Background and Objectives: This study aims to identify risk factors associated with MDRO infections and assess their impact on patient outcomes in Egyptian ICUs. Materials and Methods: The widespread overuse of antimicrobials has led to antibiotic multidrug resistance, posing significant challenges in intensive care units (ICUs) and leading to increased morbidity, mortality, and healthcare costs. A prospective observational study was conducted over 12 months, including 113 adult patients admitted to the ICU with confirmed bacterial infections. Comprehensive medical assessments and routine investigations were performed, including multisource cultures based on clinical suspicion. Patient histories, underlying conditions, and disease progression were documented. Patients were classified into two groups: those infected with MDROs and those without MDRO infections. Results: Significant differences were observed between patients with and without MDRO infections regarding temperature, pH, PaO₂, HCO₃, serum creatinine levels, high-dose inotropes, and inotrope dependence (p-values: 0.01, 0.028, 0.036, 0.008, <0.001, 0.013, 0.029, 0.039, <0.001, and 0.003, respectively). Additionally, cerebrovascular stroke and renal failure were significantly more frequent in MDRO-infected patients (p-values: 0.048 and 0.007, respectively). MDROs accounted for 42% of infections. The most commonly detected MDRO was Klebsiella spp. (52%). Patients with MDRO infections showed significantly higher mortality (42.6%), increased incidence of ARDS, invasive ventilation, and longer ventilation durations. Independent risk factors included prior antibiotic use (OR: 3.2; 95% CI: 1.5–6.8) and invasive device presence (OR: 2.7; 95% CI: 1.2–5.9). Conclusions: Cerebrovascular stroke and renal failure appear to be risk factors for MDRO infections. MDRO infections in ICUs are associated with poor clinical outcomes and increased complications. Improved antimicrobial stewardship and targeted prevention strategies are urgently required.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a global health challenge due to its complex pathophysiological processes. Systemic inflammation may profoundly affect disease progression, but the correlation between inflammatory markers and disease severity remains inadequately explored. This cross-sectional analysis within a prospective cohort evaluated associations of inflammatory markers (IL-6, TNF-α, hsCRP) with MASLD severity (five non-invasive scores) and metabolic indices, primarily with early-stage disease (66.7% mild fibrosis by TE). Methods: We recruited 120 patients diagnosed with MASLD. Assessment included anthropometric measurements, laboratory analyses, and non-invasive fibrosis evaluation using five validated scoring systems (APRI, FIB-4, NAFLD fibrosis score, FAST score, and transient elastography). Inflammatory markers were quantified using high-sensitivity ELISA techniques. Medication/comorbidities were recorded (statins 23.3%, diabetes drugs 26.7%), and multivariate regressions and FDR correction were applied. Results: Patients showed remarkably elevated inflammatory markers compared to reference ranges: IL-6 (15.1 ± 9.3 pg/mL), TNF-α (38.8 ± 29.1 pg/mL), and hsCRP (12.3 ± 11.1 mg/L). No correlations were found between inflammatory markers and disease severity across any non-invasive scoring system. However, TNF-α correlated significantly with waist circumference (r = 0.28, p = 0.002) and ALT (r = 0.19, p = 0.03), while showing inverse correlations with total cholesterol (r = −0.27, p = 0.03) and LDL (r = −0.22, p = 0.02). In contrast, hsCRP correlated positively with LDL (r = 0.20, p = 0.02) and WBC count (r = 0.24, p = 0.008). Conclusion: This study reveals a dissociation between systemic inflammatory markers and hepatic fibrosis severity in MASLD. Inflammatory Markers showed stronger metabolic associations than fibrosis, limiting their utility as fibrosis surrogates in early MASLD. These findings support a dual-pathway approach to MASLD management, targeting metabolic and hepatic components independently. The divergent associations of TNF-α and hsCRP with lipid profiles suggest distinct inflammatory mechanisms in MASLD.

Background and Objectives: The rising prevalence of drug-resistant organisms presents a significant challenge to healthcare, underscoring the importance of implementing effective antimicrobial stewardship programs. The success of these programs depends on access to accurate, evidence-based data reflecting local patterns of antibiotic resistance. This study aims to assess the antimicrobial susceptibility profiles of gram-positive bacteria isolated from pediatric patients in a tertiary care hospital in Egypt. Materials and Methods: We carried out a retrospective study over a five-year period, from January 2018 to December 2022, using microbiology laboratory records. Clinical samples included blood, urine, respiratory secretions, pus, wound, cerebrospinal fluid (CSF), and pleural fluid. The analysis focused on the resistance patterns of gram-positive pathogens identified through routine culture procedures. Antimicrobial susceptibility testing was performed using the Kirby–Bauer disc diffusion method, and vancomycin MIC was confirmed using the VITEK 2 system. Results: A total of 3223 gram-positive bacterial isolates were identified. Staphylococcus aureus, including 82.5% methicillin-resistant strains (MRSA), exhibited high resistance to erythromycin (47.3%) and gentamicin (low potency) (32.1%). Coagulase-negative staphylococci (CoNS) showed the highest erythromycin resistance (up to 88.3%), while Enterococcus spp. demonstrated declining susceptibility to vancomycin, levofloxacin, and erythromycin. Across all isolates, vancomycin and gentamicin (high potency) showed the highest overall susceptibility. Resistance to cotrimoxazole and doxycycline declined over the five-year period. Conclusions: While a decline in resistance was noted for some agents, persistent resistance to key antibiotics (particularly erythromycin and gentamicin) among MRSA and CoNS remains concerning. These findings underscore the importance of targeted antimicrobial stewardship interventions and continuous surveillance to inform empirical therapy in pediatric settings.

β-thalassemia is a genetic disorder affecting chromosome 16, inherited from one or both parents. In spite of the improved treatment of the hematological disorder and its complications, β-thalassemic patients still exhibit an imbalance in bone mineral turnover, resulting in diminished bone mineral density (BMD), more evident in the lumbar spine. The purpose of this study was to investigate the association between genetic polymorphism of the PPAR-γ gene and the presence of osteopenia or osteoporosis in children with β-thalassemia. This case–control study was conducted on 50 children with β-thalassemia from the pediatric hematology unit of Beni-Suef University Hospital, including 50 healthy children as the control group. The age range was 8 to 18 years. Samples of patients and control subjects were analyzed for the presence of polymorphisms of the PPAR-γ gene and other blood labs. An assay of BMD measure using dual-energy X-ray absorptiometry (DXA) was performed to investigate osteopenia or osteoporosis. Statistical analysis was used to investigate the relationship between the risk of osteopenia or osteoporosis and the presence of PPAR-γ Pro12Ala gene polymorphism. Eighteen (eleven males and seven females) of fifty patients (representing 36% of the patients group) have osteopenia with low bone mineral density (Z-score is −1 or less than 1). There was no statistically significant difference between BMD measurements in males and females. By comparing the frequency of 12 Ala gene polymorphisms between the patient group and the control group, we found that no statistically significant difference was detected. The BMD values were not significantly different between the groups of PPAR-γ Pro12Ala gene polymorphism. In conclusion, decreased BMD levels are frequent in β-thalassemia patients. PPAR-γ Pro12Ala gene polymorphism is not common in Egyptian patients with β-thalassemia. No significant relationship was found between the PPAR-γ Pro12Ala gene polymorphism and low BMD levels or osteopenia in Egyptian β-thalassemia patients. However, further studies on a larger population of Egyptian patients are needed to confirm this finding.

Background: Chronic hepatitis C virus (HCV) infection remains an important cause of progressive liver disease and fibrosis. Toxoplasma gondii infection is highly prevalent worldwide and may influence inflammatory and fibrotic pathways; however, its clinical significance in patients with chronic HCV infection remains unclear. This study aimed to assess the prevalence of anti-T. gondii antibodies among patients with chronic HCV infection and to evaluate potential differences in liver fibrosis biomarkers and elastography findings according to T. gondii serostatus. Methods: In this case–control study conducted between December 2023 and October 2024 at Beni-Suef University Hospital, Beni-Suef, Egypt, 58 treatment-naive patients with chronic HCV infection, confirmed by documented anti-HCV positivity together with detectable serum HCV RNA, and 20 healthy controls were enrolled. Anti-T. gondii IgG and IgM antibodies were detected using a qualitative rapid immunochromatographic assay (OnSite Toxo IgG/IgM Combo Rapid Test, CTK Biotech, Poway, CA, USA). In HCV patients, liver fibrosis was assessed using transient elastography and circulating fibrosis-related biomarkers, including tissue inhibitor of metalloproteinase-1 (TIMP-1), macrophage colony-stimulating factor (M-CSF), and YKL-40, the latter three measured by quantitative sandwich enzyme-linked immunosorbent assay. Clinical, biochemical, and fibrosis-related parameters were compared between HCV patients and controls and according to T. gondii serological status. Results: Anti-T. gondii IgG seropositivity was detected in 26/58 (44.8%) patients with chronic HCV infection and 8/20 (40.0%) healthy controls, whereas IgM seropositivity was observed in 4/58 (6.9%) and 2/20 (10.0%), respectively. No statistically significant differences were observed between patients and controls in either IgG or IgM seropositivity rates. Patients with chronic HCV infection showed significantly higher circulating concentrations of TIMP-1, M-CSF, and YKL-40 than healthy controls (all p < 0.001). Among HCV patients, anti-T. gondii IgG serostatus was not significantly associated with FibroScan-defined fibrosis category, platelet count, AST, GGT, TIMP-1, M-CSF, or YKL-40. Analyses involving IgM-positive patients were considered exploratory because of the small number of IgM-positive participants. Conclusions: Anti-T. gondii IgG and IgM seropositivity did not differ significantly between patients with chronic HCV infection and healthy controls. Among HCV patients, serological evidence of previous T. gondii exposure was not significantly associated with transient elastography-defined fibrosis severity or the evaluated circulating fibrosis biomarkers. Because seropositivity reflects exposure rather than active parasitic infection, the findings should not be interpreted as evidence of active hepatic toxoplasmosis. Larger multicenter longitudinal studies incorporating molecular confirmation of active T. gondii infection are warranted.