Keyword: Drug Resistance
2 results found.
Original Article
Oncology, Nuclear Medicine and Transplantology, 2(3, Suppl. 1), 2026, onmt_A9, https://doi.org/10.63946/onmt/19326
ABSTRACT:
Introduction: Infections caused by multidrug-resistant gram-negative microorganisms are one of the causes of adverse outcomes in critically ill patients with oncohematological diseases. Given the limited availability of modern antibacterial agents, colistin remains a reserve drug; however, its use is associated with concerns regarding nephrotoxicity. Objective: To evaluate clinical outcomes, microbiological profile, and renal function dynamics during colistin therapy in an oncohematological intensive care unit.
Materials and Methods: A single-center retrospective study was conducted on 48 consecutive episodes of colistin therapy in an oncohematological intensive care unit in 2024. Clinical and microbiological data, treatment characteristics, creatinine dynamics, use of renal replacement therapy, and in-hospital outcomes were analyzed. The primary outcome was in-hospital mortality. Comparisons were made using the Mann–Whitney U test and Fisher's exact test; differences were considered statistically significant at p < 0.05.
Results: Neutropenia was observed in 36 of 48 episodes (75.0%), and mechanical ventilation and/or vasopressor support prior to therapy initiation was required in 41 episodes (85.4%). Positive cultures were obtained in 30 episodes (62.5%). Klebsiella pneumoniae was isolated in 26 episodes (54.2%); 25 of the 26 isolates exhibited a multidrug-resistant phenotype. Among episodes with positive cultures, 26 of 30 isolates (86.7%) were susceptible to colistin. In-hospital mortality was 60.4% (29 of 48). Compared with survivors, non-survivors more frequently had neutropenia (96.6% vs. 42.1%; p < 0.001) and required mechanical ventilation and/or vasopressor support before therapy initiation (100.0% vs. 63.2%; p < 0.001). They also had higher median procalcitonin concentrations (17.67 [5.40–34.91] vs. 3.15 [0.87–6.35] ng/mL; p < 0.001) and higher median baseline serum creatinine concentrations (108 [96–180] vs. 93 [89.5–102] µmol/L; p = 0.006). Colistin susceptibility was not associated with mortality (p = 0.584). An increase in creatinine of at least 26.5 µmol/L was observed in 21 episodes (43.8%), and an increase to at least 1.5 times the baseline value was observed in 13 episodes (27.1%). Renal replacement therapy after colistin initiation was required in 7 of 39 episodes without prior renal replacement therapy (17.9%).
Conclusions: Colistin therapy in the oncohematological intensive care unit was predominantly administered to patients with severe infection, neutropenia, and a need for organ support. Adverse outcomes were primarily associated with the baseline severity of the condition, whereas laboratory susceptibility to colistin did not determine prognosis. Worsening renal function during treatment was frequent; however, the retrospective design and concomitant organ dysfunction preclude attributing it exclusively to colistin. These findings underscore the need for early microbiological diagnosis and careful monitoring of renal function.
Materials and Methods: A single-center retrospective study was conducted on 48 consecutive episodes of colistin therapy in an oncohematological intensive care unit in 2024. Clinical and microbiological data, treatment characteristics, creatinine dynamics, use of renal replacement therapy, and in-hospital outcomes were analyzed. The primary outcome was in-hospital mortality. Comparisons were made using the Mann–Whitney U test and Fisher's exact test; differences were considered statistically significant at p < 0.05.
Results: Neutropenia was observed in 36 of 48 episodes (75.0%), and mechanical ventilation and/or vasopressor support prior to therapy initiation was required in 41 episodes (85.4%). Positive cultures were obtained in 30 episodes (62.5%). Klebsiella pneumoniae was isolated in 26 episodes (54.2%); 25 of the 26 isolates exhibited a multidrug-resistant phenotype. Among episodes with positive cultures, 26 of 30 isolates (86.7%) were susceptible to colistin. In-hospital mortality was 60.4% (29 of 48). Compared with survivors, non-survivors more frequently had neutropenia (96.6% vs. 42.1%; p < 0.001) and required mechanical ventilation and/or vasopressor support before therapy initiation (100.0% vs. 63.2%; p < 0.001). They also had higher median procalcitonin concentrations (17.67 [5.40–34.91] vs. 3.15 [0.87–6.35] ng/mL; p < 0.001) and higher median baseline serum creatinine concentrations (108 [96–180] vs. 93 [89.5–102] µmol/L; p = 0.006). Colistin susceptibility was not associated with mortality (p = 0.584). An increase in creatinine of at least 26.5 µmol/L was observed in 21 episodes (43.8%), and an increase to at least 1.5 times the baseline value was observed in 13 episodes (27.1%). Renal replacement therapy after colistin initiation was required in 7 of 39 episodes without prior renal replacement therapy (17.9%).
Conclusions: Colistin therapy in the oncohematological intensive care unit was predominantly administered to patients with severe infection, neutropenia, and a need for organ support. Adverse outcomes were primarily associated with the baseline severity of the condition, whereas laboratory susceptibility to colistin did not determine prognosis. Worsening renal function during treatment was frequent; however, the retrospective design and concomitant organ dysfunction preclude attributing it exclusively to colistin. These findings underscore the need for early microbiological diagnosis and careful monitoring of renal function.
Review Article
Oncology, Nuclear Medicine and Transplantology, 1(2), 2025, onmt007, https://doi.org/10.63946/onmt/17300
ABSTRACT:
Spatial tumour heterogeneity, which denotes the changes in cellular and molecular attributes across distinct locations within a tumour, significantly influences cancer diagnosis and treatment resistance. The heterogeneity of tumour cells inside a singular mass facilitates tumour development, metastasis, and the ineffectiveness of standard therapy. Comprehending the geographical distribution of tumour cells is crucial for formulating more efficient treatment regimens. Diverse methodologies are employed to investigate spatial heterogeneity, encompassing modern imaging techniques such as MRI, PET, and multiplexed imaging, alongside omics approaches including genomes, transcriptomics, and proteomics. These instruments offer insights into the tumour microenvironment and facilitate the identification of resistant subpopulations. The amalgamation of imaging and genomic data via radiogenomics has emerged as a viable methodology, providing an extensive perspective on the spatial and molecular intricacies of tumours. Principal findings reveal that spatial heterogeneity fosters medication resistance by establishing microenvironments characterised by varying oxygen levels, immunological infiltration, and genetic alterations, hence complicating the efficacy of monotherapy strategies. Hypoxic environments and immunological evasion significantly contribute to treatment resistance. Addressing geographical heterogeneity has the potential to enhance cancer treatments. By analysing the molecular and geographical characteristics of tumours, physicians can customise therapies more efficiently, minimising resistance and improving therapeutic results. This methodology signifies a vital advancement in precision medicine, providing more individualised and efficacious cancer therapies in the future.