular and popular items.
The actual fact is that you can find a lot of people who are not able to get a good deal on a lot of things.
The actual fact that the prostate gland is rich in alpha-adrenoceptors, after being cold, can cause sympathetic nerve activity, leading to increased pressure in the urethra, preventing excretion, and the prostate gland is also contracted to prevent excretion, resulting in depressed congestion.
The allergic reaction to a virus can also lead to inflammation.
Psychosomatic health factors: Some say this factor is as high as 50%.
Pathogenesis.
Only 5% of patients with prostatitis have evidence of bacterial infection. In patients without evidence of infection, a proportion of patients have leukocytosis of prostatic secretions. This evidence suggests that an inflammatory response within the prostate (although without infection) is responsible for the symptoms of prostatitis. Other patients with prostatitis do not even have inflammatory changes. brunner’s study showed that 64% and 31% of patients with symptoms of prostatitis had inflammatory manifestations and no inflammatory manifestations, respectively.
Acute bacterial prostatitis: Acute bacterial prostatitis results in significant inflammation of part or the entire prostate in roughly 3 stages.
Congestive phase: The posterior urethra, prostatic ducts and surrounding interstitial tissue show congestion, edema and round cell infiltration with patches of lobulated nucleated granulocytes. The epithelial cells of the glandular ducts are sometimes hyperplastic and desquamated.
The vesicular phase: The inflammation continues to develop, the prostate ducts and vesicles become more edematous and congested, the prostate ducts and vesicles swell and many small abscesses form.
The parenchymal phase: The tiny abscesses gradually increase in size and invade more of the parenchyma and surrounding stroma; this is more common with staphylococcal infections.
It is uncommon to find acute prostatitis alone without any of the pathological manifestations of chronic prostatitis, accounting for only 13.1 to 20 percent of prostatitis, and most cases coexist with chronic prostatitis.
The pathogenic bacteria of prostatitis are mainly Escherichia coli, accounting for about 80%, followed by Proteus, Klebsiella, Enterobacter, Pseudomonas, and Serratia. Gram-positive bacteria, except for enterococci, rarely cause disease. In addition, gonococcus, tuberculosis, fungi, and trichomonas can also cause associated prostatitis. The pathogenic role of Chlamydia trachomatis, Mycoplasma solium and Mycoplasma humanum in prostatitis is still controversial. The incidence of gonorrheal prostatitis has been increasing in recent years.
The classification of prostatitis
Prostatitis can be classified into 4 categories as follows.
Acute bacterial prostatitis;
Chronic bacterial prostatitis;
Chronic non-bacterial prostatitis/chronic pelvic pain syndrome;
Asymptomatic inflammatory prostatitis.
Diagnosis and differential diagnosis of prostatitis
Diagnosis of prostatitis
Acute bacterial prostatitis is easy to diagnose because of its obvious and typical clinical manifestations; the clinical features of chronic prostatitis syndrome are more variable and inexact, and many symptoms, signs and pathological examinations are often indistinguishable in chronic bacterial prostatitis, non-bacterial prostatitis and prostatodynia. radiology and urethral cystoscopy, which may be of some help in diagnosis, cannot confirm the diagnosis either. Histological examination of the prostate is only needed in some rare types of prostatitis, such as granulomatous prostatitis. In chronic bacterial prostatitis histological changes are not specific for determining inflammation as a bacterial etiology. 1 group of 162 consecutive surgical resections for prostate enlargement found a 98% incidence of prostate inflammation. Six definite morphologic types of inflammation were observed, but there was no significant difference between positive and negative cultures for bacterial infection of the prostate. The inflammatory response was focal in most cases, involving only a small portion of the entire prostate, so prostate biopsy is rarely a guide in the management of prostatitis. The tissue culture of prostate biopsy specimens is of little value in the diagnosis of chronic prostatitis.
Differential diagnosis of prostatitis
Differential Diagnosis of Acute Bacterial Prostatitis
Acute pyelonephritis: also manifests as acute chills and fever with frequent, urgent and painful urination. It usually also presents with lumbago and back pain on the affected side; not suprapubic or perineal pain and no difficulty in urination. There is no prostate pressure on rectal examination and the prostate fluid examination is normal.
Abscess kidney: It also presents with acute chills and fever with frequent, urgent and painful urination. It also shows obvious lumbar pain on the affected side; but no suprapubic or perineal pain, no difficulty in urination, and no prostate pressure on rectal finger examination. Prostate fluid examination is normal.
Prostate abscess: also manifested as acute chills, fever. It is the result of the development of acute prostatitis. The diagnosis can be clarified by rectal ultrasound and CT examination, which reveals a fluid occupancy in the prostate, and by puncture and extraction of pus.
The differential diagnosis of chronic bacterial prostatitis
Prostate cancer: late stage also shows discomfort in urination, which may include frequency, urgency and difficulty in urination. Rectal examination reveals that the prostate gland is hard and may have nodules; serum PSA is significantly elevated, and the diagnosis can be confirmed by rectal ultrasound, which shows heterogeneous light clusters in the prostate gland.
Prostate tuberculosis: It also manifests as frequent, urgent and painful urination with urethral drip, with pain in the lower abdomen and perineum. There is usually a history of genitourinary tuberculosis. Rectal finger examination may reveal irregular nodules in the prostate, and antacid bacilli may be found in the prostate fluid.
Chronic aseptic prostatitis: also presents as frequent urination with urethral drip, with pain in the lower abdomen and perineum. The two are mainly differentiated based on bacterial cultures of VB1, EPS and VB3. Bacterial cultures of VB1, EPS and VB3 in aseptic prostatitis are negative.
Prostatic hyperplasia: It also manifests as frequent urination with dyspareunia. It occurs mostly in older men, with dyspareunia predominating. Rectal finger examination reveals a significantly enlarged prostate, while routine prostate fluid is generally free of white blood cells.
Spermatorrhea: It also manifests as frequent urination, urgent urination, painful urination with urethral drip, with pain in the lower abdomen and perineum. There is often hematospermia, and red and white blood cells are seen in the seminal vesicle fluid examination.
Chronic cystitis: also presents as frequent, urgent and painful urination with pain in the lower abdomen and perineum. leukocytes are seen in VBl and VB3, and bacterial growth is seen in culture, but EPS examination is normal.
Differential diagnosis of aseptic prostatitis
Chronic bacterial prostatitis: also manifested as frequent, urgent and painful urination with urethral drip, with pain in the lower abdomen and perineum. The two are mainly differentiated based on bacterial cultures of VB1, EPS, and VB3. Chronic bacterial prostatitis VB1 may or may not have bacteria, EPS usually has bacterial growth, and VB3 has a positive bacterial culture; while chronic non-bacterial prostatitis VB1, EPS, and VB3 all have negative bacterial cultures.
Chronic cystitis: also manifests as frequent, urgent and painful urination with pain in the lower abdomen and perineum. However, bacterial cultures for chronic cystitis VB1 and VB3 were positive, while EPS showed no bacterial growth.
Chronic urethritis: also manifested as frequent, urgent and painful urination. bacterial culture of VB1 was positive, while bacterial culture of VB3 and EPS showed no bacterial growth.
Differential diagnosis of prostatodynia
Acute, with pain in the lower abdomen and perineum. The two are differentiated mainly on the basis of bacterial cultures of VB1, EPS, and VB3. In chronic bacterial prostatitis, VB1 may or may not have bacteria, EPS usually has bacterial growth, and VB3 has a positive bacterial culture; whereas in patients with prostate pain, VBl, EPS, and VB3 have a negative bacterial culture.
Treatment of Prostatitis
Acute bacterial prostatitis
General treatment: bed rest, plenty of water or fluids, and enhanced systemic supportive therapy.
Antibiotics: Active application of effective antibiotics. The quinolones such as ciprofloxacin, ofloxafloxacin, levofloxacin (levofloxafloxacin) 0.2g, intravenous infusion, 2 to 3 times / d; aminoglycosides such as amikacin, netilmicin 0.4g, intravenous infusion, 1 time / d. After the control of acute inflammatory symptoms can be changed to oral administration, the course of treatment should be maintained for 1 month.
Other treatment: antipyretic and analgesic drugs can be used, such as Somitol (go to pain tablets), acetaminophen (Sanli pain), acetaminophen (Benadryl), etc.. If you have difficulty in urinating, you can use alpha-blockers such as Nadol 25mg, Terazosin 2mg or Tylosin 0.2mg, taken orally, 1 time/d. For acute urinary retention, it is not advisable to place a catheter, but to make a suprapubic cystocentesis fistula, and if the prostate abscess is complicated, it should be incised and drained.
The actual fact is that you can find a lot of people who are not able to get a good deal on a lot of things.
Hot water bath and physical therapy: can reduce local inflammation and promote absorption.
Prostate massage: 1 time per week to drain inflammatory secretions.
Botanical preparations: such as Sernitone, Prostacyxin capsule, Zegui retention gel capsule, etc.
Application of antispasmodic and analgesic drugs: ibuprofen 60mg, orally, 4 times/d; indomethacin (anti-inflammatory pain) suppository 0.1g, administered intrarectally, 1 time/d. For obvious symptoms of urinary irritation, tolterodine 2mg, orally, 2 times/d or flavone permethrin (urinary spirit) 0.2g, orally, 3 times/d.
Application of α-blocking drugs: It can relieve the patient’s symptoms of urinary difficulty.
Application of antibiotics.
Chronic bacterial prostatitis: antibacterial drugs that are fat-soluble, weakly alkaline and have a low binding rate with plasma proteins should be chosen, such as methotrexate (methamphetamine pyrimethamine, trimethoprim, TMP) 160mg, 1 time/d; compound sulfamethoxazole (SMZ) 800mg, 1 time/d; treatment course 4-12 weeks. Fluoroquinolones, such asloxafloxacin or levofloxacin (levofloxafloxacin) 200-300mg, orally, 2 times/d, for a course of at least 6 weeks. Erythromycin such as roxithromycin 0.15g, 2 times/d, for a course of 6 weeks. Minocycline (memantin) 0.1g, 2 times/d or doxycycline, etc., for the same course of treatment.
For chronic non-bacterial prostatitis, if the examination reveals mycoplasma, chlamydia infection, you can first try the above antibiotics for 2 weeks, if the symptoms improve then continue the medication; if the symptoms do not improve then stop the medication.
The actual fact is that you can find a lot of people who are not able to get a good deal on this.
Other treatments: radiofrequency thermotherapy, transrectal microwave therapy, posterior urethral drug infusion therapy, intraprostatic drug injection therapy, transurethral prostate needle ablation, etc.