野生型产 AmpC β-乳酰胺酶肠杆菌是血流感染患者经验性治疗失败的风险因素之一

Diseases Pub Date : 2024-03-02 DOI:10.3390/diseases12030052
Matteo Vassallo, R. Fabre, L. Lotte, Sabrina Manni, Christian Pradier
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摘要

导言:β-内酰胺酶是治疗革兰氏阴性血流感染(BSI)的常用药物。然而,染色体编码的产AmpC肠杆菌(AE)在接触第三代头孢菌素(3GCs)时可能会过量产生β-内酰胺酶,从而导致临床治疗失败。这方面的体内数据很少。我们的目标是评估 AE 作为 BSI 患者临床失败预测因素的潜在作用。材料和方法:我们对 2021 年至 2022 年期间因肠杆菌 BSI 而入住戛纳医院的患者进行了回顾性分析。我们收集了患者的人口统计学特征、合并症以及住院期间的主要临床和实验室指标。采用单变量和多变量分析评估了 48 小时后临床不稳定或死亡的风险因素,以及初始经验疗法无效的风险因素。研究结果从2021年1月到2022年12月,共纳入101名受试者(平均年龄79岁,60%为男性,97%有合并症,17%有医源性感染,13%有脓毒性休克,82%qPitt严重程度评分<2,58%有尿路感染,18%有AE)。脓毒性休克[调整后比值比(ORadj)=5.30,95% 置信区间(CI):1.47-22.19,P = 0.014]和初始经验疗法无效[ORadj 5.54,95% CI:1.95-17.01,P = 0.002]是临床不稳定或死亡的独立预测因素。广谱β-内酰胺酶[ORadj 9.40,95% CI:1.70-62.14,p = 0.012]、AE 组[ORadj 5.89,95% CI:1.70-21.40,p = 0.006]和临床不稳定或死亡[ORadj 4.71,95% CI:1.44-17.08,p = 0.012]与经验疗法无效独立相关。结论AE感染与治疗失败有关。如果经验疗法仅限于3GC,则可能导致治疗失败。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Wild-Type AmpC Beta-Lactamase-Producing Enterobacterales Are a Risk Factor for Empirical Treatment Failure in Patients with Bloodstream Infection
Introduction: Beta-lactamases are frequently prescribed for Gram-negative bloodstream infections (BSIs). However, chromosomally encoded AmpC-producing Enterobacterales (AE) could overproduce beta-lactamases when exposed to third-generation cephalosporins (3GCs), with a risk of clinical failure. There are few available in vivo data on the subject. Our goal was to assess the potential role of AE as a predictive factor for clinical failure in patients with BSIs. Materials and Methods: We retrospectively analyzed patients admitted to Cannes hospital between 2021 and 2022 for BSIs due to Enterobacterales. Patient demographics, comorbidities, and main clinical and laboratory parameters during hospitalization were collected. The risk factors for clinical instability after 48 h or death, as well as for ineffective initial empirical therapy, were assessed using univariate and multivariate analyses. Results: From January 2021 to December 2022, 101 subjects were included (mean age 79 years, 60% men, 97% with comorbidities, 17% with healthcare-associated infection, 13% with septic shock, 82% with qPitt severity score < 2, 58% with urinary tract infection, and 18% with AE). Septic shock [adjusted odds ratio (ORadj) = 5.30, 95% confidence interval (CI): 1.47–22.19, p = 0.014] and ineffective initial empirical therapy [ORadj 5.54, 95% CI: 1.95–17.01, p = 0.002] were independent predictive factors for clinical instability or death. Extended-spectrum beta-lactamases [ORadj 9.40, 95% CI: 1.70–62.14, p = 0.012], AE group [ORadj 5.89, 95% CI: 1.70–21.40, p = 0.006], and clinical instability or death [ORadj 4.71, 95% CI: 1.44–17.08, p = 0.012] were independently associated with ineffective empirical therapy. Conclusions: Infection with AE was associated with treatment failure. Empirical therapy may result in failure if restricted to 3GC.
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