AMIKACIN is a bactericidal aminoglycoside. Aminoglycosides inhibit bacterial protein synthesis. The antibacterial spectrum of AMIKACIN is the broadest of aminoglycosides. Because of its resistance to many of the aminoglycosides-inactivating enzymes, it has a special role in hospitals where gentamicin-and tobramycin-resistant microorganisms are prevalent. AMIKACIN is active against the majority of aerobic gram-negative bacilli in the community and in the hospitals. This includes most strains of Serratia, Proteus, Enterobacter, and Escherichia coli that are resistant to gentamicin and tobramycin. AMIKACIN is active against Mycobacterium tuberculosis (99% of strains are inhibited by 4 μ g/ml AMIKACIN), including streptomycin-resistant strains atypical mycobacteria. The gastrointestinal absorption of AMIKACIN is minimal and is largely excreted through the renal glomerulus. In neonates, the dose of AMIKACIN is 15 mg/kg. In the first week of life, a loading dose of 10 mg/kg followed by a maintenance regimen of 7. 5 mg/kg has been suggested. After the first week of life, the corresponding doses are 17 mg/kg (loading dose) and 15 mg/kg (maintenance dose). The peak and trough doses of AMIKACIN should be 20-30 μ g/ml and <5 μ g/ml, respectively. In neonates, the half-life of AMIKACIN is 7 to 8 hours and in adults it is 1. 3 hours. In infants, the half-life of AMIKACIN inversely correlates with postnatal age and body weight. AMIKACIN therapeutic serum concentrations are not ototoxic and nephrotoxic in term neonates. The aim of this study is to review the clinical pharmacology of AMIKACIN in term neonates.

Background and Objectives: The most common problems limiting the medical use of aminoglycosides have been the nephro- and oto-toxicities as well as the increasing bacterial resistance.Encapsulation of drugs into liposomes enhances their efficacy while reducing their toxicities. The aim of this study was to evaluate the antimicrobial activity of free and liposomal AMIKACIN.Material and Methods: Encapsulated AMIKACIN into liposome was prepared by sonication. The drug contained in the liposome was measured by HPLC after lysis of vesicles by 0.2% Triton X-100. The AMIKACIN kinetic released from liposomes in the presence of normal human pooled plasma was also evaluated. The MICs of this drug for Pseudomonas. aeruginosa (ATCC 27853), Escherichia. Coli (ATCC 25922), Streptococcus. faecalis (ATCC 29212) and Staphylococcus. aureus (ATCC 29213) were determined and compared to those of the respective free drug using a broth dilution method.Results: In the presence of plasma, liposomal retention of AMIKACIN was 80.25 ± 0.55% (P £ 0.05) after 1 h of incubation and then remained nearly constant over a 24 h period of the study. The encapsulation efficiency of liposomal preparation was 24.36% ± 0.14 (P£0.05) of the initial amount of the drug in solution. The MICs of liposomal AMIKACIN against all bacterial strains tested were lower than MICs of free AMIKACIN.Conclusion: The AMIKACIN appears a promising approach in the management of bacterial infections and should be further evaluated in vivo experiments.

AMIKACIN has been shown to irreversibly suppressCochlear activity.The aim of this study is to assess the incidence of AMIKACINototoxicity in multidrug-resistant tuberculosis patients and riskfactors associated withthis ototoxicity.In this cross-sectional study, 41 patientswith multidrug-resistant tuberculosis (MDR-TB) were included.All patients received fixed dose of intravenous AMIKACIN (500 mg/day) and anti-TB medications for six months. Baseline Pure-Tone Audiometry (PTA) was performed on all patients, before and during the drug treatment with the frequency range between 250 Hz and 8000 Hz. Patients were closely observed for the occurrence of symptomatic ototoxicity using a questionnaire.To find an association between the incidence of cochlear damage and patients’ demographics, all patients’ data were recorded.A total of 29 patients suffered from hearing loss (70.1%) (Male: n=18; Female: n=20).Using logistic regression, the incidence ofAMIKACINototoxicity was higher in men than in women. There was a negative correlation between the duration of the AMIKACINtreatment and the difference in hearing thresholds (r=-0.34, p=0.03). The mean of hearing threshold wassignificantly increased before and after theAMIKACINtreatment ((23.68 ± 19.26 vs.38.93 ± 22.80) (p<0.0001)). The incidence of hearing loss was remarkable in MDR-TB patients treating with AMIKACIN. However, risk factors’ determination and monitoring of audiometric result variations could haveinfluenced the incidence of the AMIKACIN ototoxicity.

Background: Infection and its treatment as a common problem in children may induce different complications. Ampicillin and aminoglycosides, as choice drugs for this condition, may have many important side effects, such as nephrotoxic side effects. Therefore, the aim of this study was to evaluate the nephrotoxic effect of gentamicin and AMIKACIN in neonates with infection. Methods: This clinical trial and double blind study was conducted on 80 children with aminoglycosides addministration. Initially, during hospital admission, serum and urine samples were collected for diagnosis of infection. Children based on their treatment were divided to 2 groups, 40 children were treated by ampicillin and AMIKACIN and 40 children were treated by ampicillin and gentamicin, during a 7-day period. At the end of the treatment period, serum and urine samples were taken for measurment of laboratory variables, and GFR, for evaluation of kidney function. Results: Blood Urea Nitrogen (BUN), creatinine and GFR before and after treatment in the two groups did not have statistically significant differences (P > 0. 05). In addition age, gender, birth age, infection type, occupation, and education of parents and milk type were equal in the 2 groups. Conclusions: Based on the present study, there were no significant differences between nephrotoxic effect of gentamicin and AMIKACIN in the two groups.