Search Menu Abstract Prostatitis is characterized by voiding symptoms and genitourinary pain and is sometimes associated with sexual dysfunction. The causes and treatment of nonbacterial prostatitis are largely unknown, but bacterial prostatitis is caused by infection with uropathogens, especially gram-negative slid prosztatitis, although infection is sometimes due to gram-positive and atypical microorganisms.
Acute bacterial prostatitis is easily diagnosed by abrupt urogential and often systemic symptoms, along with bacteriuria and treated by systemic antibiotic therapy. Chronic bacterial prostatitis is characterized by prolonged or recurrent symptoms and relapsing bacteriuria; diagnosis traditionally requires comparing urinary specimens obtained before with specimens obtained after prostatic massage.
Treating chronic bacterial prostatitis requires prolonged therapy with an antibiotic that penetrates the prostate ie, one with high lipid solubility, a low degree of ionization, high dissociation constant, low protein binding, and small molecular size.
We review recent pharmacological and clinical data on treating bacterial prostatitis. Prostatitis is a common syndrome that usually presents with voiding symptoms irritative or obstructive and pain genitourinary, pelvic, or rectal and is sometimes associated with sexual dysfunction eg, ejaculatory discomfort and hematospermia.
Characteristic features include a high prevalence, substantially impaired quality of life, and frequent recurrences [ 1 ]. Although some cases are clearly infectious, most men who receive a diagnosis slid prosztatitis prostatitis have no evidence of a genitourinary bacterial infection and the slid prosztatitis is usually unknown [ 2 ].
Disagreement persists over how to define prostatitis, including debates over the relative importance of various clinical, microbiological, and histopathological findings [ 3 ].
Advances in the past decade, however, have spurred better-designed clinical trials and generated more robust evidence regarding treatment. One major change was the development of a National Institutes of Health NIH consensus definition and classification system Table 1 [ 45 ].
This scheme, although limited by the lack of a reliable comparison standard, clarified that a small minority of men with prostatitis have bacterial infection ie, acute bacterial prostatitis [ABP; category I] or chronic bacterial prostatitis [CBP; category II] [ 6 ]. The rest have nonbacterial prostatitis. A new syndrome, asymptomatic inflammatory prostatitis category IVis defined by an abnormal semen analysis, elevated prostate-specific antigen PSAor incidental findings of prostatitis on examination of a biopsy specimen.
This questionnaire scores disorders relating to pain, voiding, and quality of life.
Prostate : Acute Inflammation
The slid prosztatitis area of uncertainty in treating prostatitis concerns the approach to nonbacterial prostatitis. This review, however, will focus on treatment of bacterial prostatitis and will only briefly discuss nontreatment slid prosztatitis or nonbacterial disorders.
Because of the familiarity of the prostatitis categories, we will generally refer to them by their classical rather than NIH designations. Our recommendations are derived from a comprehensive review of the literature and our combined clinical experience. Reported rates of prostatitis are similar in North America, Europe, and Asia [ 15 ]. In addition to discomfort, prostatitis syndromes are responsible for substantial physical and emotional distress [ 1617 ] and financial costs [ 14 ].
Pathophysiology The prostate gland has several natural defenses against infection, including the production of slid prosztatitis substances and mechanical flushing of the prostatic urethra by voiding and ejaculation [ 18 ]. However, poor drainage of secretions from peripheral ducts or reflux of urine into prostatic tissue may lead to inflammation, fibrosis, or stones.
Urinalysis involves testing a urine sample. A health care provider tests the sample during an office visit or sends it to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated slid prosztatitis, called a dipstick, into the urine. Patches on the dipstick change color to indicate signs of infection in urine. The health care provider can diagnose the bacterial forms of prostatitis by examining the urine sample with a microscope.
Most bacterial prostatitis probably follows a urinary tract infection UTIespecially with uropathogens that demonstrate special slid prosztatitis factors [ 19 ]. Risk factors for developing prostate infection include urinary tract instrumentation, having a urethral stricture, or urethritis usually due to sexually transmitted pathogens. The formation of either bacterial biofilm or prostatic calculi favors chronic, treatment-resistant infection [ 22 ].
Histopathological findings in bacterial prostatitis are poorly defined, with infection primarily in the acinar rather than slid prosztatitis interstitial spaces [ 22 ] and primarily luminal rather than parenchymal.
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Clinical Presentation and Diagnostic Evaluation ABP typically presents abruptly with voiding symptoms and distressing but poorly localized pain and is often associated with systemic findings eg, malaise and fever [ 5 ]. Clinicians should enquire about urogenital disorders, recent genitourinary instrumentation, and new sexual contacts. Between symptomatic UTIs, patients may be asymptomatic, despite ongoing prostatic slid prosztatitis.
Physical examination should include obtaining vital signs and examining the lower abdomen seeking a distended bladderback seeking costovertebral-angle tendernessgenitalia, and rectum. Digital prostate palpation in ABP can cause discomfort and can potentially induce bacteremia but is safe if done gently.
Prostatitis: Misdiagnosed and Misunderstood
Few laboratory tests are diagnostically useful in evaluating possible prostatitis. Any patient at risk slid prosztatitis be screened for sexually transmitted infections. All patients with possible prostatitis need a urinalysis and urine culture. Blood cultures and a complete blood count are useful in ABP. For patients with possible CBP, the 4-glass test is considered to be the diagnostic criterion standard.
Diagnosis is based on finding substantially lower leukocyte and slid prosztatitis counts in voided bladder urine specimens from the urethra VB1 slid prosztatitis bladder VB2compared with counts in post-prostatic massage voided urine VB3 or expressed prostatic secretions EPS.
Adding a culture of ejaculated semen improves the diagnostic utility of the 4-glass test [ 2526 ], but semen cultures are positive more often than are cultures of VB3 or EPS in men with nonbacterial prostatitis [ slid prosztatitis ]. The 4-glass test is cumbersome, inadequately validated, and rarely performed, even by urologists [ 2829 ].
It may be diagnostically helpful on first presentation, but its value is limited in previously treated patients with chronic symptoms. A simpler 2-glass test comparing pre- with post-prostatic massage urine specimens provides similar results [ 30 ].
Evaluating patients with chronic prostatitis should usually include administering the NIH-CPSI and perhaps measuring urinary flow rate and post-void residual urine; only selected patients need further urodynamic or imaging studies [ 32 ].
Various imaging studies can detect a suspected prostatic abscess. Figure 1 shows our approach to evaluating a patient with possible prostatitis. Causative Pathogens in Prostatitis Aerobic gram-negative bacilli are the predominant pathogens in bacterial prostatitis. Some debate the role of gram-positive organisms other than enterococci [ 3637 ], but most accept Staphylococcus and Streptococcus species as pathogens [ 37—39 ].
The increasing prevalence slid prosztatitis gram-positive pathogens may represent changing disease epidemiology perhaps related to fluoroquinolone therapy or acceptance of their pathogenicity by health care providers. Limited data suggest a prosztatitis miramistin kezelése obligate anaerobes may rarely cause chronic prostatitis [ 40 ].
Some cases of prostatitis are caused by atypical pathogens [ 34 ]. Other possible prostatitis pathogens include Mycoplasma genitalium, Neisseria gonorrhoeae, Mycobacterium slid prosztatitis, various fungi, and several viruses [ 34 ]. Treatment of Bacterial Prostatitis The approach gyakori vizelési inger viszketés treating bacterial elektródák prosztatitis of the prostate largely centers slid prosztatitis appropriately selected antibiotic therapy.
Overview of antibiotic therapy. Treatment of bacterial prostatitis is hampered by the lack of an active antibiotic transport mechanism and the relatively poor penetration of most antibiotics into infected prostate tissue and fluids. Most antibiotics are either weak acids or bases that ionize in biological fluids, which inhibits their crossing slid prosztatitis epithelium Figure 2 [ 23 ]. Only free, non-protein-bound antibiotic molecules enter tissues.
- Every year, thousands of men are diagnosed with prostatitis.
- A kaporok infúziója a prosztatitisből
Passage of a drug through prostatic capillary endothelium and prostatic epithelium is enhanced by a high concentration gradient, high lipid solubility, low degree of ionization, high dissociation constant pKa; allowing diffusion of the unionized component into the prostatelow protein binding, slid prosztatitis small molecular size [ 42 ].
A pH gradient allows electrically neutral molecules to pass through membranes, become ionized, and be trapped. Although ion trapping may increase prostatic drug concentration, slid prosztatitis charged fraction has an unclear antimicrobial role. Many early studies of prostatic antibiotic slid prosztatitis used dogs, which generally have acidic prostatic fluid. Human studies have mostly used adenoma tissue derived from prostate resection.
These uninfected samples of mixed tissues and fluids with varied pH levels generally have antibiotic concentrations that exceed those in plasma. In humans, alkaline drugs eg, trimethoprim and clindamycin undergo ion trapping, which leads to high prostatic concentrations.
Acidic drugs, such as beta-lactams, achieve lower levels, but more drug is in the active unionized state. Fluoroquinolones have emerged as the preferred antibiotics for treating bacterial prostatitis, and several have been approved by the US Food and Drug Administration FDA for this indication.
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Compared with concentrations in plasma, drug levels are generally higher in urine, similar in seminal fluid and prostatic a prosztatitisből előírva, and lower albeit therapeutic in prostatic fluid [ 4344 ]. One concern with these agents is the growing problem of fluoroquinolone resistance, which generally requires treatment with a third-generation cephalosporin eg, ceftazidime or ceftriaxone or a carbapenem eg, imipenem or ertapenem népi kezelés a prosztatitishez 45 ].
Table 2 provides information on other antibiotics that may be useful for treating bacterial prostatitis, based on pharmacodynamic data, case reports, or FDA approval for treating UTIs. Although penicillin G achieves poor prostatic concentrations, piperacillin has good levels and has been used successfully to treat CBP.
Cephalosporins, despite being weak acids with low lipid solubility, can attain therapeutic levels in prostatic fluid or tissue Table 2. Aztreonam, imipenem, and some aminoglycosides can attain levels in prostatic tissue that exceed the minimum inhibitory concentrations slid prosztatitis most Enterobacteriaceae.
Prostatitis: Inflammation of the Prostate
Erythromycin—and probably other macrolides, as well—can develop high prostate concentrations. Clindamycin and trimethoprim readily enter prostatic fluid, and levels of these drugs in prostatic fluid may exceed levels in plasma.
The prostatic concentration of sulfamethoxazole is much lower, raising doubts that it synergizes with trimethoprim. Nitrofurantoin prostatic levels are likely nontherapeutic.
Table 3 outlines the advantages and disadvantages of commonly used antimicrobial agents for the treatment of CBP. Antibiotic therapy for ABP. For systemically ill patients with ABP, parenteral antibiotic therapy is preferable, at least initially.
Most antibiotic agents penetrate the acutely inflamed prostate, but slid prosztatitis favors empirical treatment with a broad-spectrum beta-lactam drug—either a penicillin eg, piperacillin- tazobactam or a cephalosporin eg, cefotaxime or ceftazidime —perhaps combined with an aminoglycoside for patients who are severely ill or who have recently received antibiotic therapy.
Clinicians should consider local drug-resistance patterns in choosing antibiotics, especially with the emergence of extended-spectrum beta-lactamase-producing strains in complicated UTIs [ 21 ], and should adjust therapy on the basis of culture results.
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Clinically stable patients may be treated with oral therapy usually a fluoroquinolone. Duration of therapy for ABP is usually 2 weeks, although it can be continued for up to 4 weeks for severe illness or treatment of patients with concomitant bacteremia. Two recent studies provide insights on treating ABP. A multicenter retrospective survey revealed vizeletben a prosztatitisben community -acquired slid prosztatitis were 3 times more common than slid prosztatitis infections; E.
A similar study found a high rate of ciprofloxacin- resistant pathogens and that nosocomial acquisition or prior instrumentation were slid prosztatitis with increased antibiotic resistance and higher rates of clinical failure [ 47 ]. Ancillary measures for ABP include ensuring adequate fluid intake and urinary drainage.
CBP should be treated with 4—6 weeks of antibiotic therapy. When persistent infection is caused by infected prostate stones or other types of genitourinary pathology, patients who have shown some response may benefit from more-prolonged antibiotic therapy [ 48 ].
In contrast with treatment of ABP, treatment of CBP can usually be delayed until culture and susceptibility results are available. Fluoroquinolones are the preferred drugs, except when resistance to these agents is confirmed or strongly suspected.
Clinical and microbiological response rates are similar in those whose prostatic specimens grow either well-accepted uropathogens or coagulase-negative Staphylococcus or Streptococcus species [ 39 ]. Giving repeated courses of antibiotics is generally unwise.
Surgically removing infected prostatic stones may help when other measures fail. Some case reports suggest apparent benefit from direct injection of antimicrobials into the prostate, but the evidence is insufficient to slid prosztatitis this approach. Long-term suppressive therapy with low doses of oral antibiotics eg, trimethoprim- sufamethoxazole may reduce symptomatic recurrences, but evidence is lacking.
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Clinicians often treat nonbacterial prostatitis because of concern over missing infections that slid prosztatitis due to pathogens that are difficult to culture, and because many apparently uninfected patients appear to respond to treatment. This may be at least partly related to the fact that some antibiotics eg, macrolides and tetracyclines have direct antiinflammatory effects. There is no validated test of cure for bacterial prostatitis. If the patient's symptoms resolve after therapy, we would usually not treat asymptomatic bacteriuria, if present.
If symptoms that are thought to be related to prostatitis persist, culture-directed antibiotic therapy with a more prolonged course, higher dosage, or different agent should be considered. To interrogate the literature on the possible value of antibiotic therapy for chronic prostatitis bacterial or presumed nonbacterialwe identified studies published in the previous decade that reported rates of either symptom improvement or microbiological eradication Table 4. In all 8 trials involving patients with CBP, the patients experienced significant symptomatic and microbiological improvement usually defined slid prosztatitis improved prostate symptom scores and infection eradication with antibiotic therapy.