We collected 76 clinical isolates of Acinetobacter baumannii (amikacin MIC by Vitek 2 AST-N055 card: < or =2microgram/mL, 11 isolates; 4microgram/mL, 19 isolates; 8microgram/ mL, 17 isolates; 16microgram/mL, 27 isolates; and > or =64microgram/ mL, 2 isolates) from a university hospital and evaluated the Vitek 2 AST-N055 card vs the broth microdilution as a reference method for testing susceptibility to amikacin. Vitek 2 AST-N055 card yielded very major errors in 15 isolates (19.7%) and minor errors in 26 isolates (34.2%). Of the 15 isolates shown very major errors, 14 had Vitek 2 MICs ranging from 8 to 16microgram/mL. The results of our study suggest strongly that it is unreliable to test the amikacin susceptibility by Vitek 2 AST-N055 card of A. baumannii with the Vitek 2 MICs ranging from 8 to 16microgram/mL. In those cases, another susceptibility test, such as broth microdilution (BMD), should be performed to confirm the results.
Acinetobacter ; Acinetobacter baumannii ; Amikacin

No abstract available.
Amikacin* ; Cefuroxime* ; Hysterectomy* ; Sodium*

We implemented a carbapenem-saving strategy in hemato-oncology patients from 2013, using an empirical combination of piperacillin-tazobactam and amikacin for high-risk hemato-oncology patients with febrile neutropenia, who remain hemodynamically unstable > 72 hours despite initial cefepime treatment. All-cause mortality was not different between the two periods (6.54 and 6.57 deaths per 1,000 person-day, P = 0.926). Group 2 carbapenem use significantly decreased after strategy implementation (78.43 vs. 67.43 monthly days of therapy, P = 0.018), while carbapenem-resistant gram-negative bacilli did not show meaningful changes during the study period. Our carbapenem-saving strategy could effectively suppress carbapenem use without an increase of overall mortality.
Amikacin* ; Febrile Neutropenia ; Humans ; Mortality

Mycobacterium massiliense, an emerging pathogen that is increasingly reported as a causative agent in infections occurring during medical procedures, is difficult to be identified using conventional methods. Here we report the case of a cutaneous M. massiliense infection that was associated with repeated surgical procedures and that was identified via a comparative sequence analysis of rpoB and hsp65. The patient showed a substantial response to treatment with a combination of antimicrobial therapies consisting of clarithromycin, amikacin, and cefoxitin for 6 months.
Amikacin ; Cefoxitin ; Clarithromycin ; Humans ; Mycobacterium ; Sequence Analysis

Pathogenic gram-negatives that produce 16S ribosomal RNA methyltransferases (16S RMTases) have already been distributed all over the world. To investigate the predominance of aminoglycoside resistance associated with 16S RMTases in Korea, we collected a total of 222 amikacin resistant Gram-negative clinical isolates from patient specimens between 1999 and 2015 from three hospital banks across Korea. ArmA and rmtB were the predominant 16S RMTase genes responsible for aminoglycoside-resistant isolates circulating in Korean community settings although only one rmtA-producing isolate was detected in 2006.
Amikacin ; Humans ; Korea* ; Methyltransferases ; RNA, Ribosomal, 16S

Nephrotoxicity is a major factor limiting the clinical utility of aminoglycoside antibiotics(AG). In this study, we have therefore investigated the usefulness of the renal tubular protein for a predictor of the nephrotoxicity of AG. We have also compared the nephrotoxicity among different AG. Among the simple fracture patients visiting orthopedics, for whom an AG seemed warrantable, we have sampled thirty-nine subjects--excluding those suffering from severe bleeding, taking drugs, or having renal disease which can affect the renal function. We have set three different groups by the following criteria; ten subjects in group I were given 250mg of Amikacin sulfate twice a day; fifteen subjects in GroupII were given 60mg of Micronomicin sulfate twice a day; and fourteen subjects in GroupIII were given 200mg of Isepacin sulfate twice a day. Urine from each patient was collected for 24 hours before, one week after, and two weeks after the drugs were given, and then the urinary concentrations of NAG, beta2-Microglobulin(beta2-MG), and electrolyte(Na+, K+, Cl-) were measured. The measurement of 24-hour urinary concentrations of NAG shows that, for all three groups, significant increase of the concentrations(P<0.01) is seen between the different times in the same group. The results of measurements of the 24-hour urinary concentrations of beta2-MG, and electrolyte(Na+, Ke+, Cl-) show their increase for all three groups but whithin the normal range. For the samples collected two weeks after the drugs were given, there is a significant decrease in the twenty-four-hour urinary concentrations of NAG(P<0.05) of Group III compared to Group I and II. The resulta of measurements of 24-urinary concentrations of beta2-MG, and electrolyte(Na+, K+, Cl-) show their increase for all three groups but whithin the normal range. In conclusion, we have seen that the nephrotoxicity of the AG appears for all three groups; but, when we compare the nephrotoxicity between the different antibiotics, the nephrotoxicity of Amikacin sulfate and that of Micronomicin sulfate appear stronger than that of Isepacin sulfate. Our data suggest the usefulness of sequential NAG measurements in monitoring and predicting aminoglycoside nephrotoxicity.
Amikacin ; Anti-Bacterial Agents ; Hemorrhage ; Humans ; Orthopedics ; Reference Values

OBJECTIVES: This experimental study investigated the possible protective effect of beta glucans on amikacin ototoxicity. METHODS: Thirty-eight rats with normal distortion product otoacoustic emissions (DPOAEs) were divided into four groups. Group K was the control group. Group A was injected intramuscularly (i.m.) with amikacin 600 mg/kg/day between days 1-15. Group AB was given beta glucan gavage 1 mg/kg/day on days 0-15 and given amikacin 600 mg/kg/day i.m. on days 1-15. Group B was administered only beta glucan gavage, 1 mg/kg/day, on days 0-15. The DPOAEs were elicited in different frequency regions between 2,003 and 9,515 Hz, as distortion product diagrams (DPgrams), before and after the medication was administered, in all groups, on days 1, 5, 10, and 15. RESULTS: No significant changes in the DPgrams were observed in group K. In group A, significant deterioration was observed at the 8,003 and 9,515 Hz frequencies on day 10, and at the 3,991, 4,557, 5,660, 6,726, 8,003, and 9,515 Hz frequencies on day 15. For group AB, statistically significant deterioration was observed at the 2,824, 8,003, and 9,515 Hz frequencies on day 15. The results for group B showed a significant improvement of hearing at the 2,378, 2,824, 3,363, and 3,991 Hz frequencies on day 1, at the 3,363, 3,991, and 8,003 Hz frequencies on day 10, and at the 8,003 Hz frequency on day 15. CONCLUSION: This study suggests that amikacin-induced hearing loss in rats may be limited to some extent by concomitant use of beta glucan.
Amikacin ; Animals ; beta-Glucans ; Hearing ; Hearing Loss ; Rats

OBJECTIVES: In this study we investigated the probable protective effects of thymoquinone on amikacin-induced ototoxicity in rats. METHODS: Thirty-two healthy rats were divided into four groups (amikacin, amikacin+thymoquinone, thymoquinone, and no treatment). Thymoquinone was fed to the rats via oral gavage in a dose of 40 mg/kg/day throughout the study period of 14 days. Amikacin was given by the intramuscular route in a dose of 600 mg/kg/day. Audiological assessment was conducted by the distortion product otoacoustic emission (DPOAE) and auditory brainstem response (ABR) tests, administered to all rats at the beginning of the study, and also on days 7 and 15. Biochemical parameters were calculated at the termination of the study to evaluate the oxidative status. RESULTS: There were significant decreases in DPOAE values and significant increases in ABR thresholds of the amikacin group on days 7 and 15, as compared to the amikacin+thymoquinone group. While ABR thresholds of the amikacin group increased significantly on days 7 and 15 as compared to their initial values, there were no significant differences between the initial and the 7th and 15th day values of ABR thresholds in the amikacin+thymoquinone group. Total oxidant status and oxidative stress index values of the amikacin+thymoquinone group were significantly lower than those of the amikacin group. Total antioxidant status values of the amikacin+thymoquinone group were significantly higher than those of the amikacin group. CONCLUSION: Our study has demonstrated that the ototoxic effect brought forth by amikacin could be overcome with the concurrent use of thymoquinone.
Amikacin ; Animals ; Evoked Potentials, Auditory, Brain Stem ; Oxidative Stress ; Rats*

We analysed retrospectively pharmacokinetic parameters of gentamicin and amikacin in 44 and 58 Korean pediatric patients, respectively, with normal renal function. Pharmacokinetic parameters were calculated from two concentrations in serum by method of Sawchuck. There was wide individual variation in peak serum concentrations of gentamicin and amikacin, Administration of the usually recommended doses yielded subtherapeutic concentrations in 47% and 82%, respectevely, of patients in the peak concentrations of gentamicin and amikacin. The volumes of distribution of gentamicin and amikacin in children of over 1 year of age were 0.37+/-0.13L/kg and 0.41+/-0.13L/kg which are greater than those reported from the western countries. We conclude that the wide individual variation and high frequency of subtherapeutic levels in the peak concentrations of gentamicin and amikacin obtained by usually recommended dosage as well as the narrow safety margin of these drugs necessitate monitoring of serum concentration and adjustment of individual dosage regimen early in the course of treatment with aminoglycosides.
Amikacin* ; Aminoglycosides ; Child* ; Gentamicins* ; Humans ; Pharmacokinetics* ; Retrospective Studies

OBJECTIVE: Using pre- and post-treatment otoacoustic emission (OAE) tests, this study aimed to assess the ototoxic effect of meropenem, amikacin and meropenem plus amikacin among neonates treated for sepsis neonatorum in a neonatal intensive care unit versus untreated outpatient controls.METHODS: Design: Prospective Quasi-Experimental Controlled Clinical Trial Setting: Tertiary Government Hospital Subjects: Neonates treated for sepsis neonatorum in the Neonatal Intensive Care Unit between August to October 2012 who met inclusion criteria were included in this study. Controls were neonates born in the same institution who were not admitted and did not receive any antibiotic treatment. Excluded were those with APGAR < 5 at first minute, birth weight < 1000 grams, clinically evident congenital anomalies and initial "refer" results on OAE. Neonates were subjected to OAE testing before and after seven days treatment with amikacin, meropenem or a combination of both drugs. Results were analysed using chi-square test. Maternal drug intake, family history of hearing impairment and clinical outcomes (whether expired or discharged improved) were not included in this study. Assessment of ototoxic effects were limited to OAE alone and not confirmed by ABR.RESULTS: OAE "refer" rates were as follows: no amikacin and no meropenem, 0% (0/42); amikacin only, 33.3% (3/9); meropenem only, 25% (2/8) and amikacin and meropenem, 50% (10/20). Statistical analysis showed that hearing loss was dependent on treatment (c2 =23.741, p = < 0.001). Overall, statistical analysis showed that there is an increased risk of hearing loss when treated with amikacin and/or meropenem as compared to no treatment.CONCLUSION: There is an increased risk of ototoxicity when amikacin, meropenem or a combination of both drugs is administered to neonates. While the ototoxic effects of amikacin have been elucidated, further studies involving meropenem and its potential ototoxic effect are recommended.
Human ; Male ; Female ; Infant Newborn ; amikacin ; meropenem ; hearing loss