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1.
Clin Microbiol Infect ; 30(2): 223-230, 2024 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-38267096

RESUMEN

OBJECTIVES: To assess the mortality attributable to infections caused by carbapenem-resistant Enterobacterales (CRE) and to investigate the effect of clinical management on differences in observed outcomes in a multinational matched cohort study. METHODS: A prospective matched-cohorts study (NCT02709408) was performed in 50 European hospitals from March 2016 to November 2018. The main outcome was 30-day mortality with an active post-discharge follow-up when applied. The CRE cohort included patients with complicated urinary tract infections, complicated intra-abdominal infections, pneumonia, or bacteraemia from other sources because of CRE. Two control cohorts were selected: patients with infection caused by carbapenem-susceptible Enterobacterales (CSE) and patients without infection. Matching criteria included type of infection for the CSE group, hospital ward of CRE detection, and duration of hospital admission up to CRE detection. Multivariable and stratified Cox regression was applied. RESULTS: The cohorts included 235 patients with CRE infection, 235 patients with CSE infection, and 705 non-infected patients. The 30-day mortality (95% CI) was 23.8% (18.8-29.6), 10.6% (7.2-15.2), and 8.4% (6.5-10.6), respectively. The difference in 30-day mortality rates between patients with CRE infection when compared with patients with CSE infection was 13.2% (95% CI, 6.3-20.0), (HR, 2.57; 95% CI, 1.55-4.26; p < 0.001), and 15.4% (95% CI, 10.5-20.2) when compared with non-infected patients (HR, 3.85; 95% CI, 2.57-5.77; p < 0.001). The population attributable fraction for 30-day mortality for CRE vs. CSE was 19.28%, and for CRE vs. non-infected patients was 9.61%. After adjustment for baseline variables, the HRs for mortality were 1.87 (95% CI, 0.99-3.50; p 0.06) and 3.65 (95% CI, 2.29-5.82; p < 0.001), respectively. However, when treatment-related time-dependent variables were added, the HR of CRE vs. CSE reduced to 1.44 (95% CI, 0.78-2.67; p 0.24). DISCUSSION: CRE infections are associated with significant attributable mortality and increased adjusted hazard of mortality when compared with CSE infections or patients without infection. Underlying patient characteristics and a delay in appropriate treatment play an important role in the CRE mortality.


Asunto(s)
Cuidados Posteriores , Gammaproteobacteria , Humanos , Estudios de Cohortes , Alta del Paciente , Estudios Prospectivos , Carbapenémicos/farmacología , Carbapenémicos/uso terapéutico , Estudios de Casos y Controles
2.
Rev. esp. quimioter ; 31(1): 78-100, feb. 2018. tab
Artículo en Inglés | IBECS (España) | ID: ibc-171349

RESUMEN

Pseudomonas aeruginosa is characterized by a notable intrinsic resistance to antibiotics, mainly mediated by the expression of inducible chromosomic β-lactamases and the production of constitutive or inducible efflux pumps. Apart from this intrinsic resistance, P. aeruginosa possess an extraordinary ability to develop resistance to nearly all available antimicrobials through selection of mutations. The progressive increase in resistance rates in P. aeruginosa has led to the emergence of strains which, based on their degree of resistance to common antibiotics, have been defined as multidrug resistant, extended-resistant and panresistant strains. These strains are increasingly disseminated worldwide, progressively complicating the treatment of P. aeruginosa infections. In this scenario, the objective of the present guidelines was to review and update published evidence for the treatment of patients with acute, invasive and severe infections caused by P. aeruginosa. To this end, mechanisms of intrinsic resistance, factors favoring development of resistance during antibiotic exposure, prevalence of resistance in Spain, classical and recently appeared new antibiotics active against P. aeruginosa, pharmacodynamic principles predicting efficacy, clinical experience with monotherapy and combination therapy, and principles for antibiotic treatment were reviewed to elaborate recommendations by the panel of experts for empirical and directed treatment of P. aeruginosa invasive infections (AU)


Pseudomonas aeruginosa se caracteriza por una notable resistencia intrínseca a los antibióticos mediada fundamentalmente por la expresión de β-lactamasas cromosómicas inducibles y la producción constitutiva o inducible de bombas de expulsión. Además de esta resistencia intrínseca, P. aeruginosa posee una extraordinaria capacidad para desarrollar resistencia a prácticamente todos los antimicrobianos disponibles a través de la selección de mutaciones. El aumento progresivo de la resistencia en P. aeruginosa ha llevado a la aparición de cepas que, de acuerdo con el grado de resistencia frente a los antibióticos habituales, se han definido como multirresistentes, extensamente resistentes y panresistentes. Estas cepas se están diseminando mundialmente, complicando progresivamente el tratamiento de las infecciones por P. aeruginosa. En este escenario, el objetivo de las presentes recomendaciones es la revisión y puesta al día de la evidencia publicada para el tratamiento de pacientes con infección aguda, invasiva y grave por P. aeruginosa. Con este fin, se han revisado los mecanismos de resistencia intrínseca, factores que favorecen el desarrollo de resistencia durante la exposición a antibióticos, prevalencia de la resistencia en España, antibióticos clásicos así como los de reciente introducción activos frente a P. aeruginosa, principios farmacodinámicos predictores de eficacia, experiencia clínica con tratamientos en monoterapia o terapia combinada y principios del tratamiento antibiótico para elaborar por un panel de xpertos recomendaciones para el tratamiento empírico o dirigido de infecciones invasivas por P. aeruginosa (AU)


Asunto(s)
Humanos , Pseudomonas aeruginosa/patogenicidad , Infecciones por Pseudomonas/tratamiento farmacológico , Antibacterianos/uso terapéutico , Evaluación Preclínica de Medicamentos/métodos , Enfermedad Aguda/terapia , Pruebas de Sensibilidad Microbiana/métodos , Resistencia a Múltiples Medicamentos
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