Browsing by Author "Kilinc, Metin"

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Antibiotic Resistance and Mortality in Icu Patients: a Retrospective Analysis of First Culture Growth Results
(Mdpi, 2025) Kilinc, Metin
Objectives: This study aimed to analyze the antibiotic resistance patterns of microorganisms isolated from intensive care unit (ICU) patients and evaluate their impact on mortality and length of ICU stay. Given the increasing prevalence of multidrug-resistant (MDR) pathogens in critically ill patients, understanding their resistance profiles is crucial for optimizing empirical antibiotic therapy and improving patient outcomes. Methods: This retrospective study included 237 ICU patients admitted between 1 July 2022, and 1 January 2024. The initial culture growth results from blood and urine samples were analyzed. Microorganism identification was performed using VITEK 2 Compact and conventional bacteriological methods, while antibiotic susceptibility testing followed CLSI 2022 and EUCAST 2022 guidelines. Results: A total of 237 ICU patients were included in this study. The most frequently isolated microorganisms were Escherichia coli (E. coli) (44.3%), Klebsiella pneumoniae (K. pneumoniae) (35.0%), and Pseudomonas aeruginosa (P. aeruginosa) (25.3%), with Acinetobacter baumannii (A. baumannii) (31.2%) being the most resistant pathogen. Among Gram-positive bacteria, methicillin-resistant Staphylococcus aureus (MRSA) (12.2%) and vancomycin-resistant enterococci (VRE) (21.5%) were the most frequently identified multidrug-resistant (MDR) pathogens. Regarding antimicrobial resistance, carbapenem resistance was highest in A. baumannii (55%), followed by P. aeruginosa (40%) and K. pneumoniae (30%). Additionally, ESBL-producing E. coli (43.2%) and K. pneumoniae (38.5%), as well as carbapenemase-producing K. pneumoniae (18.6%) and E. coli (9.2%), were identified as key resistance mechanisms impacting clinical outcomes. Patients with MDR infections had significantly longer ICU stays (p < 0.05) and higher mortality rates. The Kaplan-Meier survival analysis revealed that A. baumannii infections were associated with the highest mortality risk (HR: 4.6, p < 0.001), followed by MRSA (HR: 3.5, p = 0.005) and P. aeruginosa (HR: 2.8, p = 0.01). Among laboratory biomarkers, elevated procalcitonin (>= 2 ng/mL, OR: 2.8, p = 0.008) and CRP (>= 100 mg/L, OR: 2.2, p = 0.01) were significantly associated with ICU mortality. Additionally, patients who remained in the ICU for more than seven days had a 1.4-fold increased risk of mortality (p = 0.02), further emphasizing the impact of prolonged hospitalization on adverse outcomes. Conclusions: MDR pathogens, particularly A. baumannii, MRSA, P. aeruginosa, and K. pneumoniae, are associated with longer ICU stays and higher mortality rates. Carbapenem, cephalosporin, fluoroquinolone, and aminoglycoside resistance significantly impact clinical outcomes, emphasizing the urgent need for antimicrobial stewardship programs. ESBL, p-AmpC, and carbapenemase-producing Enterobacterales further worsen patient outcomes, highlighting the need for early infection control strategies and optimized empirical antibiotic selection. Biomarkers such as procalcitonin and CRP, alongside clinical severity scores, serve as valuable prognostic tools for ICU mortality.
Association of Inflammatory and Metabolic Markers With Mortality in Patients With Postoperative Femur Fractures in the Intensive Care Unit
(Mdpi, 2025) Akelma, Hakan; Celik, Enes; Demir, Ibrahim; Aydemir, Semih; Akelma, Hakan
Background and Objectives: Postoperative femur fracture in elderly patients is associated with high morbidity and mortality, especially in the intensive care unit (ICU). Various factors, including demographic and laboratory parameters, may influence mortality in this population. The aim of this study was to evaluate the association of inflammatory and metabolic markers with mortality in ICU patients with postoperative femur fractures and to identify key predictors to enhance risk stratification and improve patient outcomes. Materials and Methods: In this retrospective single-center study, we analyzed 121 patients aged over 65 years with postoperative femur fractures who were admitted to the ICU between January 2023 and January 2024. Demographic and clinical data, including comorbidities, Charlson Comorbidity Index (CCI), and Acute Physiology and Chronic Health Evaluation (APACHE II) score, were collected. Laboratory parameters such as white blood cell count (WBC), albumin, C-reactive protein (CRP), D-dimer, Pan-Immune-Inflammation Value (PIV), CRP-to-albumin ratio (CAR), neutrophil-to-lymphocyte ratio (NLR), and others were analyzed. Linear regression, logistic regression, and Receiver Operating Characteristic (ROC) analyses were performed to determine the predictive value of these markers for ICU mortality. Results: The mean age of the patients was 76.3 +/- 9.6 years, and 52.1% were female. The most common comorbidities were hypertension (67.8%) and diabetes (49.6%). ICU mortality occurred in 24 patients (20%). Significant predictors of mortality included higher CRP (>62.8 mg/L), NLR (>10.0), PIV (>450), and APACHE II scores (>23) (p < 0.001 for all). Lower albumin levels (<2.5 g/dL) were strongly associated with increased mortality (p < 0.001). ROC analysis demonstrated that the APACHE II score had the highest predictive accuracy for mortality (AUC = 0.83), followed by albumin (AUC = 0.79) and PIV (AUC = 0.76). Extended ICU stay (>10 days) was also significantly correlated with increased mortality (p < 0.001). Conclusions: This study successfully demonstrates the utility of combining traditional clinical markers, such as APACHE II score, with novel inflammatory markers, such as PIV, CAR, and NLR, in predicting mortality in ICU patients following femur fracture surgery. The integration of emerging biomarkers with well-established scoring systems offers enhanced predictive accuracy and provides valuable insights into patient management.
Elevated Urotensin-Ii and Tgf-Β Levels in Copd: Biomarkers of Fibrosis and Airway Remodeling in Smokers
(Mdpi, 2024) Kilinc, Metin; Demir, Ibrahim; Aydemir, Semih; Gul, Rauf; Dokuyucu, Recep
Background and Objectives: Small airway fibrosis plays a critical role in the progression of chronic obstructive pulmonary disease (COPD). Previous research has suggested that Urotensin-II (U-II) and transforming growth factor-beta (TGF-beta) may contribute to pathological fibrosis in various organs, including the cardiovascular system, lungs, and liver. However, their specific relationship with airway fibrosis in COPD has not yet been thoroughly investigated. This study aims to evaluate the concentrations of U-II and TGF-beta in individuals with COPD, as well as in healthy smokers and non-smokers, to explore their potential roles in COPD-related fibrosis. Materials and Methods: The study included three distinct groups: a healthy non-smoker control group (n = 98), a healthy smoker group (n = 78), and a COPD group (n = 80). All participants in the COPD group had a smoking history of at least 10 pack-years. COPD was defined according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, with only patients classified as GOLD stage 2 or higher being included in the study. Urotensin-II (U-II) and transforming growth factor-beta (TGF-beta) levels were measured using a commercially available ELISA kit. Results: COPD patients had a significantly lower FEV1 (58 +/- 15.4%) compared to smokers (79 +/- 4.5%) and non-smokers (92 +/- 3.7%) (p < 0.001). Similarly, COPD patients had a lower FEV1/FVC ratio (55 +/- 9.4%) compared to smokers (72 +/- 4.2%) and non-smokers (85 +/- 3.6%) (p < 0.01 and p < 0.05, respectively). SaO(2) was significantly lower in COPD patients (87%) compared to smokers (96.5%) and non-smokers (98%) (COPD vs. smokers: p < 0.05 and smokers vs. non-smokers: p > 0.05). U-II levels were significantly higher in COPD patients (175.10 +/- 62.40 pg/mL) compared to smokers (118.50 +/- 45.51 pg/mL) and non-smokers (85.29 +/- 35.87 pg/mL) (p < 0.001 and p < 0.05, respectively). COPD patients also had significantly higher levels of TGF-beta (284.60 +/- 60.50 pg/mL) compared to smokers (160.00 +/- 41.80 pg/mL) and non-smokers (92.00 +/- 25.00 pg/mL) (p < 0.001 and p < 0.05, respectively). Conclusions: Our study supports the growing body of evidence that U-II and TGF-beta play central roles in the development and progression of fibrosis in COPD. The negative correlation between these markers and lung function parameters such as FEV1 and FEV1/FVC indicates that they may be key drivers of airway remodeling and obstruction. These biomarkers could serve as early indicators of fibrotic changes in smokers, even before the onset of COPD.