Prostate disease diagnostics increasingly integrate PSA-derived parameters, molecular assays, risk calculators, and multiparametric MRI, yet important limitations remain in distinguishing benign inflammatory changes from clinically significant prostate cancer and in capturing biological heterogeneity. This narrative review summarizes current evidence on inflammatory and epigenetic biomarkers in prostate disease, focusing on YKL-40, mannose-binding lectin, and global DNA methylation/hydroxymethylation. The reviewed evidence indicates that chronic inflammation, innate immune variability, tumor microenvironment remodeling, and epigenetic dysregulation contribute to prostate disease progression and may provide biological information not fully reflected by conventional diagnostic tools. YKL-40 may reflect inflammatory stromal remodeling and angiogenic activity, mannose-binding lectin may represent innate immune variability, while DNA methylation and hydroxymethylation may indicate systemic molecular adaptation and long-term inflammatory imprinting. However, these biomarkers remain largely investigational and should currently be considered adjunctive biological layers rather than validated standalone diagnostic tools. Future studies should prioritize analytical standardization, prospective prostate-specific validation, and assessment of incremental clinical utility beyond PSA, molecular assays, and mpMRI within clearly defined contexts of use.

Background and Objectives: Oxidative stress is widely recognized as a key contributor to both the development and progression of chronic obstructive pulmonary disease (COPD), particularly during acute exacerbations (AECOPD). 8-Hydroxy-2′-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage, has been insufficiently investigated as a systemic biomarker in this setting. This study evaluated the relationship between serum 8-OHdG levels, airflow limitation severity, and smoking status in patients hospitalized with AECOPD. Materials and Methods: We conducted a cross-sectional study including 176 patients admitted for AECOPD and stratified according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages. The study population comprised patients with comparable distributions of age, sex, smoking status, diabetes, cardiovascular comorbidities, and area of residence across GOLD categories. Serum 8-OHdG, leukocyte count, neutrophil percentage, C-reactive protein (CRP), fibrinogen, and procalcitonin were measured. Group comparisons, multivariable logistic regression analyses, and smoking-status subgroup analyses were performed. Results: Serum 8-OHdG levels increased significantly with advancing airflow limitation severity (p = 0.038), with higher concentrations observed in patients with GOLD 4 disease compared to GOLD 1–2 disease (p = 0.023). In multivariable analysis, 8-OHdG was the only biomarker independently associated with GOLD stage (OR = 2.44, 95% CI: 1.12–5.31, p = 0.025). Higher serum 8-OHdG levels were also independently associated with smoking status (OR = 1.20, 95% CI: 1.05–1.37, p = 0.022). Ever-smokers demonstrated significantly higher 8-OHdG concentrations than never-smokers in GOLD 1–2 and GOLD 3 disease, whereas procalcitonin levels were higher among never-smokers with advanced COPD. Conclusions: Serum 8-OHdG levels measured during AECOPD are associated with both airflow limitation severity and smoking status. These findings support the potential role of oxidative DNA damage as a clinically relevant component of COPD pathophysiology and suggest that serum 8-OHdG may represent a useful biomarker for disease characterization in patients experiencing acute exacerbations.

Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are characterized by intensified systemic inflammation, yet the relationship between inflammatory biomarker profiles and underlying GOLD-defined airflow limitation severity remains incompletely understood. This exploratory cross-sectional study investigated inflammatory and hematological biomarkers across the spectrum of stable-state GOLD-defined airflow limitation severity in patients hospitalized for AECOPD. A total of 100 participants were included, comprising non-COPD controls and patients with mild-to-moderate (GOLD 1–2), severe (GOLD 3), and very severe (GOLD 4) COPD (n = 25/group). Absolute leukocyte count, C-reactive protein (CRP), erythrocyte sedimentation rate, interleukin-6 (IL-6), procalcitonin, and hemoglobin were analyzed using non-parametric statistics, ordinal logistic regression, and Spearman correlation analysis. Absolute leukocyte counts, CRP, IL-6, and procalcitonin differed significantly across the airflow limitation continuum (p < 0.05). Among all variables examined, CRP was the only biomarker independently associated with increasing GOLD-defined airflow limitation severity (OR = 1.15, 95% CI: 1.01–1.31, p = 0.034). Correlation analyses revealed stage-dependent alterations in biomarker interaction patterns, with strong CRP-centered associations observed in GOLD 1–2 progressively weakening in advanced disease stages. These findings suggest that COPD severity is associated not only with quantitative changes in inflammatory biomarkers but also with progressive reorganization of inflammatory biomarker relationships, supporting the potential value of CRP as a complementary marker of disease stratification during AECOPD.

Chronic kidney disease (CKD) is associated with intestinal dysbiosis, barrier dysfunction, uremic toxin accumulation, and systemic inflammation. This narrative review critically evaluates the gut–kidney axis, focusing on the distinction between NLRP3 [Nucleotide-binding Oligomerization Domain (NOD)-like receptor pyrin domain-containing protein 3] inflammasome priming and direct activation. It also examines the diagnostic and prognostic relevance of related biomarkers. Preclinical studies, clinical investigations, systematic reviews, meta-analyses, and relevant clinical trials within the past decade were considered. CKD-associated barrier dysfunction increases exposure to lipopolysaccharides and gut-derived metabolites. Lipopolysaccharide (LPS)-mediated TLR4/NF-κB (Toll-like receptor 4/nuclear factor kappa B) signaling provides well-supported inflammasome priming. Indoxyl sulfate acts predominantly as a priming stimulus, although its effects vary among cell types. Direct NLRP3 activation by p-cresyl sulfate has not been demonstrated. Trimethylamine N-oxide has the strongest experimental evidence for inflammasome activation. Candidate biomarkers include these metabolites, microbial profiles, intestinal permeability markers, and inflammasome-related mediators. However, their interpretation is limited by dependence on renal clearance, assay heterogeneity, absent standardized thresholds, and uncertain added value beyond estimated glomerular filtration rate and urinary albumin-to-creatinine ratio. Interventional studies remain small and predominantly use surrogate endpoints. The gut–toxin–inflammasome axis is mechanistically plausible, but evidence for priming is substantially stronger than that for direct activation. Its biomarkers remain research tools and require assay harmonization, prospective validation, and demonstration of independent clinical value before routine implementation.

Background and Clinical Significance: Cutaneous aspergillosis caused by Aspergillus flavus is rare and coinfection with Klebsiella pneumoniae was reported only in pulmonary disease. Case Presentation: We describe a 57-year-old woman with no prior comorbidities who developed septic shock requiring intensive care, broad-spectrum antibiotics, corticosteroids, and renal replacement therapy. Six days after discharge, she was readmitted with fever, leukopenia, thrombocytopenia, cavitary lung lesions, and multiple erythematous nodules on the limbs and mammary regions. Bronchial aspirate cultures detected K. pneumoniae, while progressive cutaneous lesions required surgical debridement. Histopathology revealed angioinvasive septate hyphae, and MALDI-TOF identified A. flavus. The K. pneumoniae strain was extensively drug resistant; A. flavus was susceptible only to azoles. Despite targeted therapy, lesions progressed requiring bilateral mastectomy. Conclusions: This case illustrates a previously unreported scenario in which secondary immunosuppression after severe sepsis led to concurrent cutaneous A. flavus infection and extensively drug-resistant (XDR) K. pneumoniae. Early recognition of mixed fungal–bacterial infections is essential for appropriate management.

Background/Objectives: Early risk stratification in non-shock sepsis remains challenging, as patients may appear clinically stable despite ongoing deterioration. We used key variables across seven pathophysiological domains (cardiovascular, hematological, metabolic, hepatic, renal, immune, and comorbidity burden) to identify admission-based predictors of in-hospital mortality for these patients and derive a simple, clinically applicable triage score. Methods: This prospective pilot study included 182 adult non-shock sepsis patients transferred from the Emergency Department to the internal medicine ward in a tertiary hospital in Arad (Romania). Markers of cardiovascular (atrial fibrillation), renal (creatinine, urea), immune–inflammatory (IL-6, CRP, ESR, procalcitonin, presepsin), metabolic (FBG), hepatic (AST, ALT), and comorbidity burden (CCI) domains were analyzed using logistic and LASSO regression with bootstrap validation. Results: Non-survivors exhibited a significantly higher prevalence of atrial fibrillation (p = 0.012), as well as significantly higher creatinine, urea, IL-6, CRP, ESR, CCI, and presepsin (p ≤ 0.042). Although most variables, (except IL-6) were significant in univariate analysis (p ≤ 0.047), only atrial fibrillation (AOR = 2.31, 95% CI: 1.09–2.84, p = 0.021) and creatinine (AOR = 1.40, 95% CI: 1.00–1.95, p = 0.048) remained independent predictors in the multivariate model. LASSO regression (1000 bootstrap iterations, selection frequency ≥ 80%) confirmed their robustness. Three-parameter models combining atrial fibrillation, creatinine, and inflammatory biomarkers showed good discrimination, with the presepsin-based model achieving an AUC of 0.843, 80.0% sensitivity, 82.9% specificity, and NPV > 95% at the optimal cut-offs (creatinine > 1.49 mg/dL; presepsin > 1446 pg/mL). The Sepsis CORE score demonstrated progressive risk stratification, with mortality rising from 0% to 60.0% across score categories. Conclusions: The proposed score integrates cardiovascular, renal, and immune domains into a simple admission-based tool with high negative predictive value. It may support early triage and risk stratification in non-shock sepsis patients admitted to general wards, although external validation is required.