Prostatitis is one of the most common diseases among adult men. Although it is not a direct life-threatening disease, it has a serious impact on the quality of life of patients. At the same time, its large patient population and the high cost of medical care place a huge economic burden on public health. The pathogenesis and pathophysiological changes of prostatitis are not well understood and many physicians find it difficult to treat prostatitis clinically. This is a good way to get a better understanding of prostatitis, to determine the severity of the disease, to choose a treatment method, and to evaluate its effectiveness. The Chinese Medical Association’s Urology Section hired relevant experts, based on evidence-based medical data at home and abroad, referring to Campbell¢s Urology, Wu Jieping Urology and relevant foreign guidelines, combined with the actual clinical situation in China, repeated discussions, and completed the 2007 edition of our “Prostatitis Diagnosis and Treatment Guidelines”. After two years of promotion and application, with reference to the opinions and suggestions of colleagues from all over the world, and supplemented with new evidence-based medical information, the Diagnostic and Treatment Guide for Prostatitis was revised.
1. Overview
(1) Concept and classification
The patient’s symptoms are characterized by pain or discomfort in the pelvic region and abnormal urination due to the action of pathogens or (and) certain non-infectious factors.
The pathogenesis and pathophysiological changes of chronic prostatitis are not well understood. It is currently believed that chronic prostatitis is a clinical syndrome consisting of a group of diseases with their own unique etiology, clinical features and outcome.
a. Traditional classification methods
The Meares-Stamey “four-cup method” of classifying prostatitis was the first standardized method of classifying prostatitis by comparing the initial urine (voided bladder one, VB1), the intermediate urine (voided bladder two, VB2), the prostatic secretion (expressed prostatic secretion, VB2), and the prostatic secretion (expelled prostatic secretion, VB2). The results of the four cups of voided bladder one, voided bladder two, VB2, EPS, and voided bladder three (VB3) were used to classify prostatitis as: acute bacterial prostatitis. （The results of white blood cell count and bacterial culture in the four cups of urine specimens were used to classify prostatitis into: acute bacterial prostatitis (ABP), chronic bacterial prostatitis (CBP), chronic nonbacterial prostatitis (CNP), prostatodynia (PD), and prostate pain. This classification reflects the past practice of classifying prostatodynia as an infection.
This classification reflects the past understanding of infection as the main cause of prostatitis.
b. New classification methods
In 1995, the National Institutes of Health (NIH) developed a new classification based on the basic and clinical research on prostatitis at that time.
Type I: Equivalent to the traditional classification of ABP, with an acute onset of febrile illness, persistent and obvious lower urinary tract infection, elevated white blood cell count in the urine, and positive bacterial cultures in the blood or urine.
Type II: Equivalent to CBP in the traditional classification method, accounting for about 5% to 8% of chronic prostatitis. There are recurrent lower urinary tract infections lasting more than 3 months, elevated leukocyte count in EPS/semen/VB3, and positive bacterial culture results.
Type III: Chronic prostatitis/chronic pelvic pain syndromes (CP/CPPS), equivalent to CNP and PD in the traditional classification, is the most common type of prostatitis, accounting for about 90% of chronic prostatitis. The main manifestation is prolonged, recurrent pelvic pain or discomfort lasting more than 3 months, which can be accompanied by varying degrees of urinary symptoms and sexual dysfunction, seriously affecting the patient’s quality of life; negative EPS/semen/VB3 bacterial culture results.
Based on the results of routine EPS/semen/VB3 microscopy, the type can be subdivided into two subtypes, IIIA (inflammatory CPPS) and IIIB (non-inflammatory CPPS): type IIIA patients have elevated leukocyte counts in EPS/semen/VB3; type IIIB patients have leukocytes in EPS/semen/VB3 in the normal range. Subtypes IIIA and IIIB each account for about 50% of the cases.
Type IV: asymptomatic inflammatory prostatitis (AIP). This is a condition in which there are no subjective symptoms and only evidence of inflammation is found during examinations of the prostate (EPS, semen, prostate tissue biopsy and pathology of prostatectomy specimens, etc.).
In addition to the addition of asymptomatic prostatitis, the above classification also combines the traditional classification of CNP and PD into one category, reflecting the new understanding of chronic prostatitis (type III) as a clinical syndrome. In addition, the division of type III into inflammatory (IIIA) and non-inflammatory (IIIB) subcategories, which are not equivalent to CNP and PD because of the expansion of the classification from EPS to EPS/seminal fluid/VB3 leukocyte counts, makes these two subcategories not equivalent to CNP and PD, respectively. The shift in the understanding of chronic prostatitis and the consequent new classification has led to a shift in the treatment strategy towards symptom improvement and a more targeted approach to the different subcategories. According to the International Prostatitis Collaborative Network (IPCN), after 3 years of clinical application, the classification is considered to be a significant improvement over the traditional classification, and has some guidance in clinical application, but there are still shortcomings that need further improvement. However, there are still shortcomings and further improvement is needed.
(2) Epidemiology
Prostatitis is a common disease in adult men. It has been shown that approximately 50% of men will be affected by prostatitis at some point in their lives. Some cases of prostatitis may seriously affect the quality of life of patients and impose a significant economic burden on public health .
a. Morbidity
Patients with prostatitis account for 8-25% of urology outpatients.
The prevalence of prostatitis in the general population: due to the application of different epidemiological survey methods and the different structure of the population selected for the survey, the prevalence of prostatitis reported in the literature varies widely. In the Americas, the prevalence of prostatitis in men aged 20-79 years ranged from 2.2% to 16.0%, in Europe, the prevalence of prostatitis in men aged 20-59 years was 14.2%, and in different Asian countries and regions, the prevalence of prostatitis in men aged 20-79 years ranged from 2.7% to 8.7%.
The detection rate of histological inflammation: recent studies have found that the detection rate of histological inflammation in puncture or surgical specimens of benign prostatic hyperplasia is 49.5% to 100%.
Prevalence in autopsy: According to autopsy reports, the prevalence of prostatitis is 24.3%~44.0%.
b. Factors influencing the onset of prostatitis
The prevalence of prostatitis can affect adult males of all ages, and is higher in adult males under 50 years of age.
3. Etiology and pathogenesis
(1) Type I prostatitis
The pathogenic infection is the main causative factor. The main reason for this is the low resistance of the body, the infection of the prostate by virulent bacteria or other pathogens and their rapid growth and multiplication, mostly bloodstream infection, retrograde infection through the urethra. The main pathogen is Escherichia coli, followed by Staphylococcus aureus, Klebsiella pneumoniae, Aspergillus, Pseudomonas, etc. The majority of these are single pathogen infections.
(2) Type II prostatitis
The pathogenic factors are also mainly pathogenic infections, but the body is more resistant or/and the pathogens are less virulent, mainly retrograde infections, the pathogens are mainly Staphylococcus spp, followed by Escherichia coli, Corynebacterium spp and Enterococcus spp. Prostate stones and urinary reflux may be important reasons for the persistence of pathogens and recurrence of infection.
(3) Type III prostatitis
The pathogenesis is unknown and the etiology is complex and widely debated: there may be multiple etiologies acting simultaneously, with one or more playing a key role; or there may be many different diseases that are difficult to identify but have the same or similar clinical manifestations; or even these diseases have been cured and the damage and pathological changes caused by them continue to act independently. Most scholars believe that the primary etiology may be a combination of pathogenic infection, inflammation, and abnormal pelvic floor neuromuscular activity.
a. Pathogenic infections
Although no pathogens have been isolated by routine bacterial examination, some specific pathogens, such as anaerobic bacteria, L-shaped Aspergillus, nanobacteria, or Chlamydia trachomatis and mycoplasma, may still be associated with this type of infection. Some studies have shown that local prokaryotic DNA detection rates can be as high as 77% in patients with this type of disease; some clinical “aseptic” prostatitis with chronic inflammation and recurrent or worsening episodes may be associated with these pathogens. The most important thing is that it is not only the most common type of disease, but also the most common type of disease.
b. Urinary dysfunction
The fact that some factors cause excessive contraction of the urethral sphincter, resulting in bladder outlet obstruction and residual urine formation, causes urine to flow back into the prostate, which not only brings pathogens into the prostate, but also directly stimulates the prostate and induces aseptic “chemical prostatitis”, causing abnormal urination and pain in the pelvic region.
Many patients with prostatitis have a variety of urodynamic changes, such as decreased urinary flow rate, functional urinary tract obstruction, and dysfunctional forced urinary muscle-urethral sphincter synergy. These functional abnormalities may only be a clinical phenomenon, and their nature may be related to various underlying pathogenic factors.
c. Psychosomatic factors
These mental and psychological factors can cause phytonadic dysfunction, resulting in posterior urethral neuromuscular dysfunction, leading to pelvic area pain and urinary dysfunction; or cause changes in the function of the hypothalamus-pituitary-gonadal axis and affect sexual function, further aggravating the symptoms, eliminating mental tension can make the symptoms ease or heal. However, it is not clear whether the psychosomatic changes are the direct cause or secondary manifestations.
d. Neuroendocrine factors
Patients with prostate pain are often prone to fluctuations in heart rate and blood pressure, suggesting that they may be related to autonomic responses. The pain is characteristic of visceral organ pain. Local pathological stimulation of the prostate and urethra triggers spinal reflexes through the afferent nerves of the prostate, activating astrocytes in the lumbar and sacral medulla, and nerve impulses are transmitted through the genitofemoral and ilioinguinal nerves. This leads to abnormal activity of the perineum and pelvic floor muscles, resulting in referred pain in the corresponding areas other than the prostate.
e. Abnormal immune response
It is believed that prostatitis may be an allergic inflammatory response or an autoimmune disease. The prostate gland produces certain seminal protein antigens such as PSA that can act as autoantigenic substances; residual debris or necrotic tissue of pathogens can also act as antigens that stimulate the body to produce antibodies, which can cause an immune response in the prostate gland, resulting in the deposition of antigen-antibody complexes, leading to a series of clinical manifestations.
In recent years, it has been found that in some patients with chronic prostatitis, cellular immunosuppressive factors (IAP) in the prostate fluid are significantly reduced, while immunoglobulin levels are significantly increased, and treatment with immunosuppressive drugs is effective.
f. The theory of oxidative stress
Under normal circumstances, the production, utilization and removal of oxygen free radicals in the body are in a dynamic balance. The production of oxygen free radicals or/and the scavenging system of free radicals is relatively reduced in patients with prostatitis, thus reducing the body’s ability to respond to oxidative stress and increasing the products or/and by-products of oxidative stress, which may also be one of the pathogenic mechanisms.
g. Pelvic-related disease factors
The fact that some patients with prostatitis often have dilated prostate peripheral plexus, hemorrhoids and varicose veins suggests that some patients with chronic prostatitis may have symptoms related to pelvic venous congestion and blood stagnation, which may also be one of the reasons for the persistent treatment. The reason for this is that some patients with a clinical diagnosis of chronic prostatitis may also have an interstitial cystitis.
(4) Type IV prostatitis
The actual fact that there are no clinical signs and symptoms, often found during the examination of other related diseases, so there is a lack of research data on the pathogenesis of the disease, may be the same as the partial etiology and pathogenesis of type III prostatitis.
(5) Predisposing factors of prostatitis
The most important triggers for the development of prostatitis include: smoking, alcohol consumption, spicy food, inappropriate sexual activity, prolonged congestion of the prostate caused by sedentary and chronic extrusion of the pelvic floor muscles, cold, fatigue, etc., resulting in decreased body resistance or idiosyncratic body.
4.Diagnosis
(1) Diagnostic principles
The diagnosis of prostatitis is recommended according to NIH typing.
Type I: The diagnosis mainly relies on medical history, physical examination and bacterial culture results of blood and urine. Rectal examination of the patient is mandatory, but prostate massage is contraindicated. Before applying antibiotic treatment, a midstream urine culture or blood culture should be performed. If the patient’s condition does not improve after 36 hours of standardized management, transrectal ultrasound and other tests are recommended to evaluate the lower urinary tract lesions comprehensively and to clarify the presence of prostatic abscesses.
Types II and III (chronic prostatitis): Detailed history, thorough physical examination (including rectal examination), routine urine and prostate massage fluid examination are required. The NIH chronic prostatitis symptom index (NIH-CPSI, see Appendix I) is recommended for scoring symptoms. The “two-cup method” or “four-cup method” is recommended for pathogen localization testing (see Appendix IV).
For diagnosis and differential diagnosis, the following tests are available: semen analysis or bacterial culture, prostate-specific antigen (PSA), urine cytology, transabdominal or transrectal ultrasound (including residual urine measurement), urine flow rate, urodynamics, CT, MRI, urethral cystoscopy, and prostate puncture biopsy.
Type IV: asymptomatic, detected during prostate massage fluid (EPS), semen, post-prostate massage urine, prostate tissue biopsy and pathological examination of prostatectomy specimens.
(2) Diagnostic methods
The specific diagnostic methods of prostatitis include
a. Clinical symptoms
When diagnosing prostatitis, a detailed history should be taken to understand the causes or triggers of the disease; to inquire about the nature, characteristics, location, degree of pain and abnormal urination; to understand the treatment and recurrence; to evaluate the impact of the disease on quality of life; and to understand past history, personal history and sexual life.
Type I: The onset of the disease is often sudden, with general symptoms such as chills, fever, fatigue and weakness, accompanied by pain in the perineum and suprapubic area, urinary tract irritation and difficulty in urination, and even acute urinary retention.
Types II and III: The clinical symptoms are similar, with pain and abnormal urination. Type II may manifest as recurrent lower urinary tract infections. Type III mainly presents with pain in the pelvic region, which can be seen in the perineum, penis, perianal region, urethra, pubic bone or lumbosacral region. Urinary abnormalities may include urgency, frequency, painful urination and increased nocturia. Due to the chronic pain, the quality of life of the patient is reduced and there may be sexual dysfunction, anxiety, depression, insomnia, and memory loss.
Type IV: No clinical symptoms.
Chronic Prostatitis Symptom Score
The NIH-CPSI is recommended for symptom assessment due to the relative lack of objective indicators for diagnosing chronic prostatitis and the many controversies surrounding it. the NIH-CPSI consists of 3 main parts with 9 questions (0-43 points). The first part assesses the site, frequency and severity of pain and consists of questions 1-4 (0-21 points); the second part assesses the severity of dysuria and frequency of urination and consists of questions 5-6 (0-10 points); the third part assesses the impact on quality of life and consists of questions 7-9 (0-12 points). It has been translated into several languages and is widely used to assess the symptoms and efficacy of chronic prostatitis.
b. Physical examination
To diagnose prostatitis, a thorough physical examination should be performed, focusing on the genitourinary system. The patient’s lower abdomen, lumbosacral region, perineum, penis, urethral orifice, testes, epididymis and spermatic cord should be examined for abnormalities to aid in diagnosis and differential diagnosis. Rectal examination is very important for the diagnosis of prostatitis and helps to identify perineal, rectal, neurological lesions or other diseases of the prostate, as well as to obtain EPS through prostate massage.
Type I: Physical examination may reveal pressure and discomfort over the pubic bone, and in cases of urinary retention, a bulging bladder over the pubic bone may be palpable. Rectal examination may reveal enlargement of the prostate, tenderness, increased local temperature and irregular shape. Prostate massage is contraindicated.
The prostate should be massaged to obtain EPS. Before rectal examination, it is recommended that urine be retained for routine analysis and urine bacterial culture.
c. Laboratory tests
Routine EPS examination
Routine examination of EPS is usually performed by wet smear method and microscopic examination by hematocrit plate method, the latter having better accuracy.
A normal EPS with <10 leukocytes ph="">10/HP and a reduced number of leukocytes vesicles has diagnostic significance. The number of leukocytes does not correlate with the severity of symptoms. Macrophages containing components such as phagocytosed lecithin vesicles or cellular debris in the cytoplasm are also characteristic of prostatitis [9]. Pathogens such as bacteria, fungi and trichomonads can be detected in EPS when the prostate is infected with these pathogens.
In addition, in order to clearly distinguish the components of EPS such as leukocytes, EPS can be identified using methods such as Gram staining.
If EPS cannot be collected after prostate massage, it is not advisable to repeat the massage several times, and the patient can be allowed to retain the urine after prostate massage for analysis.
Routine urine analysis and urine sedimentation examination
Routine urine analysis and urine sediment examination are auxiliary methods to exclude urinary tract infections and diagnose prostatitis.
Bacteriological examination
1) Type I Stain microscopy, bacterial culture and drug sensitivity test of the middle urine, and blood culture and drug sensitivity test should be performed.
2) Chronic prostatitis (type II and III) The “two-cup” or “four-cup” pathogen localization test is recommended.
”The four-cup method: In 1968, Meares and Stamey [6] proposed the use of sequential collection of segmental urine and EPS for separate culture (referred to as the “four-cup method”) to differentiate between urethral, bladder and prostate infections in men. infections.
”The two-cup method: The four-cup method is complex, time-consuming and expensive, so the two-cup method is usually recommended in clinical practice. The “two-cup method” is done by obtaining urine before and after prostate massage for microscopic examination and bacterial culture.
d. Other pathogens examination
1) Chlamydia trachomatis detection Chlamydia trachomatis (Ct) detection methods are culture method, immunofluorescence method, spot gold immuno-permeation method , polymerase chain reaction (PCR) and ligase chain reaction (LCR) etc. The cultivation method only detects live Ct and is not recommended for clinical application due to cost, time and technical level. Currently, PCR and LCR techniques with high sensitivity and specificity are mainly used to detect the nucleic acid component of Ct.
The main mycoplasmas that may cause prostate infection are Ureaplasma urealyticum (Uu) and Mycoplasma hominis (Mh). Culture is the gold standard for the detection of Uu and Mh, and in combination with drug sensitivity testing, it can be used for clinical diagnosis and treatment; immunological testing and nucleic acid amplification techniques are also used for mycoplasma detection.
Since Chlamydia trachomatis and mycoplasma may also be present in the male urethra, it is recommended that urethral swabs be taken first and then EPS testing be performed after urethral infection has been ruled out to further clarify whether it is a prostate infection.
In addition, other pathogens in EPS, such as fungi, are detected by direct smear staining microscopy and isolation culture; viruses are usually detected by prostate tissue culture or PCR techniques.
(5) Other laboratory tests
Patients with prostatitis may have abnormal semen quality, such as leukocytosis, semen non-liquefaction, hematospermia and decreased sperm quality. Elevated PSA may also be seen in some patients with chronic prostatitis [28]. Urine cytology examination has some value in differentiating from carcinoma in situ of the bladder and other .
d. Instrumental examinations
(1) Ultrasound: Although ultrasound examination in patients with prostatitis can reveal manifestations such as uneven prostate echogenicity, prostate stones or calcifications, and dilated periprostatic plexus, there is still a lack of specific manifestations of ultrasound for the diagnosis of prostatitis, and it is not possible to use ultrasound for the staging of prostatitis. However, ultrasound can provide a more accurate picture of the kidneys, bladder, and residual urine in patients with prostatitis, which can be helpful in excluding organic lesions of the urinary tract. Transrectal ultrasound is valuable for identifying prostate, seminal vesicle and ejaculatory duct lesions and for diagnosing and draining prostatic abscesses.
(2) Urodynamics: (1) urine flow rate, urine flow rate examination can give a general idea of the patient’s voiding status and help to differentiate prostatitis from diseases related to voiding disorders; (2) invasive urodynamic examination, studies have shown that invasive urodynamic examination in patients with prostatitis can detect bladder outlet obstruction, functional urethral obstruction, bladder detrusor hyporeflexia or detrusor instability and other bladder detrusor dysfunction. urethral dysfunction. If there is clinical suspicion of these voiding dysfunctions, or if there are significant abnormalities in urinary flow rate and residual urine, invasive urodynamic testing may be indicated to clarify the diagnosis.
(3) Cystourethroscopy
Cystourethroscopy is an invasive test and is not routinely recommended for patients with prostatitis. In some cases, such as patients with hematuria, significant abnormalities in urinalysis, and other tests suggesting cystourethral lesions, cystourethroscopy may be chosen to clarify the diagnosis.
e. CT and MRI
There are potential applications for identifying pelvic organ lesions such as seminal vesicles and ejaculatory ducts, but the diagnostic value for prostatitis itself is still unclear.
(3) Differential diagnosis
Type III prostatitis lacks an objective and specific diagnostic basis. The clinical diagnosis should be differentiated from diseases that may cause pain in the pelvic region and abnormal urination, and patients with predominantly abnormal urination should be clearly identified with or without bladder outlet obstruction and abnormal bladder function. Diseases to be differentiated include: benign prostatic hyperplasia, testicular epididymal and spermatic cord disease, overactive bladder, neurogenic bladder, interstitial cystitis, adenocystitis, sexually transmitted diseases, bladder tumors, prostate cancer, anorectal disease, lumbar spine disease, central and peripheral neuropathy, etc.
5.Treatment
(1) Treatment principles
Prostatitis should be treated in a comprehensive manner.
Type I: mainly broad-spectrum antibiotics, symptomatic treatment and supportive therapy. If you have urinary retention, you can use fine tube catheterization or suprapubic cystostomy to drain urine, and if you have prostate abscess, you can use surgical drainage.
Type II: Treatment is based on oral antibiotics, with sensitive drugs chosen for a course of 4-6 weeks, during which the patient should be evaluated for efficacy in stages. If the efficacy is not satisfactory, other sensitive antibiotics can be used instead. Alpha-blockers can be used to improve urinary symptoms and pain. Botanicals, NSAIDs, and M-blockers can also improve the symptoms.
Type IIIA: Oral antibiotics can be given for 2 to 4 weeks, and then the decision to continue antibiotic therapy is based on their efficacy feedback. Alpha-blockers are recommended to improve urinary symptoms and pain, and NSAIDs, botanicals and M-blockers are also available.
Type IIIB: alpha-blockers, NSAIDs, botanicals, and M-blockers are available for treatment.
Type IV: No treatment is generally required.
(2) Treatment methods
Type Ⅰ
Antibiotic treatment for type I prostatitis is necessary and urgent. Once the clinical diagnosis or blood and urine culture results are obtained, antibiotics should be applied immediately. In the beginning, antibiotics such as broad-spectrum penicillin, triple cephalosporins, aminoglycosides or fluoroquinolones can be applied via static pulse. After the patient’s fever and other symptoms improve, the patient can be switched to oral medications (e.g., fluoroquinolones) for at least 4 weeks. Patients with milder symptoms should also be treated with antibiotics for 2 to 4 weeks.
For acute bacterial prostatitis with urinary retention, suprapubic cystostomy can be used to drain urine, or fine catheterization can be used, but the catheter should not be left in place for more than 12 hours. In cases with abscess formation, transrectal ultrasound-guided fine needle aspiration drainage, transurethral resection prostatic abscess drainage or perineal aspiration drainage can be used.
Types II and III
The clinical progressiveness of chronic prostatitis is not clear enough to threaten the life and vital organ function of patients, and not all patients require treatment. The goal of treatment for chronic prostatitis is to relieve pain, improve urinary symptoms and improve quality of life, and the evaluation of efficacy should be based on symptom improvement.
a. General treatment
Health education, psychological and behavioral counseling have a positive effect. Patients should abstain from alcohol, spicy and stimulating food; avoid holding urine, sitting for a long time, pay attention to warmth and strengthen physical exercise.
b.Medication
The three most commonly used drugs are antibiotics, alpha-blockers and non-steroidal anti-inflammatory analgesics, and other drugs also have different degrees of efficacy in relieving symptoms.
（The most common first-line drug used in clinical practice for the treatment of prostatitis is antibiotics, but only about 5% of patients with chronic prostatitis have a clear bacterial infection.
Type II: Antibiotics are chosen based on the results of bacterial cultures and the ability of the drug to penetrate the prostate. The ability of the drug to penetrate the prostate depends on the degree of ionization, lipolysis, protein binding, relative molecular mass, and molecular structure. The choice of antibiotics includes fluoroquinolones (e.g., ciprofloxacin, levofloxacin, lomefloxacin, and moxifloxacin), tetracyclines (e.g., minocycline), and sulfonamides (e.g., cotrimoxazole).
After the diagnosis of prostatitis, the course of antibiotic treatment is 4-6 weeks, during which the patient should be evaluated in stages of efficacy. If the results are not satisfactory, the patient can be switched to other sensitive antibiotics. Intraprostatic injection of antibiotics is not recommended as a treatment method.
Type IIIA: Antibiotic therapy is mostly empirical and is based on the theory that certain pathogens that are routinely culture-negative are presumed to cause this type of inflammation. Therefore, oral antibiotics such as fluoroquinolones are recommended for 2 to 4 weeks, followed by a decision to continue antibiotic therapy based on feedback on efficacy. Continuation of antibiotics is recommended only if the patient shows a definite reduction in clinical symptoms. The recommended total course of treatment is 4 to 6 weeks. Some patients with this type may have intracellular pathogens such as Chlamydia trachomatis, Ureaplasma lysis or Mycoplasma humanum, and may be treated with oral antibiotics such as tetracyclines or macrolides.
Type IIIB: Antibiotic treatment is not recommended.
(2) Alpha-blockers Alpha-blockers can relax the smooth muscles of the prostate and bladder to improve lower urinary tract symptoms and pain, making them the basic treatment for type II/III prostatitis.
The choice of alpha-blocker can vary depending on the patient’s condition. The recommended alpha-blockers are: doxazosin, naftopidil, tamsulosin and terazosin. Controlled studies have shown that these drugs have shown varying degrees of improvement in urinary symptoms, pain and quality of life index. The adverse effects of these drugs, such as vertigo and postural hypotension, should be noted in the treatment. The current meta-analysis of studies suggests that alpha-blockers may be more effective in patients with untreated or newly diagnosed prostatitis than in chronic, refractory patients, that longer courses (12 to 24 weeks) may be more effective than shorter courses, and that less selective agents may be more effective than more selective agents.
Alpha-blockers should be used for at least 12 weeks. alpha-blockers can be used in combination with antibiotics for the treatment of type IIIA prostatitis and the combination should be used for at least 6 weeks.
(3) Non-steroidal anti-inflammatory analgesics Non-steroidal anti-inflammatory analgesics are used empirically to treat the symptoms associated with type III prostatitis. Their primary purpose is to relieve pain and discomfort. To date, only a few randomized, placebo-controlled studies have evaluated the efficacy of such drugs. Controlled clinical studies have confirmed the effectiveness of celecoxib in improving pain and other symptoms in patients with type IIIA prostatitis!
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