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Imipenem–Cilastatin and Imipenem–Relebactam
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Yoshiro Hayashi, David L. Paterson
Imipenem–cilastatin is one of the alternatives of initial antimicrobial therapy for neutropenic fever in high-risk patients. Imipenem has activity against most of the causative pathogens in neutropenic fever, such as P. aeruginosa, Enterobacteriaceae (including ESBL producers), Streptococcus spp., and Entero-coccus faecalis. As noted previously, imipenem will not reliably cover MRSA, MRSE, Enterococcus faecium, and non-bacterial pathogens. Imipenem–cilastatin therapy for neutropenic fever has been supported by substantial clinical experience. There have been 19 RCTs (see Table 37.11) for empirical treatment of neutropenic fever (each of which enrolled more than 100 patients) that compared imipenem–cilastatin with other regimens: cefepime, ceftazidime with or without tobramycin or amikacin, cefoperazone–sulbactam, cefuroxime plus tobramycin, piperacillin–tazobactam, piperacillin plus gentamicin or amikacin, cefoperazone plus piperacillin, ceftazidime plus piperacillin, aztreonam, latamoxef plus tobramy-cin, clinafloxacin, imipenem–cilastatin plus amikacin, and imipenem–cilastatin itself in different dose (Norrby et al., 1987; Liang et al., 1990; Matsui et al., 1991; Winston et al., 1991; Leyland et al., 1992; Rolston et al., 1992; Miller et al., 1993; Erjavec et al., 1994; Freifeld et al., 1995; Aparicio et al., 1996; Bode et al., 1996; Raad et al., 1996; Biron et al., 1998; Bohme et al., 1998; Marra et al., 1998; Winston et al., 1998; Winston et al., 2001; Raad et al., 2003; Cherif et al., 2004). None of these studies showed inferiority of imipenem–cilastatin in clinical success for this condition, and 2 studies demonstrated that imipenem–cilastatin was significantly superior to ceftazidime in clinical success rate (Liang et al., 1990; Rolston et al., 1992).
Advancements in the pharmacological management of sepsis in the elderly
Published in Expert Opinion on Pharmacotherapy, 2023
Christos Psarrakis, Evangelos J. Giamarellos-Bourboulis
Another promising intravenous broad spectrum β-lactamase inhibitor, Durlobactam, is currently being evaluated in combination with sulbactam for infections caused by Acinetobacter baumannii including carbapenem-resistant strains. The part A of the global, non-inferiority, phase III RCT (ATTACK trial) evaluated the clinical efficacy of the novel combination Sulbactam/Durlobactam (SUL-DUR) vs Colistin in 125 patients with pneumonia or bacteremia caused by Acinetobacter baumanii-calcoaceticus complex (ABC). All patients also received imipenem/cilastatin as adjunctive treatment. The primary study endpoint was 28-day all-cause mortality among patients with carbapenem-resistant ABC (CRABC) infections in mMITT population. The preliminary results showed that Sulbactam/Durlobactam was non-inferior to colistin regarding the primary outcome (19% vs 32.3%, difference: −13.2%, 95% CI: −30–3.5%) and was associated with higher clinical cure rate at both EOT (74.6% vs 45.2%, difference: 29.4%, 95% CI: 11.4–47.4) and TOC visits (61.9% vs 40.3%, difference: 21.6%, 95% CI: 2.9–40.3) [100].
Safety evaluation of current therapies for high-risk severely ill patients with carbapenem-resistant infections
Published in Expert Opinion on Drug Safety, 2022
Matteo Bassetti, Antonio Falletta, Giovanni Cenderello, Daniele R. Giacobbe, Antonio Vena
Based on current evidences coming from pivotal trials, imipenem-cilastatin-relebactam is generally well-tolerated and shows a good safety profile consistent with that established for imipenem-cilastatin alone [49,50]. In RESTORE IMI-1 trial (an RCT comparing the efficacy and safety of imipenem-cilastatin-relebactam 500 mg-500 mg-250 mg iv every 6 hours vs colistin 300 mg loading dose followed by 150 mg every 12 hours plus imipenem-cilastatin 500 mg-500 mg every 6 hours in patients with imipenem-nonsusceptible bacterial infections) [50], treatment emergent nephrotoxicity was significantly less frequent (p = 0.002) with imipenem-cilastatin-relebactam than with colistin plus imipenem-cilastatin (10% vs 59%) (Table 2). In this study, the most common AEs reported with imipenem-cilastatin-relebactam were pyrexia (13%) and increased in aspartate aminostransferase (AST) (13%) or in alanine aminotransferase (ALT) above the upper limit of normal range (ULN) (11%). Although the incidence of pyrexia was similar between groups, a significantly lower percentage of patients receiving imipenem-cilastatin-relebactam (0%) than colistin plus imipenem-cilastatin (13%) experienced clinically relevant elevations in hepatic transaminases (elevations in hepatic transaminases were per protocol defined as AST or ALT ≥3 X ULN and total bilirubin ≥ 2 X ULN and alkaline phosphatase >2 X ULN or AST or ALT ≥ 5 X ULN) [50].
Transient appearance of EDTA dependent pseudothrombocytopenia in a patient with 2019 novel coronavirus pneumonia
Published in Platelets, 2020
Han Li, Bangqin Wang, Leping Ning, Yu Luo, Shulin Xiang
In addition to the antiviral treatment, the patient was also under an antibiotic treatment with Imipenem Cilastatin in ICU. We collected the blood samples in EDTA tubes and monitored the routine blood cell counts. Two days later, we suddenly found a low platelet count of 91 × 109/L. Her platelet count was decreasing progressively from then on. She was treated with platelet infusion twice but failed to respond. In spite of the lowest value of 17 × 109/L, the patient had no signs or symptoms of bleeding. The peripheral blood smear presented platelet aggregation. Meanwhile, the IgG/IgM antibody of SARS-CoV-2 in her serum was conformed qualitatively to be positive. We collected the blood samples with both EDTA tube and citrate tube on the same day. The number of platelet with citrate was normal (118 × 109/L), while that with EDTA was lower with 17 × 109/L. Thus, the patient was diagnosed with EDTA-PCTP. With the remission of COVID-19, the platelet count in the citrate anticoagulant samples remained normal, and the platelet count in the EDTA anticoagulant samples eventually returned to normal (Figure 1). One week after discharged, the patient was negative to the repeated result of IgG/IgM antibody of SARS-CoV-2, and her platelet count in the EDTA anticoagulant samples remained normal.