Etiology, pathogenesis and treatment of chronic prostatitis
Chronic prostatitis is the most common disease in urology, and its incidence accounts for 33% of urological outpatients. The clinical features are extensive and lack specificity, and the individual differences in patients are large. This is because the company’s products and services are not only available in the market, but also in the marketplace.
1, the classification of chronic prostatitis
In 1968, Meares “divided chronic prostatitis (CP) into: chronic bacterial prostatitis (CP); chronic non-bacterial prostatitis (CNBP); and prostate pain (PDY) based on segmented quantitative bacterial culture and EPS white blood cell count. 1978 Drach proposed to divide acute and chronic bacterial prostatitis, non-bacterial prostatitis and prostate pain. The classification of acute and chronic bacterial prostatitis, non-bacterial prostatitis and prostatodynia was proposed by Drach in 1978. In 1995, at the NIH symposium on chronic prostatitis, a new classification of prostatitis was proposed based on microscopic examination and culture of prostate-specific specimens: acute bacterial prostatitis (type I), chronic bacterial prostatitis (type II), chronic aseptic prostatitis/chronic pelvic area pain syndrome (type III), and asymptomatic inflammatory prostatitis. asymptomatic inflammatory prostatitis (type IV). m type is divided into two subtypes (IIIa, IIIb), inflammatory and non-inflammatory, based on the number of white blood cells in the prostatic fluid and semen. This new classification was confirmed at the International Prostatitis Collaborative Network meetings held in November 1998, 1999 and November 2000. The NIH classification literally seems to be a little more stringent, but it is thought that this method is not superior to the Drach typing method and has not been widely promoted in China.
2. The pathogenesis and pathogenesis of chronic prostatitis
The main cause of CBP is bacterial infection, with an incidence of 5%-10%. The pathogenic bacteria are the same as acute bacterial prostatitis (ABP), with non-specific infections predominating, such as E. coli accounting for about 80% of infections, followed by S. pyogenes and Klebsiella. The pathogenicity of Gram-positive cocci is still debated. The pathway of bacterial invasion into the prostate is mainly due to increased urethral pressure caused by inflammation, edema or obstruction of the lower urethra, leading to the return of the inoculated urine into the prostatic ducts and alveoli.
CNBP and chronic pelvic pain syndrome (CPPS) The incidence of CNBP is about 64% of the overall CP and 8 times that of CBP. In contrast, the incidence of CPPS is about 30%. Both have unsatisfactory treatment results, and their etiology and pathogenesis are complex. There are many hypothetical theories, which have caused a lot of controversies, and some of them are still not recognized by everyone, which are divided as follows.
2.2 Sympathetic theory The theory is based on the fact that the internal sphincter of the bladder, the anterior sphincter of the prostate, the prostatic peritoneum, the muscles, the smooth muscle of the vesicles, the muscles around the ducts, the random muscle portion of the external urethral sphincter, and the seminal vesicles, vas deferens, and ejaculatory ducts are rich in. Adrenergic fibers.
2.3 Immune mechanism In people with normal systemic immune function, the pathogen may not show symptoms or react mildly after infection, but there are also rapid and obvious reactions, but the process and outcome are good; after the occurrence of infection in people with low systemic immune function, the inflammatory reaction is often not obvious, but it is easy to form a bun process. Therefore, some people believe that the inflammatory response of chronic non-invasive prostatitis is a manifestation of low systemic immune function. However, the local immune function of the prostate often shows abnormally enhanced, and both cellular and humoral immune responses are involved in the immune response process of steamed-bun prostatitis. It was found that the immunosuppressive factors in the prostatic fluid of patients with steamed-bun nonbacterial prostatitis were significantly reduced, while the levels of immunoglobulin IgG, IgA, IgM and SLgA were significantly increased, suggesting that the occurrence of chronic nonbacterial prostatitis is related to the enhanced local immunity of the prostate. The complex process of changes in cytokine gene expression levels may play an important role in the pathogenesis of prostatitis, which can often be seen in the prostate fluid of patients with prostatitis as IL-1ß and TNFa. changes in cytokine levels.
3 , diagnosis
3.1 Type I Clinical manifestations include urinary frequency, urinary urgency, painful urination, urethral discharge during urination. And urethral discomfort or burning sensation; perineum, lower abdomen vague pain and discomfort, even lumbosacral, suprapubic, inguinal area with soreness and swelling; may have erectile dysfunction, premature ejaculation; dizziness, head swelling, weakness, fatigue, insomnia, depressed mood and other psychoneurotic symptoms. There are pathogenic bacteria in the prostate massage tuck, prostate fluid leukocytes >10/high magnification field, and lecithin vesicles are reduced. Rectal examination shows a full, enlarged, soft and mildly painful prostate. In those with long duration of disease, the prostate is shrunken, hard and uneven, with small hard nodules. The urine Stemey-Meares method is negative for VB3>VB110 times or VBl and VB2, and positive for VB3: fine inoculum culture. In milder cases, the size of the prostate morphology and internal echogenicity are nearly normal on ultrasound examination; in patients with prolonged or severe disease, the prostate gland is slightly enlarged or reduced in size, the edge of the envelope is mostly intact and continuous, the echogenicity of the gland parenchyma is evenly distributed but strong and dense, calcification points are common, and in a few cases, the echogenic boundary at the envelope is unclear and the surface is not smooth.
3.2 Type IIIA/IIIB The main clinical manifestations are pain or discomfort in the pelvic area lasting for more than 3 months, which may be accompanied by abnormal symptoms of urination and sexual life, but without a history of UTLs, and laboratory tests cannot confirm infection. Among them, type IIIA is inflammatory bun pelvic pain syndrome, also known as aseptic prostatitis. The presence of leukocytes in the patient’s semen, prostatic fluid or urine specimen after prostate massage has diagnostic significance and is the most common type of prostatitis. type IIIB is a non-inflammatory steamed bun pelvic pain syndrome with no leukocytes in semen, prostatic fluid or urine after prostate massage.
3.3 Type IV Patients have no subjective symptoms and are diagnosed due to incidental evidence of inflammatory reaction in their prostate biopsy tissue, semen, prostatic fluid or urine specimens after prostate massage. The International Prostatitis Collaborative Network (1PCN) meeting held in 2000 concluded that the diagnosis of chronic prostatitis should be made with the following items.
Medical history ;
Physical examination including rectal examination;
4-cup or 2-cup test. Recommended items.
Bun Prostatitis Symptom Score;
Urine flow rate ;
Residual urine (ultrasound). Optional items.
Semen specimen test ;
Urethral swab culture;
Pressure flow measurement;
TV urodynamic measurements, including electromyography;
Transrectal ultrasound ;
PSA.
4. Differential diagnosis
4.1 Prostate abscesses Most of them are complications of acute fine prostatitis, mostly occurring in 50-60 years old, with rectal symptoms and urinary retention being more common. The prostate is enlarged on the diseased side of the rectum and is soft to the touch with a sense of fluctuation.
The patient can show all kinds of symptoms of chronic prostatitis, but the rectal examination can feel the friction of stones in the prostate, the pelvic X-ray has a positive stone shadow on the side of the pubic symphysis, the ultrasound examination can appear in the prostate stone area with strong light band and sound shadow.
4.2 Prostate tuberculosis Symptoms are similar to chronic prostatitis, but there is often a history of urological tuberculosis or other sites of tuberculosis. The prostate is irregularly nodular on rectal examination, the epididymis is enlarged and hardened, the vas deferens has bead-like nodules, and the prostate fluid is directly stained for Mycobacterium tuberculosis.
4.3 Prostate cancer Advanced stage of prostate cancer can show symptoms such as frequent urination, painful urination and difficulty in urination, but patients often have systemic symptoms such as wasting, weakness, anemia and loss of appetite, etc. There is a hard stone like mass in the prostate gland with uneven surface on rectal examination, and the serum prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) are increased. The prostate gland may be found to be cancerous by puncture. ultrasonography may show an enlarged gland with uneven or defective border echogenicity and uneven internal light spots. ct examination may show asymmetry of the prostate gland. if the tumor infiltrates into the outer envelope, the tissue gap between the seminal vesicles and the posterior wall of the bladder may disappear.
4.4 Osteitis pubis Clinically, it shows symptoms of chronic prostatitis, but rectal examination and prostatic fluid examination are normal. The main features are obvious pressure pain at the pubic symphysis, pelvic radiographs showing widening of the pubic symphysis gap >10mm, bilateral difference of the suprapubic branch >2mm, irregularity of the pubic symphysis margin, erosion and reactive osteosclerosis.
5.Treatment
5.1 Western medical treatment
5.1.1 Treatment of CBP
It should be treated with antibiotics estimated to be sensitive and efficacious for 8-12 weeks, and continued in full doses for 6-8 weeks in recurrent or untreated cases, along with prostate massage (2-3 times/week), hot water therapy or other thermal treatments.
For recurrent episodes or refractory cases with cysts, stones, enlarged glands, focal inflammatory calcification and ineffective antibiotic therapy, TURP or focal debridement may be considered (but is rarely used in actual clinical practice).
If the treatment of CBP with antibiotics alone is not satisfactory, a-blockers should be given as an appropriate adjunct. a-blockers are used to reduce urethral resistance, relax the glandular ducts and smooth muscles, and promote the discharge of secretions in the lumen of the glandular ducts.
5.2 Treatment of CNBP There are many drugs for the treatment of CNBP, but there are no specific drugs. Different drugs have different improvement of symptoms, so a combination of drugs is recommended.
①If chlamydia or mycoplasma infection can be clearly identified, erythromycin class or minocycline is preferred for treatment.
②If there is no chlamydial or mycoplasma infection or other clear pathogen, antibiotics are often ineffective, and the medication should be used to improve symptoms at this time. A-blocker therapy is available.
③ patients with mainly painful symptoms can be treated with antipyretic and analgesic drugs, and can also be tried with other