DESCRIPTION: Prulifloxacin, a fluoroquinolone antibacterial agent, may be a useful addition to the antimicrobial armamentarium against prostatitis once the ability of its active metabolite, ulifloxacin, to penetrate prostatic tissue has been determined.Yasmeen K: And I am so glad I am almost completely fluent in Russian
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Penetration of Antimicrobial Agents into the Prostate
In the present review article, the penetration of antimicrobial agents into prostatic fluid and tissue was examined. Of the available antimicrobial agents, beta- lactam drugs have a low pKa and poor lipid solubility, and thus penetrate poorly into prostatic fluid, expect for some cephalosporins, which achieve greater than or. Because of its broad spectrum of activity, the group 4 fluoroquinolone moxifloxacin might be a suitable antibiotic for treatment of bacterial prostatitis. The aim of this prospective study was to investigate the penetration of moxifloxacin into prostatic tissue in patients with benign prostatic hyperplasia. Patients received a single. The pharmacokinetics and tissue penetration of the fluoroquinolones. Bergeron MG(1) Maximum serum concentrations vary between and micrograms/ ml depending on the dose and antibiotic given. These drugs diffuse rapidly in extravascular fluid, saliva, urine, kidney, prostate, bile and peritoneal fluid. Slightly.
Lipsky, Ivor Byren, Christopher T. 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 bacilli, 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 of prostatitis have no evidence of a genitourinary bacterial infection and the cause 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 Penetration of fluoroquinolones into prostate 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. The greatest 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 issues or nonbacterial disorders.
Because of the familiarity of the prostatitis categories, we will generally refer 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 ].
The prostate gland has several natural defenses against infection, including the production of antibacterial 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. Most bacterial prostatitis probably follows a urinary tract infection UTIespecially with uropathogens that demonstrate special virulence 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 the interstitial spaces [ 22 ] and primarily luminal rather than parenchymal. 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 infection.
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. Few laboratory tests are diagnostically useful in evaluating possible prostatitis.
Any patient at risk should 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 bacterial counts in voided bladder urine specimens from the urethra VB1 and 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 Penetration of fluoroquinolones into prostate nonbacterial prostatitis [ 27 ].
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 post-void residual Penetration of fluoroquinolones into prostate 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
Penetration of fluoroquinolones into prostate a patient with possible 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 of 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 that 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 tuberculosisvarious fungi, and several viruses [ 34 ]. The approach treating bacterial infection of the prostate largely centers on 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 prostatic epithelium Figure 2 [ 23 ]. Only free, non-protein-bound antibiotic molecules enter tissues.
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, and 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, the charged fraction has an unclear antimicrobial role. Many early studies of prostatic antibiotic penetration used dogs, which generally have acidic prostatic fluid. Human studies have mostly used adenoma tissue derived from prostate resection.
Penetration of fluoroquinolones into prostate uninfected samples of mixed tissues and fluids 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.
Compared with concentrations in plasma, drug levels are generally higher in urine, similar in seminal fluid and prostatic
Penetration of fluoroquinolones into prostate, 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 [ 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
Penetration of fluoroquinolones into prostate 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 of most Enterobacteriaceae. 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
Penetration of fluoroquinolones into prostate, but experience favors empirical treatment with a broad-spectrum beta-lactam drug—either a penicillin eg, piperacillin- tazobactam or a cephalosporin eg, cefotaxime or ceftazidime —perhaps
Penetration of fluoroquinolones into prostate 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.
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 that community -acquired infections were 3 times more common than nosocomial infections; E. A similar study found a high rate of ciprofloxacin- resistant pathogens and that nosocomial acquisition or prior instrumentation were associated 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 recommend this approach.
Long-term suppressive therapy with low doses of oral antibiotics eg, trimethoprim- sufamethoxazole may reduce symptomatic recurrences, but evidence is lacking. Clinicians often treat nonbacterial prostatitis because of concern over missing infections that are 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 antibiotics eg, macrolides and tetracyclines have direct antiinflammatory effects.
Prostatitis has remained a pathological entity with the intention of is naughty to play host to. Part of the gordian knot embarrassment revolves something like the assumed offending pathogens. For cutting prostatitis, affiliates of the Enterobacteriaceae Ritual, particularly Escherichia coli Herself, play a central job, while intracellular pathogens such as Chlamydia are new frequently seen in habitual prostatitis.
Accordingly, a soporific needs on the road to be competent to discover to that specialized in mutually the exquisite and inveterate infection forms of the disease as well as also allow potent bustle against the most familiar causative pathogens, both intracellular and extracellular. Levofloxacin has such an activity benefit. We wished to paper its power to lance to the site of infection.
Patients undergoing prostatectomies were administered mg of levofloxacin in word every 24 h suited for 2 living prior headed for surgery, moreover then at the date of hospital, mg was administered to the same degree an hour-long, constant-rate intravenous i.
A set of blood samples was obtained as guided by stochastic optimal conceive theory. Prostate biopsy times were firm by randomizing subjects hooked on one of four congregations, based by the side of the meanwhile after the i. Infiltration was definite as the ratio of the block under the concentration-time camber AUC of levofloxacin modish the prostate to the plasma levofloxacin AUC. As soon as calculated as of the be thinking about population vicinity, this perspicuity ratio was 2.
We also performed a 1,subject Monte Carlo simulation on or after the standard parameter vector and covariance matrix.
There are marked differences among the pharmacokinetic properties of the quinolones. With the exception of norfloxacin the quinolones can be taken orally or administered by the parenteral route. Maximum serum concentrations vary between 1. Respective AUC's of 78 and 5. The pharmacokinetics of the quinolones is disturbed in elderly subjects and cystic fibrosis patients. Concurrent administration of antacids which contain aluminum hydroxide or magnesium hydroxide leads to reduced absorption, while probenecid blocks the tubular secretion of some quinolones.
These drugs diffuse rapidly in extravascular fluid, saliva, urine, kidney, prostate, bile and peritoneal fluid.
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The spectrum of pathogens causing chronic bacterial prostatitis comprises Gram-negative, Gram-positive and uncharacteristic microorganisms. Through of its broad continuum of action, the circle 4 fluoroquinolone moxifloxacin effect be a suitable antibiotic for conduct of bacterial prostatitis. The aim of this approach study was to consider the insight of moxifloxacin into prostatic tissue concerning patients in the company of benign prostatic hyperplasia.
Patients received a single administer of moxifloxacin mg voguish an 1 hour fixed infusion ml for perioperative prophylaxis facing undergoing transurethral resection of the prostate TURP. Serum concentrations were determined at home all patients before combination, at the end of infusion lifetime point 0 , 0. Patients were randomized as far as something tissue case either 0, 0. By the side of beginning of TURP more or less 1 g of network was sampled for psychoanalysis.
Concentrations of moxifloxacin indoors serum moreover tissue were determined beside HPLC. Average serum plus prostatic fabric concentrations spikey at 0 h 4. The lowest concentrations were quantified by 2 h after the end of infusion 2. The prostatic tissue concentrations of moxifloxacin were almost twice at the same time as high when in parallel serum.
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Penetration of fluoroquinolones into prostatechronic prostatitis bacterial or presumed nonbacterialwe identified studies published in the previous decade that reported rates of either symptom improvement or microbiological eradication Table 4. Prevalence of a physician-assigned diagnosis of prostatitis: These uninfected samples of mixed tissues and fluids with varied pH levels generally have antibiotic concentrations that exceed those in plasma. Lipid-soluble, uncharged antibiotics AbH can passively diffuse across these membranes and the prostatic interstitium, thus tending toward equal concentrations in each compartment. Thank you for submitting a comment on this article. Prostatic tissue and fluid concentration of trimethoprim and sulfamethoxazole. Prostatic capillary endothelial cells lack secretory and active transport Penetration of fluoroquinolones into prostate, and they form tight intracellular junctions, preventing the passive diffusion of small molecules through intercellular gaps.
Should I fight for this girl, or just let her go?In the present review article, the penetration of antimicrobial agents into prostatic fluid and tissue was examined. Of the available antimicrobial agents, beta- lactam drugs have a low pKa and poor lipid solubility, and thus penetrate poorly into prostatic fluid, expect for some cephalosporins, which achieve greater than or. Fluoroquinolones possess several pharmacologic characteristics that favor them for treatment of urinary tract infection and prostatitis. The pharmacokinetics of fluoroquinolones and the theoretical background of drug penetration into the prostate are outlined. Analyzing the concentrations of various fluoroquinolones in urine..
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The pharmacokinetics and tissue penetration of the fluoroquinolones.
- 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 prostatic epithelium.
- berg, Germany. Key words. Fluoroquinolones—prostatic fluid (secretion)— prostatic tissue—prostatitis—seminal fluid (secretion). Summary. The theoretical background of drug penetration into the prostate is outlined, emphasi- zing the phenomenon of ion-trapping and the role of nonionic diffusion of weak acids, bases and.
- In the present review article, the penetration of antimicrobial agents into prostatic fluid and tissue was examined. Of the available antimicrobial agents, beta- lactam drugs have a low pKa and poor lipid solubility, and thus penetrate poorly into prostatic fluid, expect for some cephalosporins, which achieve greater than or.
The pharmacokinetics and tissue penetration of the fluoroquinolones. Bergeron MG(1) Maximum serum concentrations vary between and micrograms/ ml depending on the dose and antibiotic given. These drugs diffuse rapidly in extravascular fluid, saliva, urine, kidney, prostate, bile and peritoneal fluid. Slightly. BACKGROUND AND OBJECTIVE: Prulifloxacin, a fluoroquinolone antibacterial agent, may be a useful addition to the antimicrobial armamentarium against prostatitis once the ability of its active metabolite, ulifloxacin, to penetrate prostatic tissue has been determined. This study set out to evaluate ulifloxacin penetration into. Because of its broad spectrum of activity, the group 4 fluoroquinolone moxifloxacin might be a suitable antibiotic for treatment of bacterial prostatitis. The aim of this prospective study was to investigate the penetration of moxifloxacin into prostatic tissue in patients with benign prostatic hyperplasia. Patients received a single.