In order to clarify the clinical significance of a suspected drug interaction, we sought to determine if the international normalized ratio (INR) is affected when levofloxacin is administered in patients receiving long-term warfarin therapy.
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This single-center retrospective study compared clinical outcomes of patients with Legionella pneumonia (LP) treated with AZM versus FQ from January 1999 to May 2011.
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Preventive effects against endophthalmitis were similar between antibiotic-treated IOL implantation and intracameral antibiotic administration.
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Two hundred and seven clinical isolates of Pseudomonas aeruginosa were collected at Tenri Hospital between April 2003 and March 2004. We determined the minimum inhibitory concentration (MIC) of 16 antimicrobial agents, including prulifloxacin, pazufloxacin and biapenem which were recently published in Japan, against these isolates according to the guidelines of the Clinical and Laboratory Standards Institute. For the fluoroquinolones, the rank order of activity was prulifloxacin (MIC50, 0.5 microg/ml)>ciprofloxacin (1 microg/ml)> pazufloxacin (2 microg/ml)=levofloxacin (2 microg/ml)>gatifloxacin (4 microg/ml). For the carbapenems, the rank order of activity was meropenem (MIC50, 1 microg/ml)=biapenem (1 microg/ml)>imipenem (2 microg/m)>panipenem (8 microg/ml). For the cephalosporins and monobactam, the overall rank order of activity was cefozopran (MIC50, 4 microg/ml)= ceftazidime (4 microg/ml)>cefepime (8 microg/ml)=piperacillin/tazobactam (8 microg/ml)>aztreonam (16 microg/ml)= cefoperazone/sulbactam (16 microg/ml)=cefpirome (16 microg/ml). The rates of susceptibility to antimicrobial agents as per the criteria of the Japanese Society of Antimicrobial Chemotherapy were especially high for cefozopran (63%), biapenem and meropenem (61%), and pazufloxacin (53%) and ciprofloxacin (53%). These findings suggest that prulifloxacin, pazufloxacin and biapenem, which are newly introduced, are clinically effective in the treatment of infection caused with P. aeruginosa.
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Impurity analysis plays an important role to guarantee the quality and safety of pharmaceuticals. However, identification of impurities remains challenging, especially for those unknown or at trace levels. We present an integrated approach to detect and characterize the trace impurities in drugs.
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Carbapenems had superior in vitro activity against bacteria that produced ESBLs compared with fluoroquinolones. Pharmacodynamic modeling based on local ESBL-producing isolates and pharmacokinetic data from healthy humans indicated that imipenem and meropenem may have a greater likelihood of achieving pharmacodynamic targets against bacteria that produce ESBLs than ertapenem or fluoroquinolones.
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Data was retrospectively collected by chart review during the pre-intervention period (PIP). During the intervention proactive conversion period (PCP), pharmacists reviewed and intervened on all levofloxacin orders. The detailed reimbursements for medications and inpatient expenses from the Bureau of National Health Insurance (NHI), Taiwan were calculated. The clinical impacts during the PIP and PCP were compared with the duration of the i.v. levofloxacin therapy, total used i.v./p.o. ratio levofloxacin, and total length of hospital stay. The financial impact was compared with medication costs and total inpatient expenditures.
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The susceptibility and pharmacodynamic activity of ciprofloxacin and new fluoroquinolones were studied against low-level (MIC 4 mg/L) and high-level (MIC 16 mg/L) ciprofloxacin-resistant Streptococcus pneumoniae. An in vitro pharmacodynamic model simulating free fluoroquinolone (protein unbound) serum concentrations, using Cp(max) and AUC(0-24) achieved (in healthy volunteers) after standard oral doses that are used for community-acquired respiratory infections, was used to compare bacterial killing by five fluoroquinolones against six ciprofloxacin-resistant S. pneumoniae isolates (four different resistance mutant phenotypes: ParC, efflux, ParC with efflux, and ParC and GyrA) obtained from an ongoing Canadian respiratory organism surveillance study. The potency (MIC only) of fluoroquinolones was gemifloxacin > moxifloxacin > gatifloxacin > levofloxacin > ciprofloxacin. Ciprofloxacin (free AUC(0-24)/MIC 0.9-3.5) produced no reduction of growth at 6, 24 or 48 h compared with the initial inoculum in all six strains. Levofloxacin (free AUC(0-24)/MIC 18-35) was bactericidal (> or = 3 log(10) killing) at 6, 24 and 48 h for the ParC as well as the efflux mutants, but only bactericidal at 24 h for the ParC with efflux strain. Levofloxacin (free AUC(0-24)/MIC 4.4) demonstrated no reduction of growth relative to the initial inoculum against the ParC and GyrA mutants. Gatifloxacin and moxifloxacin (free AUC(0-24)/MIC 48 and 60, respectively) were bactericidal at 6, 24 and 48 h against the ParC, efflux, and ParC with efflux mutants, but demonstrated little to no growth reduction (free AUC(0-24)/MIC 6 and 7.5, respectively) in ParC and GyrA mutants. Gemifloxacin (free AUC(0-24)/MIC 67-133) was bactericidal (> or = 3 log(10) killing) at 6, 24 and 48 h in all low-level ciprofloxacin-resistant S. pneumoniae mutants. Against two of the ParC and GyrA mutants, gemifloxacin (free AUC(0-24)/MIC 32) was bactericidal at 6, 24 and 48 h but against one ParC and GyrA mutant (free AUC(0-24)/MIC 16) gemifloxacin demonstrated reduced activity with initial killing at 24 h but with subsequent regrowth. These data indicate that ciprofloxacin produces no inhibition of growth of low- or high-level ciprofloxacin-resistant S. pneumoniae, whereas gatifloxacin, levofloxacin and moxifloxacin (moxifloxacin>gatifloxacin>levofloxacin) were bactericidal for low-level resistant strains but produced little or no inhibition of high-level resistant strains. Gemifloxacin at simulated free AUC(0-24)/MIC > or = 32, was bactericidal against low- and high-level resistant strains. When simulated free AUC(0-24)/ MIC was <16, gemifloxacin allowed regrowth of high-level ciprofloxacin-resistant strains.