Little information exists on YKL-40—a key protein in tissue remodeling—and complete blood count (CBC) parameters during acute exacerbations of advanced chronic obstructive pulmonary disease (COPD). This pilot exploratory study (August 2020–January 2021) investigated the connection between serum YKL-40 levels and CBC profile in sex- and age-matched individuals with severe COPD (GOLD stage III, n = 23, median age = 66 years, 65.21% males) and very severe COPD (GOLD stage IV, n = 24, median age = 66.5 years, 74.81% males). The measured parameters were serum YKL-40, absolute leukocyte count (ALLC), absolute neutrophil count (ANC), neutrophil percentage, absolute lymphocyte count (ALC), lymphocyte percentage, neutrophil-to-lymphocyte ratio (NLR), absolute eosinophil count (AEC), eosinophil percentage, absolute monocyte count (AMC), monocyte percentage, absolute basophil count (ABC), basophil percentage, hemoglobin levels, and hematocrit concentrations. No significant inter-group differences were observed. However, high YKL-40 subjects (n = 23)—as stratified via median YKL-40 (3934.5 pg/mL)—showed significantly increased neutrophil percentage and NLR but significantly lower lymphocyte-, eosinophil-, and basophil-related parameters compared to low YKL-40 patients (n = 24). These results reveal multidimensional, YKL-40-associated changes in leukocyte profile of patients with advanced COPD during acute exacerbations, with potential implications for personalized treatment.

Background and Objectives: episodes of acute decompensation in chronic heart failure (ADHF), a common health problem for the growing elderly population, pose a significant socio-economic burden on the public health systems. Limited knowledge is available on both the endothelial function in and the cardio-metabolic health profile of old adults hospitalized due to ADHF. This study aimed to investigate the connection between asymmetric dimethylarginine (ADMA)—a potent inhibitor of nitric oxide—and key health biomarkers in this category of high-risk patients. Materials and Methods: this pilot study included 83 individuals with a known ADHF history who were admitted to the ICU due to acute cardiac decompensation. Selected cardiovascular, metabolic, haemogram, renal, and liver parameters were measured at admission to the ICU. Key renal function indicators (serum creatinine, sodium, and potassium) were determined again at discharge. These parameters were compared between patients stratified by median ADMA (114 ng/mL). Results: high ADMA patients showed a significantly higher incidence of ischemic cardiomyopathy and longer length of hospital stay compared to those with low ADMA subjects. These individuals exhibited significantly higher urea at admission and creatinine at discharge, indicating poorer renal function. Moreover, their lipid profile was less favorable, with significantly elevated levels of total cholesterol and HDL. However, no significant inter-group differences were observed for the other parameters measured. Conclusions: the present findings disclose multidimensional, adverse ADMA-related changes in the health risk profile of patients with chronic heart failure hospitalized due to recurrent decompensation episodes.

Background and Objectives: Vitamin D deficiency is linked to adverse outcomes in chronic obstructive pulmonary disease (COPD). Limited data exist on how vitamin D levels vary by disease severity during acute exacerbations of COPD (AECOPDs). This study aimed to determine whether the vitamin D status during AECOPDs—alongside inflammatory and hematological biomarkers—is associated with COPD severity. Materials and Methods: This observational study included 105 AECOPD hospitalized patients, stratified according to GOLD stages 1–2, 3, and 4. Blood samples were collected to measure serum vitamin D—as 25-hydroxyvitamin D [25(OH)D], acute phase reactants, serum calcium, and selected hematological parameters. Inter-group differences were evaluated using Kruskal–Wallis tests, with Spearman correlations applied for intra-strata associations. ROC analysis and logistic regression assessed the discriminatory power of significant biomarkers. Results: C-reactive protein (CRP) and fibrinogen concentrations were elevated across all COPD stages, whereas calcium and vitamin D remained consistently below normal. Interleukin (IL)-6 and 25(OH)D levels varied significantly with COPD stage (p = 0.033 and p = 0.047, respectively), with a marked drop from GOLD stage 3 to stage 4. High-IL-6 patients revealed significantly elevated CRP (p = 0.045), erythrocyte sedimentation rate (ESR) (p = 0.032), fibrinogen (p = 0.011), and procalcitonin (p = 0.044). The strongest correlations were seen between CRP, ESR, and fibrinogen (r_s ≥ 0.58, p ≤ 0.05), indicating a coordinated acute-phase response that weakened with advancing disease. Serum 25(OH)D was a significant independent predictor of COPD severity (AUC = 0.631, p = 0.048), while IL-6 had a weaker predictive value, losing significance in the combined regression model. Conclusions: Vitamin D deficiency is more pronounced in very severe COPD, serving as a potential clinical indicator of disease severity during exacerbation episodes.

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: Although TRAIL is a potent propapoptotic factor, its role in cardiovascular disease (CVD) remains unclear. This pilot exploratory study investigated serum TRAIL changes along the CVD continuum. We focused on two successive phases of this spectrum (systemic arterial hypertension and heart failure), with emphasis on acute cardiac events due to their immediate clinical significance. Methods: The study population included 90 age- and sex-matched patients hospitalized with hypertensive urgencies (HTUs) or acute decompensation episodes (ADHF). Key echocardiographic, endothelial, cardiometabolic, renal, and liver markers were assessed alongside TRAIL levels. Results: ADHF patients showed significantly elevated TRAIL concentrations, suggesting a progressive rise in TRAIL levels along the CVD continuum. They exhibited worse cardiac, hematologic, and renal profiles, with longer hospital stays and the cachexic phenotype. TRAIL correlated directly with asymmetric dimethylarginine, C-reactive protein, and admission potassium in ADHF patients. In hypertensive subjects, it correlated directly with asymmetric dimethylarginine and inversely with erythrocyte size variability. TRAIL may, thus, serve as a compensatory mechanism in HF, with potential as a biomarker for acute cardiovascular events. Conclusions: TRAIL dynamics provide valuable insights into CVD pathophysiology, particularly in acute settings, warranting further investigation to clarify its role in the broader context of apoptosis and cardiovascular health.

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.