In vitro and in vivo activities of LJC10,627, a new carbapenem with stability to dehydropeptidase I.
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The activity of LJC10,627 was compared with the activities of imipenem and other antibiotics. LJC10,627 was more active against most members of the family Enterobacteriaceae, Pseudomonas spp., and Acinetobacter spp. but slightly less active than imipenem against staphylococci and streptococci. LJC10,627 showed stability to mouse dehydropeptidase I and was more effective in vivo than imipenem plus cilastatin against gram-negative bacterial infections and as effective against staphylococcal infections. (+info)
Comparison of in vivo nephrotoxicity in the rabbit by a pyrrolidinyl-thio Carbapenem CW-270031.
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CW-270031 is a novel synthesized carbapenem antibiotic with a broad antimicrobial activity. Carbapenem antibiotics are well known for their nephrotoxicity. In this study, we evaluated the nephrotoxicity potential of this compound in rabbits, which are known for being more sensitive than other animals to renal insult. CW-270031 was administered to NZW male rabbits via an ear vein (200 mg/kg, single injection). Blood samples were collected on 2, 3, and 4 days after treatment. Urea nitrogen and creatinine in plasma were quantified. Four days after the treatment, all animals were autopsied and histopathological examinations were performed on their kidneys, revealing that cephaloridine and imipenem were highly nephrotoxic, and cefazolin had mild renal toxicity, whereas CW-270031 as well as meropenem and tienam had no toxicity to the kidney. The present findings suggest that CW-270031 is a potential carbapenem antibiotic with no nephrotoxicity. (+info)
An unusual cause of seizures during subarachnoid anesthesia in a patient undergoing transurethral resection of the prostate: a case report.
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A 73-year-old, ASA I patient scheduled for transurethral resection of the prostate under subarachnoid anesthesia received, prior to the beginning of the surgery, intravenous imipenem/cilastatin 1 g for a urinary infection with multiresistant Escherichia coli. The patient developed seizures during the surgical procedure. Central nervous toxicity of imipenem/cilastatin might have been the cause of the seizures. After appropriate management, the patient recovered well and was discharged without complications. The differential diagnosis between systemic toxicity of local anesthetics and imipenem-related seizures is discussed. (+info)
Necrotizing pancreatitis after transcatheter arterial chemoembolization for hepatocellular carcinoma.
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A patient who developed necrotizing pancreatitis after transcatheter arterial chemoembolization (TACE) for hepatocellular carcinoma (HCC) is presented. A 55- year-old man had been followed for chronic hepatitis B infection for 10 years at another institution. He presented with multiple masses in the right lobe of the liver and a metastasis in the left adrenal gland. He was referred after a percutaneous liver biopsy which revealed a moderately differentiated HCC. He was treated by TACE. At the third session of TACE, the right hepatic artery was found to be thrombosed; however, angiography also demonstrated collateral feeder vessels (arising from the pancreaticoduodenal artery) which were used for treatment. He developed necrotizing pancreatitis, possibly due to regurgitation of the chemotherapeutic agents to the pancreas. He recovered without complications with imipenem-cilastatin prophylaxis. Acute pancreatitis is a rare but severe complication of TACE. Selective catheterization of the tumor vessels is the established standard in TACE. A careful risk-benefit analysis is mandatory in patients with abnormal collateral vessels. Treatment of acute necrotizing pancreatitis (ANP) after TACE is the same as the accepted approach to ANP due to other causes. (+info)
Removal of imipenem and cilastatin by hemodialysis in patients with end-stage renal failure.
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The removal of imipenem and cilastatin by hemodialysis was studied in 14 (for imipenem) and 6 (for cilastatin) subjects. Following intravenous infusion of imipenem and cilastatin at a combined concentration of 10 mg/kg of body weight, drug levels in plasma were determined serially during off- and on-hemodialysis periods, which were 2 and 4 h, respectively. The biexponential decay of the drug levels in plasma was evident in each subject for both imipenem and cilastatin. Hemodialysis accelerated the elimination of both imipenem and cilastatin: the mean elimination-phase half-life of imipenem was shortened from 200 to 78 min, and that of cilastatin was shortened from 445 to 115 min. Hemodialysis clearance of imipenem and cilastatin was calculated by five different methods, each with intrinsic assumptions. The mean hemodialysis clearance of imipenem was estimated to be 74.08 +/- 13.29 ml/min, and that of cilastatin was estimated to be 65.0 +/- 8.6 ml/min, after consideration of various methodological limitations. It was estimated that in a hypothetical anephric patient weighing 60 kg, a 4-h hemodialysis treatment would remove 54.8% of the imipenem and 62.9% of the cilastatin present in the body at the start of dialysis. (+info)
Comparative inactivation of isepamicin, amikacin, and gentamicin by nine beta-lactams and two beta-lactamase inhibitors, cilastatin and heparin.
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This study was undertaken to compare the susceptibility to inactivation of isepamicin with amikacin and gentamicin when exposed to different beta-lactams, beta-lactamase inhibitors, and heparin. The aminoglycosides (5, 10, 20, and 50 micrograms/ml) were incubated in human serum with ampicillin, azlocillin, aztreonam, carbenicillin, ceftazidime, piperacillin, and ticarcillin (100 and 600 micrograms/ml) and with clavulanate, cilastatin, 1:1 imipenemcilastatin, oxacillin, and sulbactam (20 and 120 micrograms/ml) for 48 h at 37 degrees C. Aminoglycoside concentrations were measured by fluorescence polarization immunoassay (FPI) after 0, 8, and 48 h of incubation and by radial diffusion bioassay after 48 h of incubation. Each of the three aminoglycosides was also added to whole blood containing either heparin (100 U/ml) or 0.5% EDTA as a control and assayed after 6 h by FPI. The degree of inactivation of isepamicin by the beta-lactams was significantly less than that by amikacin (P less than 0.003) and gentamicin (P less than 0.0002) when determined by bioassay. Piperacillin, carbenicillin, and azlocillin produced the greatest amount of inactivation, and cilastatin and oxacillin produced the least. A similar pattern was observed when the degree of inactivation was measured by FPI. A significant difference in the degree of inactivation was noted between isepamicin and gentamicin (P less than 0.003 at 8 h and P less than 0.006 at 48 h) but not between isepamicin and amikacin (P greater than 0.7 at 8 h and P greater than 0.08 at 48 h). Aminoglycoside determinations by FPI were not influenced by the presence of heparin. In summary, isepamicin was found to be at least as stable as amikacin against inactivation by beta-lactam compounds and beta-lactamase inhibitors. Heparin (100 U/ml) did not influence aminoglycoside determinations by FPI. (+info)
Efficacy and safety of tigecycline monotherapy vs. imipenem/cilastatin in Chinese patients with complicated intra-abdominal infections: a randomized controlled trial.
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