urethra pain
Introduction
Introduction Patients with prostatitis manifested symptoms including: dysuria, urgency, frequent urination, waiting for urine, interruption of urine, urinary weakness, urinary drip, urinary bifurcation, urinary retention, urethral drip, blood in the urine, waist and knee pain, groin and thigh root Side radiation pain, lower abdomen and perineal discomfort have pain or bulge, anal pain, dizziness, fatigue, urinary tract itch burning, testicular pain, scrotum moist, nocturnal emission. Sexual desire and sexual function decline, infertility, etc. The causes of prostatitis are diverse, and the different types of prostatitis have different causes.
Cause
Cause
(1) Causes of the disease
The causes of prostatitis are diverse, and the different types of prostatitis have different causes. Infectious factors predominate in the pathogenesis of bacterial prostatitis. In the pathogenesis of non-bacterial prostate and prostate pain, the infection factor may be an induced or initial factor, and non-infectious factors may play a leading role.
The factors that may play a role in the pathogenesis of prostatitis are as follows:
Infection factor
(1) Bacteria: Pathogenic microorganisms in bacterial prostatitis are similar to pathogenic bacteria causing genitourinary tract infections. Common pathogens are Escherichia coli (E. coli), a few are Proteus, Klebsiella, Enterococcus, etc.; Gram-positive bacteria cause less chance of infection. Absolute anaerobic bacteria rarely cause prostate infections. The role of Gram-positive bacteria in etiology is still controversial, and most researchers agree that enterococci cause chronic prostatitis. However, many Gram-positive bacteria such as Staphylococcus, Streptococcus,ococcus, and diphtheria have a pathogenic effect on prostatitis, and many scholars still have doubts. Recently, some researchers believe that Gram-positive bacteria rarely cause obvious prostatitis except for Enterococcus. In China, Staphylococcus aureus is a common bacterium in the prostatic fluid culture of patients. Whether it is different from foreign countries, it is still a contamination of urethra bacteria and needs further clarification. Most prostate infections are caused by a single consistent pathogen, but occasionally by two or more strains or types of bacteria.
Bacterial prostatitis may be caused by retrograde or reflux infection of the urine after bacterial infection. Infected urine can be invaded through the prostate duct opening to the posterior urethra. Urine influx into the prostate is more common, and certainly plays an important role in the pathogen of bacterial prostatitis. Some researchers have analyzed the crystal morphology of prostatic stones and found that many components in the stone do not appear in normal prostatic fluid but only in the urine. Others may include the spread of bacteria in the rectum through direct or lymphatic spread and blood-borne infections.
Some researchers have found that some patients with chronic bacterial prostatitis have the same pathogens as the vaginal secretions of their female sexual partners. This suggests that bacterial prostatitis may be retrograde through the external urethra during sexual intercourse. The result of the infection. Neisseria gonorrhoeae (gonococcus) or non-gonococcal urethritis patients with Neisseria gonorrhoeae prostatitis is a sexual contact disease. Anorectal intercourse without condom protection may cause urethritis, genitourinary tract infection or epididymitis due to intestinal bacterial infection, which may also cause bacterial prostatitis. Many bacterial prostatitis are the result of transurethral catheterization of the urinary tract and urinary tract infection.
The route of infection for non-bacterial prostatitis and bacterial prostatitis may be:
1 ascending urinary tract infection;
2 rows of infection of the posterior urethra to the prostate tube;
3 rectal bacteria directly spread or spread through the lymphatic vessels into the prostate;
4 blood-borne infections.
(2) Mycoplasma and Chlamydia: Chronic non-bacterial prostatitis is an unexplained inflammatory lesion. It has been shown that non-bacterial prostatitis is 8 times more than bacterial prostatitis. Some people think that it is decomposed into ureaplasma (ureaplasmas). Urealyticum and Chlamydia trachomatis may be the causative factors of non-bacterial prostatitis, but the evidence is still insufficient.
Many scholars believe that the decomposition of urea urinary tract may be the cause of this prostatitis, or it may be a saprophytes. Whether Chlamydia trachomatis is a causative factor of prostatitis is still controversial. 40% of men with non-gonococcal urethritis and most acute epididymitis under 35 years of age are caused by Chlamydia trachomatis infection, and about 1/3 of patients with non-bacterial prostatitis have urethritis. Therefore, it may be the cause of non-bacterial prostatitis, but many studies have proved that even if it is, it is not an important factor.
(3) Fungi and parasites: Fungal infections caused by prostate are mainly found in AIDS patients. The patient's resistance was severely damaged and fungal prostatitis occurred. The parasites that cause prostatitis mainly include Trichomonas vaginalis and Schistosomiasis.
2. Chemical factors
The causes and pathogens of non-bacterial prostatitis are still unclear. Pathogenic bacteria may be pathogenic microorganisms that cannot be determined. In recent years, clinical studies have found that chlamydia and mycoplasma may be the main pathogens of chronic prostatitis. Or it is a non-infectious disease, and some speculate that it may be a "chemical" prostatitis caused by urine flowing back into the prostate.
In recent years, studies have found that patients with chronic prostatitis have urinary reflux in the prostate, which may be important for the occurrence of various types of prostatitis. In addition, many adult males have found that there are stones in the prostate through B-ultrasound examination, but they cannot be detected on the X-ray. The analysis of the stone components was found to be a component of the urine rather than a component of the prostatic fluid. Therefore, it is speculated that the formation of prostatic stones is related to urine reflux. The stones after infection can exist in the gland for a long time, and it is not easy to eliminate as an infection. Some people have studied to inject the carbon powder solution into the bladder of the patient before prostatectomy, and then found the gland in the gland and the catheter in the excised prostate specimen; the non-bacterial prostatitis patient first injected the carbon powder solution into the bladder, and then carried out after 3 days. Prostate massage, there are many macrophages in the prostatic fluid containing carbon particles; non-bacterial prostatitis and prostate pain patients in the urinary bladder urethra angiography, found that urine reflux is very serious, prostate and ejaculation can be seen in the development. Therefore, it is believed that the chemical factors caused by urinary reflux in the prostate may be an important cause of the pathogenesis of non-bacterial prostatitis.
Studies have shown that urine reflux into the prostate is an important factor, affecting the metabolism of pyrimidine and purine, increasing the concentration of uric acid and causing prostatitis, the incidence of non-bacterial prostate and uric acid levels in prostate secretion. According to the above theory, allopurinol is used to treat non-bacterial prostatitis. However, some studies have concluded that contrary to the above results.
3. Immunity factors
Immunological studies on prostatitis can be traced back to the initial study of immunoglobulins in prostatic fluid, the discovery of antibody-coated bacteria, and the presence of anti-prostate antibodies. The recent application of animal models to successfully model prostatitis is an autoimmune response process. Encouragingly, the study found that bacterial products provide initial antigenic stimulation during the onset of prostatitis, causing a subsequent immune response.
(1) Immunoglobulin-coated bacteria: In 1979, Thomas published an article stating that by detecting antibodies coated in urine, pyelonephritis can be distinguished from cystitis, 35 patients with pyelonephritis In 34 cases, antibodies were coated with bacteria. Only 20 cases of antibody-coated bacteria were detected in 20 patients with cystitis. In this way, the upper urinary tract can be distinguished from the lower urinary tract infection. Subsequent studies of 14 normal people and 51 cases of prostatitis semen found that 25 patients with prostate can detect antibody-coated bacteria. Of the 25 patients, 24 found IgA antibodies and 10 found IgG antibodies. No antibody-coated bacteria were found in the semen of the normal population.
Bacterial-specific antibodies in plasma: A later study was conducted to evaluate the titer of anti-Escherichia coli (E. coli) antibodies in plasma of patients with prostatitis. Meares et al studied the titer of plasma agglutinating antibodies in patients with prostatitis caused by 25 cases of Escherichia coli (E. coli) significantly higher than the control group. In this study, the dilution titer of the control group was determined to be non-responsive. Subsequent studies have found that in patients with prostatitis, in those patients who are effective, the antibody titer is gradually reduced to normal. And those treatments did not heal, the antibody titer gradually decreased to normal. And those who did not heal the treatment, the antibody titer remained high.
(2) Immunoglobulins in prostatic fluid: Many research groups have studied immunoglobulins in prostate secretions. The initial study began in 1963, when Chodirker and Tomasi first confirmed and qualitatively determined IgG and IgA in normal human prostatic fluid, and subsequent researchers used different techniques to demonstrate systemic and local immune responses in bacterial prostatitis.
Shortliffe et al. used solid phase radioimmunoassay (RIA) to study immune responses in human acute and chronic prostatitis. They found a clear local antibody response in the prostatic fluid, mainly secretory IgA, which is independent of the plasma response and is antigen specific for the infectious agent. In the early stage of acute prostate infection, the antigen-specific IgG in plasma and prostatic fluid increased, and gradually decreased after drug treatment for 6 to 12 months. The antigen-specific IgA level in prostatic fluid increased immediately after infection, and 12 treatments were performed. After the month, it will slowly decline; however, the elevated plasma IgA level at the beginning of the infection decreases only one month. In chronic bacterial prostatitis, although antigen-specific IgA and IgG are elevated in prostatic fluid, there is no positive immunoglobulin in plasma. After chronic drug-induced prostatitis, IgA in prostate fluid increased for 1 year, while IgG lasted for 6 months. Prostatic fluid antigen-specific IgG has been maintained at elevated levels in patients with untreated chronic bacterial prostatitis. Determination of antigen-specific IgA and IgG levels in prostatic fluid not only helps to diagnose prostatitis, but also helps to clarify the effectiveness of treatment.
The increase in total immunoglobulin is clarified, and the next step is to study changes in bacterial specific antibodies. Early studies used bacterial profiles to find elevated bacterial-specific antibodies in prostatic fluid. The study found that immunoglobulins (including IgA and IgG) in the prostatic fluid of patients with non-bacterial prostatitis were moderately elevated, but failed to detect bacterial-specific antibodies.
In order to determine the true specificity of antibacterial immunoglobulins, studies have examined the specificity of antibodies using the patient's own infectious bacteria. The researchers identified bacterial immunoglobulins by detecting secretory immunoglobulins. This includes the detection of immunoglobulins in the urine after mid-stage urine and prostate massage. The study included 14 cases of bacterial prostatitis, 8 cases of non-bacterial prostatitis, and 11 cases of uninfected people. In all groups, IgA and IgG increased after prostate massage, however, after detection of specific antibacterial immunoglobulins, it was found that in normal people and non-bacterial prostatitis patients, the immunoglobulin was mainly IgG slightly elevated. High, and in patients with bacterial prostatitis, the immunoglobulins including IgA and IgG are significantly elevated.
Immunoglobulin histological localization: A localization study of immunoglobulins in the prostate was performed between the normal control group and benign prostatic hypertrophy. Studies have found that IgG is mainly in the cytoplasmic basal part of glandular cells and in the secretory granules of the ductal lumen. IgA was only found in the differentiated particles located in the lumen. In the future, immunoglobulins in prostatitis were studied. Unlike the previous studies, immunoglobulin was detected in only 1 of 21 normal controls. 57% of patients with prostatitis detect immunoglobulins in prostate tissue. IgM is the main immunoglobulin, accounting for 85%. The main deposition sites are around the glandular cells, blood vessel walls and glandular cells, which are successively reduced. IgA was detected in 35% of patients, while C4 was detected in 44% of patients. None of them failed to detect IgG.
(3) Other characteristics of the altered immune status: Prostatic 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 infertile men with fertile men and those with a history of germline infection. This study examined the levels of IL-1, IL-6, INF- and their receptors in semen. These factors are mainly produced by the reaction of macrophages against foreign antigens and, as a result of the activation of immunoglobulins, occur in chronic inflammatory reactions. 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 TNF levels. However, detection of TNF-1 receptors and IL-1 receptor antagonists revealed a decrease in the incidence of TNF-1 receptors in patients with a history of infection, while the concentration of IL-1 receptor antagonists was significantly elevated. Soluble TNF-1 receptors tend to rise in the immune response, which can be considered prostatitis is an altered immune response process. Other studies have found that IL-8 is significantly elevated in semen and prostatic fluid in patients with oligozoospermia.
(4) Autoimmune response: It has been found that the presence of anti-prostate antigen antibodies may be considered as evidence that non-bacterial prostatitis is an autoimmune disease. Studies have found that there are prostate specific antigen (PSA) antibodies in the prostate tissue of BPH patients.
(5) Animal model: In 1984, Pacheco-Rupil returned the spleen cells of rats that had been immunized with prostate extract 30 days before by returning Winstar rats. It was confirmed that T lymphocytes are required during the development of prostatitis. Subsequent studies confirmed that prostatitis was not initiated by antibody immunization against prostate extracts. Using the same model, it was found that during the inflammatory response, mast cell activation and degranulation were present. In spontaneous prostatitis in Winstar rats, prostate nerve fiber density, mast cell density and inflammatory response increase with age, and the degranulation of nerve fibers adjacent to mast cells is particularly obvious, while when mast cells are away from nerve fibers, This phenomenon has not occurred, and this phenomenon suggests a process of neuroimmunomodulation.
PSA is a tissue-specific antigen, and the interaction between tissue-specific antigens and thymus T lymphocytes is mainly due to the absence or non-reaction of related clones. Using this concept, Tagneli and others survived at birth, survived for 3 days after birth, survived for 7 days after birth, and excised the mouse thymus. Only those rats that had their thymus removed 3 days after birth developed prostatitis. Moreover, these corresponding mice produce anti-prostate IgG antibodies. Therefore, the initial immune process is mediated by T lymphocytes and is followed by antibody production. Further studies have found that returning CD4+T spleen cells from normal adult mice to these 3 days postnatal mice can prevent the occurrence of prostatitis. However, spleen cells of adolescent male rats do not have this effect.
(6) Effect of immune factors on treatment: Using animal models that form an autoimmune response, steroid technology and androgens can be successfully used in a model of recurrent prostatitis (Lewis rats) to reduce the extent of inflammatory reactions. Since the role of granules and histamine release of mast cells in the pathogenesis of prostatitis has been noted, a small amount of hydrosysin can be used in the treatment.
4. Other relevant factors
Previous studies have found that sex hormone nutrition, past urinary tract infection history, stress, mental factors, allergies and sexual life are all potential factors for prostatitis. In the following research on related factors, there are many studies in Europe and the United States, but there is still no systematic research in China.
(1) Age: Many studies have found that the incidence of prostatitis is younger than that of older men. Recently, it has been found that prostatitis can be seen in teenagers before the age of 20. However, some studies have found that older patients than young people are likely to be due to elderly patients with prostatic hypertrophy, and the symptoms are similarly misunderstood.
(2) Race: White and black Americans had no statistically significant difference in the incidence of prostatitis.
(3) Region: A US statistics from 1990 to 1994 found that the incidence of prostatitis in the southern United States was twice that of the northeast. Is it due to climatic factors or sexually active factors? Due to the definition of prostatitis and the inconsistency of various aspects of treatment, the differences in regional morbidity cannot be satisfactorily explained.
(4) Sexual activity: Some patients with chronic prostatitis have a longer sexual interval and fewer sexual life than the control group. More research shows that unclean sex is an important factor. But there are also studies. Questioning surveys through the Internet have found that sexual life is not a factor influencing prostatitis.
(5) Prostate biopsy: Prostate infection is a complication of prostate biopsy. A current study found that prophylaxis of antibiotics in 491 patients undergoing rectal biopsy was significantly better than 1/d for 2 weeks/d for 1 week. Indwelling catheters and diabetic complications are risk factors for prostate infection after prostate biopsy.
(6) prostate congestion: prostate due to various reasons for congestion, especially passive congestion, is an important cause of disease. Non-infectious, non-microbial long-term congestion, can form a non-specific inflammatory response, congestion is common in the following situations:
1 sexual life is not normal, sexual life is too frequent, forced to interrupt sexual intercourse, or excessive masturbation, can make the prostate abnormally congested. However, excessive suppression of sexual life will also produce long-term suppressed excitement, resulting in passive congestion.
2 directly oppress the perineum, cycling, horse riding, sedentary for a long time, etc. can make the prostate congestion, especially for cycling.
3 drinking, drinking can make the reproductive organs congestion and cause sexual excitement.
4 massage too heavy, prostate massage when the method is too heavy or too frequent, etc. can make the prostate congestion, can be iatrogenic congestion.
5 cold and cold, the prostate is rich in -adrenal receptors, after the cold, can cause sympathetic nerve activity, leading to increased intraurethral pressure, hindering excretion, the prostate also obstructs excretion due to contraction, resulting in stasis congestion.
(7) An allergic reaction to a virus can also cause inflammation.
(8) Factors in physical and mental health: Some people say that this factor is as high as 50%.
(two) pathogenesis
Only 5% of patients with prostatitis have evidence of bacterial infection. Among patients without evidence of infection, some patients had increased secretion of leukocytosis. These evidences suggest that the inflammatory response in the prostate (although no infection) is responsible for the symptoms of prostatitis. Some other prostatitis patients do not even have inflammatory changes. Brunner's study showed that there were inflammatory and non-inflammatory manifestations in patients with prostatitis symptoms, accounting for 64% and 31%, respectively.
Acute bacterial prostatitis: Acute bacterial prostatitis causes significant inflammation in some or all of the prostate, roughly divided into three stages:
1 Congestive period: the posterior urethra, prostatic tube and surrounding interstitial tissues showed hyperemia, edema and round cell infiltration, and there were lobular granulocytes. Glandular epithelial cells have hyperplasia and desquamation.
2 vesicle period: inflammation continues to develop, prostatic tube and vesicle edema and congestion are more obvious, prostate tubules and acinar swell, forming many small abscesses.
3 The parenchymal phase: The tiny abscess gradually enlarges and invades more parenchyma and surrounding stroma. This situation is more common with staphylococcal infection.
Simple acute prostatitis without any pathological manifestations of chronic prostatitis is uncommon, accounting for only 13.1% to 20% 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 rarely cause disease except Enterococcus. In addition, gonococcal bacteria, tuberculosis, fungi, and trichomoniasis can also cause associated prostatitis. Chlamydia trachomatis, Ureaplasma urealyticum and Mycoplasma hominis, etc., the pathogenic effect of prostatitis is still controversial. The incidence of gonococcal prostatitis has gradually increased in recent years.
Examine
an examination
Related inspection
Urethral examination for urethral secretion examination
I. Symptoms
Acute bacterial prostatitis
Sudden onset, chills and high fever, frequent urination, urgency, and dysuria. Dysuria or acute urinary retention can occur. Clinically, it is often accompanied by acute cystitis. The prostate is swollen, tender, and the local temperature rises, the surface is smooth, and the abscess is full or fluctuating.
2. Chronic bacterial prostatitis
Frequent urination, urgency, dysuria, urinary discomfort or burning when urinating. White secretions often flow from the urethra after urination and after the stool. Sometimes there may be blood, perineal pain, sexual dysfunction, and mental symptoms. The prostate is full, enlarged, soft, and tender. In the long course of the disease, the prostate shrinks, hardens, the surface is incomplete, and there is a small induration.
3. Chronic non-bacterial prostatitis and prostate pain
The clinical manifestations are similar to chronic bacterial prostatitis, but there is no history of repeated urinary tract infections. Mainly for urinary tract irritation, dysuria symptoms, especially the performance of chronic pelvic pain syndrome. Mycoplasma and chlamydia can be cultured in the prostatic fluid of some patients.
Second, diagnosis
Acute bacterial prostatitis is easy to make diagnosis because of its clinical manifestations and typical; the clinical features of chronic prostatitis syndrome vary greatly, and it is not clear. Many symptoms, signs and pathological examinations are in chronic bacterial prostatitis, non- Bacterial prostatitis and prostate pain are often unrecognizable. Radiology and urethroscopic cystoscopy may be helpful for diagnosis, but it is not certain for diagnosis. Prostate histology is only needed in some rare types of prostatitis, such as granulomatous prostatitis. Histological changes in chronic bacterial prostatitis were not specific for determining inflammation as a bacterial cause. A group of 162 consecutive cases of benign prostatic hyperplasia were surgically removed and found to have a 98% incidence of prostatitis. Six clear inflammatory morphological types were observed, but there was no significant difference between positive and negative cultures of prostate bacterial infection. In most cases, the inflammatory response is focal, involving only a small portion of the entire prostate, so prostate biopsy has little guiding significance in the treatment of prostatitis. Prostate biopsy specimen tissue culture has little value in the diagnosis of chronic prostatitis.
Diagnosis
Differential diagnosis
Urethral itching: Sexual gonococcal urethritis (acute gonorrhea): The incubation period is 1-14 days, often 2-5 days. From the beginning, it is acute anterior urethritis, redness, itching and slight tingling of the urethra, followed by thin mucus effluent, causing urination discomfort.
Urethral adhesion: normal urethra has urethral glands, which can secrete a small amount of mucus every day to play a role in lubricating and protecting the urethra. Under normal circumstances, these mucus remain in the urethra and have a protective effect on the urethra mucosa. When the urethra or prostate is inflamed, the secretions may increase. After the urethral secretions are dried in the outer urethra, the mucosa and the skin on both sides of the urethra are slightly adhered, the urinary passage is slightly unsatisfactory, and bifurcation occurs in the initial stage of urination. The urine will stick out and the fork will disappear.
There are erythema and edema in the urethra: repeated episodes of Candida balanitis appear as erythema at the glans, and there may be small pustules or small papules on the surface. It can also be expressed as local edema of the glans mucosa, mild desquamation at the edges, and the presence of papules and small pustules to expand around to form glans erosion.
