amikacin
Sources réglementaires consultées
Indications approuvées
- Infections graves dues à des bacilles à Gram négatif sensibles, notamment sepsis et infections respiratoires, urinaires, intra-abdominales, cutanées, ostéoarticulaires et du système nerveux central.
Contre-indications
Absolues
- Hypersensibilité à amikacina ou à d’autres aminosides.
Mises en garde cliniques
- Il peut provoquer une néphrotoxicité, une ototoxicité cochléaire ou vestibulaire irréversible et un bloc neuromusculaire ; surveiller la fonction rénale, l’audition, l’équilibre et les concentrations sériques. — CIMA/AEMPS, ficha técnica 57012
- Mise en garde majeure · Le risque augmente avec les fortes doses, les traitements prolongés, la déshydratation, l’âge avancé, l’insuffisance rénale et les autres médicaments néphrotoxiques ou ototoxiques. — CIMA/AEMPS, ficha técnica 57012
Interactions médicamenteuses
- SévèreAutres médicaments néphrotoxiques ou ototoxiques
Mécanisme: La toxicité rénale, cochléaire et vestibulaire peut être additive.
Recommandation: Éviter l’association si possible ; si elle est indispensable, intensifier le suivi pharmacologique, la créatinine et l’audiométrie.
CIMA/AEMPS, ficha técnica 57012
- SévèreDiurétiques de l’anse
Mécanisme: Ils peuvent augmenter l’ototoxicité, surtout lors d’une administration intraveineuse rapide.
Recommandation: Éviter l’association ou surveiller étroitement l’audition et la fonction rénale.
CIMA/AEMPS, ficha técnica 57012
- SévèreBloquants neuromusculaires et anesthésiques
Mécanisme: Le bloc neuromusculaire peut être potentialisé et provoquer une apnée.
Recommandation: Surveiller la fonction respiratoire et disposer d’une assistance ventilatoire ainsi que de calcium ou de néostigmine.
CIMA/AEMPS, ficha técnica 57012
Effets indésirables
Communs (≥1%)
Nausées, élévation de la créatinine et réaction au site d’administration
Rares mais graves
Insuffisance rénale, perte auditive irréversible, toxicité vestibulaire et bloc neuromusculaire avec apnée
Grossesse et allaitement
Il peut provoquer une atteinte fœtale, dont une surdité congénitale ; éviter pendant la grossesse sauf nécessité vitale. De faibles quantités passent dans le lait ; évaluer le bénéfice et le risque.
Bibliographie récente (PubMed)
Mycobacterium abscessus is the second most common nontuberculous mycobacterial lung disease pathogen and comprises three subspecies: abscessus, massiliense, and bolletii. Subspecies identification is critical for disease management, as subspecies abscessus and bolletii have an inducible macrolide resistance gene [erm(41)] that results in clinical macrolide resistance. In contrast, subspecies massiliense does not have an active erm(41) gene and is therefore susceptible in vitro and clinically to macrolide-containing regimens. M abscessus is also vulnerable to acquired mutational macrolide resistance. Macrolide resistance has such a profoundly negative impact on M abscessus treatment response that preserving macrolide susceptibility with adequate companion drugs for macrolides is among the highest treatment priorities. After the macrolides, amikacin is regarded as the next most important drug for M abscessus treatment, although data validating that assertion are lacking. The considerations for preventing acquired macrolide resistance also apply to amikacin. Recent guidelines suggest that treatment should be guided by in vitro susceptibilities but, aside from macrolides and amikacin, no other antibiotics have a validated minimum inhibitory concentration for M abscessus. Currently, phase therapy (intensive and continuation) is recommended for M abscessus. This approach is successful with macrolide-susceptible M abscessus but not with macrolide-resistant M abscessus, in which even more aggressive therapy is not predictably successful. Newer drugs have become available, with encouraging in vitro activity against M abscessus, but in vivo validation of their superiority to current agents is not yet available. In the absence of unequivocally effective regimens, we offer suggestions for managing this treatment-refractory organism.
Whether preventive inhaled antibiotics may reduce the incidence of ventilator-associated pneumonia is unclear. In this investigator-initiated, multicenter, double-blind, randomized, controlled, superiority trial, we assigned critically ill adults who had been undergoing invasive mechanical ventilation for at least 72 hours to receive inhaled amikacin at a dose of 20 mg per kilogram of ideal body weight once daily or to receive placebo for 3 days. The primary outcome was a first episode of ventilator-associated pneumonia during 28 days of follow-up. Safety was assessed. A total of 850 patients underwent randomization, and 847 were included in the analyses (417 assigned to the amikacin group and 430 to the placebo group). All three daily nebulizations were received by 337 patients (81%) in the amikacin group and 355 patients (83%) in the placebo group. At 28 days, ventilator-associated pneumonia had developed in 62 patients (15%) in the amikacin group and in 95 patients (22%) in the placebo group (difference in restricted mean survival time to ventilator-associated pneumonia, 1.5 days; 95% confidence interval [CI], 0.6 to 2.5; P = 0.004). An infection-related ventilator-associated complication occurred in 74 patients (18%) in the amikacin group and in 111 patients (26%) in the placebo group (hazard ratio, 0.66; 95% CI, 0.50 to 0.89). Trial-related serious adverse effects were seen in 7 patients (1.7%) in the amikacin group and in 4 patients (0.9%) in the placebo group. Among patients who had undergone mechanical ventilation for at least 3 days, a subsequent 3-day course of inhaled amikacin reduced the burden of ventilator-associated pneumonia during 28 days of follow-up. (Funded by the French Ministry of Health; AMIKINHAL ClinicalTrials.gov number, NCT03149640; EUDRA Clinical Trials number, 2016-001054-17.). Plazomicin is an aminoglycoside antibiotic similar to gentamicin and amikacin. No information is available on the use of plazomicin during breastfeeding. However,
Targeted next-generation sequencing (NGS) can rapidly and simultaneously detect mutations associated with resistance to tuberculosis drugs across multiple gene targets. The use of targeted NGS to diagnose drug-resistant tuberculosis, as described in publicly available data, has not been comprehensively reviewed. We aimed to identify targeted NGS assays that diagnose drug-resistant tuberculosis, determine how widely this technology has been used, and assess the diagnostic accuracy of these assays. In this systematic review and meta-analysis, we searched MEDLINE, Embase, Cochrane Library, Web of Science Core Collection, Global Index Medicus, Google Scholar, ClinicalTrials.gov, and the WHO International Clinical Trials Registry Platform for published and unpublished reports on targeted NGS for drug-resistant tuberculosis from Jan 1, 2005, to Oct 14, 2022, with updates to our search in Embase and Google Scholar until Feb 13, 2024. Studies eligible for the systematic review described targeted NGS approaches to predict drug resistance in Mycobacterium tuberculosis infections using primary samples, reference strain collections, or cultured isolates from individuals with presumed or confirmed tuberculosis. Our search had no limitations on study type or language, although only reports in English, German, and French were screened for eligibility. For the meta-analysis, we included test accuracy studies that used any reference standard, and we assessed risk of bias using the Quality Assessment of Diagnostic Accuracy Studies-2 tool. The primary outcomes for the meta-analysis were sensitivity and specificity of targeted NGS to diagnose drug-resistant tuberculosis compared to phenotypic and genotypic drug susceptibility testing. We used a Bayesian bivariate model to generate summary receiver operating characteristic plots and diagnostic accuracy measures, overall and stratified by drug and sample type. This study is registered with PROSPERO, CRD42022368707. We identified and scre
Non-Tuberculous mycobacteria (NTM) are opportunistic environmental bacteria. Globally, NTM incidence is increasing and modeling suggests that, without new interventions, numbers will continue to rise. Effective treatments for NTM infections remain suboptimal. Standard therapy for Mycobacterium avium complex, the most commonly isolated NTM, requires a 3-drug regime taken for approximately 18 months, with rates of culture conversion reported between 45 and 70%, and high rates of relapse or reinfection at up to 60%. New therapeutic options for NTM treatment are urgently required. A survey of ongoing clinical trials for new NTM therapy listed on ClinicalTrials.Gov using the terms 'Mycobacterium avium', 'Mycobacterium abscessus', 'Mycobacterium intracellulare', 'Non tuberculous Mycobacteria' and 'Nontuberculous Mycobacteria' and a selection criterion of interventional studies using antibiotics demonstrates that most trials involve dose and combination therapy of the guideline based therapy or including one or more of; Amikacin, Clofazimine, Azithromycin and the anti-TB drugs Bedaquiline and Linezolid. The propensity of NTMs to form biofilms, their unique cell wall and expression of both acquired and intrinsic resistance, are all hampering the development of new anti-NTM therapy. Increased investment in developing targeted treatments, specifically for NTM infections is urgently required.