Background: Heart failure (HF) is a leading cause of mortality across the globe, prompting ongoing research into novel biomarkers for improved risk stratification and patient management. Methods: This cross-sectional study aimed to investigate the relationship between two promising biomarkers, tetranectin and paraoxonase 1, and the severity of heart failure in a cohort of 87 patients with cardiovascular risk factors. Participants were categorized into three groups based on their New York Heart Association (NYHA) classification: no HF (Control), NYHA class I (G1), and NYHA class II-IV (G2). Results: Our analysis revealed a stepwise decrease in both TETRA and PON1 levels with increasing HF severity, with the Control group exhibiting the highest levels and the G2 group the lowest. Interestingly, a significant positive correlation between TETRA and PON1 was observed only in the Control group, suggesting a potential interplay between these biomarkers in healthy individuals that may be disrupted with the onset of HF. Furthermore, both TETRA and PON1 were positively associated with left ventricular ejection fraction (LVEF) and negatively associated with diastolic dysfunction, indicating their potential involvement in both systolic and diastolic cardiac function. Conclusions: These findings suggest that TETRA and PON1 may serve as valuable biomarkers for assessing HF severity and prognosis. Further research is warranted to validate these findings in larger, prospective studies and to explore their clinical utility in guiding treatment decisions.

Background/Objectives: Hypersensitivity pneumonitis (HP), a subtype of interstitial lung disease (ILD), is often misdiagnosed as idiopathic pulmonary fibrosis (IPF), particularly when the causative antigen cannot be identified. Typically resulting from chronic exposure to inhaled organic particles smaller than 5 microns, HP presents a diagnostic challenge. This report outlines a case of fibrotic HP initially misclassified as asthma. No triggering antigen was identified despite extensive investigation. The disease progressed despite corticosteroid, immunosuppressive, and antifibrotic therapy, ultimately leading to an advanced fibrotic stage and requiring lung transplantation. This clinical course is rare and infrequently reported, particularly in cases requiring lung transplantation without an identifiable causative antigen. Such progression is uncommon and underreported, especially in patients initially misclassified as having asthma. Methods: Medical records of 24 patients diagnosed with HP were reviewed. Only one case demonstrated progression to fibrotic HP; this case was selected for detailed analysis. Results: Clinical and functional deterioration occurred despite standard therapy. Given the advanced stage of fibrosis and treatment resistance, lung transplantation was deemed the next appropriate therapeutic option. Conclusions: HP remains underdiagnosed due to difficulties in identifying the causative antigen and overlapping features with other ILDs. Early and accurate differentiation from IPF is essential, particularly in progressive fibrotic forms unresponsive to conventional therapies.

Background: Tetranectin (CLEC3B), a plasminogen-binding protein involved in fibrinolysis and tissue remodeling, has been increasingly studied as a potential diagnostic and prognostic biomarker in cardiovascular disease (CVD). This review synthesizes current evidence on its clinical utility across heart failure (HF), coronary artery disease (CAD), and related conditions. Objectives: To systematically evaluate and synthesize published clinical evidence on the diagnostic and prognostic value of tetranectin in cardiovascular diseases. Methods: A systematic search of PubMed, Google Scholar, and Scopus (January 2010–June 2025) identified original human studies examining associations between tetranectin (CLEC3B) and cardiovascular diseases, including heart failure, coronary artery disease, myocardial infarction, and cardiometabolic conditions. Eligible studies included adult cohorts with observational designs; experimental, in vitro, and pediatric studies were excluded. Two reviewers independently extracted data on study design, population characteristics, biomarker assessment, and outcomes, resolving discrepancies by consensus. Results: Twelve studies were included. Tetranectin levels were consistently lower in patients with CAD, MI, and advanced HF compared to controls. Higher circulating TN levels were associated with reduced risk of HF onset, cardiovascular death, and hospitalization. In two studies, combining tetranectin with NT-proBNP improved diagnostic accuracy over NT-proBNP alone. Mechanistic studies revealed correlations between TN expression and fibrosis-related gene pathways, supporting its biological relevance. Conclusions: Tetranectin shows consistent promise as a diagnostic and prognostic biomarker in cardiovascular disease, particularly in heart failure and coronary artery disease. Its involvement in fibrotic remodeling, plasminogen activation, and vascular homeostasis underlines biological pathways relevance. Combining tetranectin with established biomarkers may improve cardiovascular risk stratification and guide more personalized therapeutic strategies. Further large-scale and longitudinal studies are needed to validate its clinical utility across diverse settings.

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.

Background and Objectives: This narrative review evaluates the potential of Tetranectin (TN) and Paraoxonase-1 (PON1) to bridge the gap between biological pathology and clinical risk stratification by mapping the “Fibrosis-Oxidative Axis”. Materials and Methods: A targeted literature search was conducted using Scopus, PubMed, and Google Scholar to identify studies examining the diagnostic and prognostic value of TN and PON1 in heart failure (HF). Evidence was synthesized qualitatively to analyze their roles in structural fibrosis and oxidative defense. Results: Tetranectin functions as a structural indicator, where its dynamics reflect fibroblast activation, extracellular matrix (ECM) deposition, and protein sequestration during tissue remodeling. On the other hand, PON1 serves as a functional metabolic barometer; its reduced activity correlates with systemic oxidative burden, loss of endothelial protection, and pro-inflammatory signaling. These markers capture a bidirectional pathology where oxidative injury drives fibrotic remodeling, which subsequently continue metabolic dysfunction. A dual-biomarker profile is proposed to stratify disease activity: early-stage metabolic stress (reduced PON1) precedes structural changes, while progressive HF involves active fibrosis (altered TN) alongside persistent oxidative injury. Conclusions: The combined assessment of TN and PON1 offers a complementary approach to HF profiling, potentially refining risk stratification beyond hemodynamic parameters. However, clinical implementation requires large-scale validation to address standardization issues and specificity limitations regarding multimorbidity.