Rifampin blood and tissue levels in patients undergoing cardiac valve surgery

Archer, Gordon L.; Armstrong, Barbara C.; Kline, Berry J.

doi:10.1128/aac.21.5.800

Cited by 11 publications

(8 citation statements)

References 10 publications

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“…The higher COL MICs values observed in our experiment with the microdilution method with respect to the E-test already have been reported and seem to be related to the adsorption of colistin to the microplate plastic wells [3,4]. Although higher COL MICs were observed with the microdilution method, the effect of adding RIF was always evident also with the lower concentrations.RIF concentrations showing synergistic activity in vitro were close to the levels reported after an oral dose of 600 mg [5]. RIF concentrations higher than 16 mg/L did not induce a further reduction of COL MIC, suggesting that higher-than-standard doses of RIF would probably not offer any significant clinical advantage.…”

supporting

confidence: 65%

Easy synergism for colistin-resistant KPC-producing Klebsiella pneumoniae: the E-test with supplemented agar

Tagliaferri

Tascini

Leonildi

et al. 2015

Clinical Microbiology and Infection

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The renewed interest in testing synergistic interactions of antimicrobial agents is mainly related to the challenge of antimicrobial resistance. Whereas time-kill curves and checkerboard methods represent the reference tests for screening synergy, the E-test with strips in a cross formation might be an interesting alternative, but requires that minimum inhibitory concentrations (MICs) of antibiotics have been previously determined [1]. However, agreement between the different tests seems to be quite variable [1]. To be clinically useful, a synergy test should be rapid and easily interpretable.We evaluated the synergistic activity of colistin (COL) plus rifampin (RIF) against 10 clinical isolates of COL-resistant Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae (KPC-Kp) comparing the checkerboard method with the E-test on Mueller-Hinton agar, alone or supplemented with RIF. The 10 tested strains resulted in KPC3 production by polymerase chain reaction and Sequence Type (ST) 512 by multilocus sequence typing (MLST) analysis (http://www.pasteur.fr/recherche/ genopole/PF8/mlst/Kpneumoniae.html). COL MICs for the checkerboard method were determined with broth microdilution in Mueller-Hinton broth alone and supplemented with RIF at the final concentration of 2, 4, 8, 16 and 32 mg/L in 96-well microtiter plates. COL MICs also were determined with the E-test method on Mueller-Hinton agar alone or supplemented with RIF at the final concentration of 2, 4, 8, 16 and 32 mg/L in Petri dishes (Fig. 1).According to the 2014 EUCAST Clinical Breakpoints, COL resistance was defined by MIC > 2 mg/L. With the checkerboard method, COL MICs for the 10 strains were 64 mg/L (5 strains) and 32 mg/L (5 strains). COL MICs decreased below the susceptibility breakpoint for 8 of 10 strains in the presence of RIF concentrations of 16 (1 strain), 8 (6 strains) and 2 mg/L (1 strain). With the E-test method, COL MICs for the 10 strains were 12 mg/L (1 strain), 8 mg/L (2 strains), 6 mg/L (4 strains) and 4 mg/L (3 strains). COL MICs for 10 of 10 strains decreased below the susceptibility breakpoint in the presence of any concentration of RIF. These results are summarized in Table 1. RIF MICs results were higher than 32 mg/L with both methods for all strains. Both methods showed similar results and were able to show that RIF decreased MICs of COL below the susceptibility breakpoint in the majority of COL-resistant KPC-Kp tested strains.The mechanism of the synergistic activity between COL and RIF might be related to the perturbation of the outer cellular membrane produced by COL that favours the penetration of RIF at intracellular concentrations able to inhibit protein synthesis [2]. The higher COL MICs values observed in our experiment with the microdilution method with respect to the E-test already have been reported and seem to be related to the adsorption of colistin to the microplate plastic wells [3,4]. Although higher COL MICs were observed with the microdilution method, the effect of adding RIF was always evident also with t...

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supporting

confidence: 65%

Easy synergism for colistin-resistant KPC-producing Klebsiella pneumoniae: the E-test with supplemented agar

Tagliaferri

Tascini

Leonildi

et al. 2015

Clinical Microbiology and Infection

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“…Rifampin is readily excreted in the bile and undergoes enterohepatic recirculation to maintain serum levels (201). It is 85% protein bound, with the unbound fraction being nonionized, allowing penetration into many tissues (7,201). Rifampin does cross the placenta and also enters breast milk (201).…”

Section: Pharmacology Pharmacokineticsmentioning

confidence: 99%

Rifampin Combination Therapy for Nonmycobacterial Infections

2010

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SUMMARY The increasing emergence of antimicrobial-resistant organisms, especially methicillin-resistant Staphylococcus aureus (MRSA), has resulted in the increased use of rifampin combination therapy. The data supporting rifampin combination therapy in nonmycobacterial infections are limited by a lack of significantly controlled clinical studies. Therefore, its current use is based upon in vitro or in vivo data or retrospective case series, all with major limitations. A prominent observation from this review is that rifampin combination therapy appears to have improved treatment outcomes in cases in which there is a low organism burden, such as biofilm infections, but is less effective when effective surgery to obtain source control is not performed. The clinical data support rifampin combination therapy for the treatment of prosthetic joint infections due to methicillin-sensitive S. aureus (MSSA) after extensive debridement and for the treatment of prosthetic heart valve infections due to coagulase-negative staphylococci. Importantly, rifampin-vancomycin combination therapy has not shown any benefit over vancomycin monotherapy against MRSA infections either clinically or experimentally. Rifampin combination therapy with daptomycin, fusidic acid, and linezolid needs further exploration for these severe MRSA infections. Lastly, an assessment of the risk-benefits is needed before the addition of rifampin to other antimicrobials is considered to avoid drug interactions or other drug toxicities.

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“…There were multiple time points available for rifampin concentrations in lung, liver, kidney, and spleen; the data at 6 h postdosing were chosen as an estimated end of a distribution phase, with an approximate equilibrium between rifampin concentrations in blood and tissues. The remaining partition coefficients were set using human and other animal data (37)(38)(39), with the heart/blood coefficient determined as the average of those for human heart valve (37) and muscle (38). The carcass/blood partition coefficient was set equal to the median value of all the other partition coefficients.…”

Section: Computationalmentioning

confidence: 99%

A Physiologically Based Pharmacokinetic Model of Rifampin in Mice

Lyons

Reisfeld

Yang

et al. 2013

Antimicrob Agents Chemother

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One problem associated with regimen-based development of antituberculosis (anti-TB) drugs is the difficulty of a systematic and thorough in vivo evaluation of the large number of possible regimens that arise from consideration of multiple drugs tested together. A mathematical model capable of simulating the pharmacokinetics and pharmacodynamics of experimental combination chemotherapy of TB offers a way to mitigate this problem by extending the use of available data to investigate regimens that are not initially tested. In order to increase the available mathematical tools needed to support such a model for preclinical anti-TB drug development, we constructed a preliminary whole-body physiologically based pharmacokinetic (PBPK) model of rifampin in mice, using data from the literature. Interindividual variability was approximated using Monte Carlo (MC) simulation with assigned probability distributions for the model parameters. An MC sensitivity analysis was also performed to determine correlations between model parameters and plasma concentration to inform future model development. Model predictions for rifampin concentrations in plasma, liver, kidneys, and lungs, following oral administration, were generally in agreement with published experimental data from multiple studies. Sensitive model parameters included those descriptive of oral absorption, total clearance, and partitioning of rifampin between blood and muscle. This PBPK model can serve as a starting point for the integration of rifampin pharmacokinetics in mice into a larger mathematical framework, including the immune response to Mycobacterium tuberculosis infection, and pharmacokinetic models for other anti-TB drugs.T uberculosis (TB), caused by Mycobacterium tuberculosis, is an infectious disease which continues to be a major cause of death in large parts of the world (1). While the current first-line therapy for drug-susceptible TB (composed of rifampin, isoniazid, pyrazinamide, and ethambutol) has been in clinical use for nearly 30 years, the emergence and spread of drug-resistant M. tuberculosis strains have motivated the search for new, more-effective combination regimens (2). Our interest here is the development of mathematical tools to supplement the animal studies necessary for the identification and testing of such new anti-TB drug regimens.The mouse is the primary animal species used for preclinical anti-TB drug development (3). Despite the differences between mice and humans, the activities of many anti-TB drugs against disease caused by M. tuberculosis are similar in both species (4, 5). Mice also provide for a range of TB susceptibility and pathology through a variety of outbred and inbred strains; a notable example is C3HeB/FeJ mice (6), which form necrotic pulmonary lesions similar to those observed in TB patients (7). The recent Critical Path to TB Drug Regimens (CPTR) Initiative (8) includes an added emphasis on the mouse for identification of new optimized three-drug regimens as a key step in advancing novel drug combinations into ...

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Rifampin blood and tissue levels in patients undergoing cardiac valve surgery

Cited by 11 publications

References 10 publications

Easy synergism for colistin-resistant KPC-producing Klebsiella pneumoniae: the E-test with supplemented agar

Easy synergism for colistin-resistant KPC-producing Klebsiella pneumoniae: the E-test with supplemented agar

Rifampin Combination Therapy for Nonmycobacterial Infections

A Physiologically Based Pharmacokinetic Model of Rifampin in Mice

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