telavancin
Sources réglementaires consultées
Indications approuvées
- Infections bactériennes compliquées de la peau et pneumonie nosocomiale ou associée à la ventilation dues à des germes à Gram positif sensibles lorsque les alternatives ne conviennent pas.
Contre-indications
Absolues
- Hypersensibilité à la télavancine ; administration d’héparine non fractionnée intraveineuse.
Mises en garde cliniques
- Dans la pneumonie nosocomiale ou associée à la ventilation avec ClCr ≤50 ml/min, une mortalité accrue a été observée ; utiliser uniquement si le bénéfice l’emporte sur le risque. Une réponse moindre a aussi été observée dans l’infection cutanée avec insuffisance rénale. — DailyMed, set_id 5359b759-db7c-4672-9e8a-59c93869bd91
- Mise en garde majeure · Il peut provoquer une néphrotoxicité et un allongement du QT ; surveiller la créatinine, l’ECG et les électrolytes chez les patients à risque. — DailyMed, set_id 5359b759-db7c-4672-9e8a-59c93869bd91
- Mise en garde majeure · Il interfère avec le TP/INR, le TCA et l’ACT pendant 0 à 18 heures après la dose ; prélever avant la dose ou utiliser des tests non affectés. — DailyMed, set_id 5359b759-db7c-4672-9e8a-59c93869bd91
Interactions médicamenteuses
- ModéréeHéparine non fractionnée IV
Mécanisme: L’interférence avec le TCA empêche une surveillance fiable.
Recommandation: Ne pas administrer simultanément d’héparine non fractionnée IV ; si une anticoagulation est nécessaire, utiliser une alternative ne dépendant pas du TCA ou un test chromogénique anti-Xa.
DailyMed, set_id 5359b759-db7c-4672-9e8a-59c93869bd91
Effets indésirables
Communs (≥1%)
Dans les cSSSI : dysgueusie, nausées, vomissements et urines mousseuses ; dans les HABP/VABP : diarrhée
Rares mais graves
Anaphylaxie et atteinte rénale aiguë
Grossesse et allaitement
Il peut provoquer une atteinte fœtale. Utiliser une contraception efficace pendant le traitement et pendant 2 jours après ; envisager d’arrêter l’allaitement ou le traitement.
Bibliographie récente (PubMed)
Vancomycin is a first-line drug for the treatment of MRSA infection. However, overuse of vancomycin can cause bacteria to become resistant, forming resistant strains and making infections more difficult to treat. This study aimed to evaluate the efficacy and safety of different antibiotics in the treatment of MRSA infections and to compare them, mainly with vancomycin, to find better vancomycin alternatives. All studies were obtained from the PubMed and Embase databases from inception to 13 April 2023. The three comprehensive indicators of clinical cure success rate, clinical microbiological success rate, and adverse reactions were evaluated, and the clinical cure success rates of three disease types, complex skin and skin structure infections (cSSSIs), complex skin and soft tissue infections (cSSTIs), and pneumonia, were analyzed in subgroups. All statistical analyses were performed using R and STATA 14.0 software for network meta-analysis. A total of 38 trials with 6281 patients were included, and 13 drug treatments were evaluated. For MRSA infections, the results of network meta-analysis showed that the clinical success rates of linezolid, the combination of vancomycin and rifampin, and the combination of minocycline and rifampin were better than that of vancomycin (RR 1.71; 95%-CI 1.45-2.02), (RR 2.46; 95%-CI 1.10-5.49) (RR, 2.77; 95%-CI 1.06-7.21). The success rate of clinical microbiological treatment with vancomycin was inferior to that with telavancin (RR 0.74; 95%-CI 0.55-0.99). Linezolid had a higher rate of adverse reactions than teicoplanin (RR 5.35; 95%-CI 1.10-25.98). Subgroup analysis showed that vancomycin had a lower clinical success rate than linezolid in the treatment of MRSA-induced cSSSIs, cSSTIs, and pneumonia (RR 0.59; 95%-CI 0.44-0.80) (RR 0.55; 95%-CI 0.35-0.89) (RR 0.55; 95%-CI 0.32-0.93). This systematic review and NMA provide a new comparison framework for the clinical treatment of MRSA infection. The NMA suggests that linezolid may be th
Nosocomial central nervous system (CNS) infections with carbapenem- and colistin-resistant Gram-negative and vancomycin-resistant Gram-positive bacteria are an increasing therapeutic challenge. Here, we review pharmacokinetic and pharmacodynamic data and clinical experiences with new antibiotics administered intravenously for the treatment of CNS infections by multi-resistant bacteria. Cefiderocol, a new siderophore extended-spectrum cephalosporin, pharmacokinetically behaves similar to established cephalosporins and at high doses will probably be a valuable addition in our therapeutic armamentarium for CNS infections. The new glycopeptides dalbavancin, telavancin, and oritavancin are highly bound to plasma proteins. Although effective in animal models of meningitis, it is unlikely that they reach effective cerebrospinal fluid (CSF) concentrations after intravenous administration alone. The β-lactam/β-lactamase inhibitor combinations have the principal problem that both compounds must achieve adequate CSF concentrations. In the commercially available combinations, the dose of the β-lactamase inhibitor tends to be too low to achieve adequate CSF concentrations. The oxazolidinone tedizolid has a broader spectrum but a less suitable pharmacokinetic profile than linezolid. The halogenated tetracycline eravacycline does not reach CSF concentrations sufficient to treat colistin-resistant Gram-negative bacteria with usual intravenous dosing. Generally, treatment of CNS infections should be intravenous, whenever possible, to avoid adverse effects of intraventricular therapy (IVT). An additional IVT can overcome the limited penetration of many new antibiotics into CSF. It should be considered for patients in which the CNS infection responds poorly to systemic antimicrobial therapy alone.
Atopic Dermatitis (AD) skin is susceptible to Staphylococcus aureus (SA) infection, potentially exposing it to a plethora of toxins and virulent determinants, including Panton-Valentine leukocidin (PVL) (α-hemolysin (Hla) and phenol-soluble modulins (PSMs)), and superantigens. Depending on the degree of infection (superficial or invasive), clinical treatments may encompass permanganate (aq) and bleach solutions coupled with intravenous/oral antibiotics such as amoxicillin, vancomycin, doxycycline, clindamycin, daptomycin, telavancin, linezolid, or tigecycline. However, when the skin is significantly traumatized (sheathing of epidermal sections), an SA infection can rapidly ensue, impairing the immune system, and inducing local and systemic AD presentations in susceptible areas. Furthermore, when AD presents systemically, desensitization can be long (years) and intertwined with periods of relapse. In such circumstances, the identification of triggers (stress or infection) and severity of the flare need careful monitoring (preferably in real-time) so that tailored treatments targeting the underlying pathological mechanisms (SA toxins, elevated immunoglobulins, impaired healing) can be modified, permitting rapid resolution of symptoms.
Several natural antimicrobial peptides (AMPs), including the novel semisynthetic lipoglycopeptide antibiotics telavancin, dalbavancin, and oritavancin, have been approved for clinical use to address the growing problem of multiple antibiotic-resistant Gram-positive bacterial infections. Nevertheless, the efficacy of these antibiotics has already been compromised. The SARS-CoV-2 pandemic led to the increased clinical use of all antibiotics, further promoting the development of bacterial resistance. Therefore, it is critical to gain a deeper understanding of the role of resistance mechanisms to minimize the consequential risks of long-term antibiotic use and misuse. Here, we summarize for the first time the current knowledge of resistance mechanisms that have been shown to cause resistance to clinically used AMPs, with particular focus on membrane proteins that have been reported to interfere with the activity of AMPs by affecting the binding of AMPs to bacteria.