Search Results (2,394)

Chronic hepatitis B virus (HBV) infection may influence extrahepatic systems, including endocrine and lipid regulation. In this cross-sectional study, 186 adults were stratified by HBV DNA status and viral load to examine thyroid function, systemic inflammation, and lipid metabolism, with further analyses by age and sex. Thyroid-stimulating hormone (TSH, a pituitary regulator of thyroid function) levels were significantly lower in HBsAg-positive individuals compared with controls; however, this association was attenuated after stratification by viral load, indicating that the relationship is not unequivocally independent of HBV DNA levels, as free thyroxine (FT4, the circulating thyroid hormone reflecting gland activity) levels remained stable. Lipid profiles displayed demographic-specific patterns: males with high viral load exhibited lower HDL cholesterol, whereas younger HBV-positive individuals showed higher LDL cholesterol. CRP levels were unaffected by HBV status or viral load, aligning with the absence of systemic inflammation in early or inactive disease stages. Age was a major determinant across biomarkers, with complex interactions involving sex and viral load. These findings indicate subtle but clinically relevant extrahepatic effects of HBV infection and underscore the need for personalized monitoring and longitudinal studies to clarify metabolic and cardiovascular implications. These subgroup trends should be interpreted with caution given the absence of BMI, liver enzyme, fibrosis, medication, and comorbidity data in this retrospective cohort. Full article

Background/Objectives: Fatigue is the most common systemic manifestation of chronic liver diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). Fatigue not only adversely affects quality of life in MASLD patients but also complicates the attainment of therapeutic goals and contributes to a worse prognosis. This study aimed to analyze the relationship between clinically significant fatigue and laboratory parameters reflecting systemic inflammation, liver function, body composition, muscle strength, and blood pressure in patients with MASLD. Methods: A total of 154 patients with a confirmed diagnosis of MASLD were enrolled in this study. All participants underwent anthropometric assessment, laboratory testing, abdominal ultrasonography, and point shear-wave elastography. Muscle strength was evaluated using handgrip strength (GS) measurement and the Five Times Sit-to-Stand Test (5TSTS). Skeletal muscle mass (SMM) was quantified using dual-energy X-ray absorptiometry (DXA). Fatigue was evaluated using the Fatigue Assessment Scale (FAS), with scores ≥ 22 indicating clinically significant fatigue. Results: Patients with FAS scores ≥ 22 exhibited significantly lower hemoglobin levels (p = 0.004) and erythrocyte counts (p = 0.011), along with a significantly elevated erythrocyte sedimentation rate (ESR; p = 0.002) and C-reactive protein level (CRP; p = 0.007). Furthermore, MASLD patients with FAS scores ≥ 22 demonstrated significantly reduced relative grip strength (p = 0.012) and took longer to complete the 5TSTS (p = 0.011). Additionally, these patients had higher maximum systolic and diastolic blood pressure values compared to those with FAS scores < 22 (p = 0.028 and p = 0.019, respectively). Conclusions: These findings underscore the multifactorial nature of fatigue in MASLD and highlight the need for a comprehensive management strategy. Such a strategy should include dietary modification, increased physical activity, targeted treatment of systemic manifestations of MASLD, and appropriate management of comorbidities. Full article

Background: Schizophrenia is a complex neuropsychiatric disorder whose pathophysiology may involve oxidative stress-induced neuronal damage and inflammation. We conducted a cross-species study to elucidate oxidative stress dysregulation in schizophrenia. Methods: We measured peripheral oxidative stress biomarkers (malondialdehyde [MDA], nitric oxide [NO], reduced glutathione [GSH], superoxide dismutase [SOD], catalase [CAT], advanced protein oxidation products [APOP]), and C-reactive protein (CRP) in antipsychotic-naïve schizophrenia patients and matched controls. We also assayed liver enzymes (ALP, ALT, AST) as indicators of systemic metabolic stress. In parallel, we re-analyzed published single-cell RNA-sequencing data from a Setd1a^+/–^ mouse model of schizophrenia, focusing on prefrontal cortex (PFC) cell types and oxidative stress-related gene expression. Results: Patients with schizophrenia showed markedly elevated MDA and NO (indicators of lipid and nitrosative stress) and significantly reduced antioxidant defenses (GSH, SOD, CAT) versus controls (p < 0.01 for all comparisons). Notably, urban patients exhibited higher oxidative stress biomarker levels than rural patients, implicating environmental contributions. Liver function tests revealed increased ALT, AST, and ALP in schizophrenia, suggesting hepatic/metabolic dysregulation. Single-cell analysis confirmed dysregulated redox pathways in the schizophrenia model; PFC neurons from Setd1a^+/–^ mice displayed significantly lower expression of key antioxidant genes (e.g., Gpx4, Nfe2l2) compared to wild-type, indicating impaired glutathione metabolism. Conclusions: Our integrative data identify convergent oxidative stress imbalances in schizophrenia across species. These findings advance a mechanistic understanding of schizophrenia as a disorder of redox dysregulation and inflammation. They also have translational implications as augmenting antioxidant defenses (for example, with N-acetylcysteine or vitamins C/E) could mitigate oxidative injury and neuroinflammation in schizophrenia, representing a promising adjunct to antipsychotic therapy. Full article

Background/Objectives: Fulminant myocarditis (FM) is an uncommon but potentially reversible form of myocardial inflammation that can rapidly progress to cardiogenic shock (CS). In patients who are refractory to conventional treatment, venoarterial extracorporeal membrane oxygenation (VA-ECMO) represents an effective life support strategy. However, the factors that determine functional recovery remain uncertain. The primary objective of this study was to characterize patients who recover ventricular function. Secondary objectives included analyzing VA-ECMO-related complications and overall patient survival. Methods: This was a retrospective, single-center, observational study including all consecutive patients diagnosed with FM between 2008 and 2025 who were supported with VA-ECMO (n = 22). Clinical, biochemical, echocardiographic, and imaging variables were collected. Patients were classified based on their outcomes as either recovery or death/transplantation. Differential factors potentially affecting myocardial recovery, survival, and complications were analyzed. Results: The mean age was 49.7 ± 11 years, with 36% being male. Severe cardiogenic shock was the most common initial presentation (86%), and the average time from symptom onset to hospital admission was 5.7 days. Regarding mechanical support, the non-recovery group required longer ECMO support (328 ± 225 h vs. 188 ± 103 h; p = 0.03). The presence of fibrosis on cardiac magnetic resonance imaging (MRI) was associated with a lower probability of recovery (100% vs. 44.4%; p = 0.03). Renal failure and vascular complications were more frequent in the non-recovery group, with a significantly higher rate of surgical reintervention (50% vs. 10%; p = 0.04). Echocardiography performed before discharge (recovery group) vs. before death/transplant (non-recovery group) showed significant differences in left ventricular ejection fraction (51.1% vs. 29.5%; p = 0.04), along with better levels of creatinine, N-terminal pro-B-type natriuretic peptide (NT-proBNP), leukocytes, and C-reactive protein (CRP) in the recovery group. In-hospital survival for the entire cohort was 63.6%, significantly higher in the recovery group (100% vs. 33.3%; p < 0.01). One-year survival was 59%, which was also greater among those who recovered (90% vs. 33.3%; p = 0.02). Conclusions: FM is associated with an acceptable in-hospital survival rate. The presence of myocardial fibrosis on MRI and longer ECMO support duration were observed to be associated with a lower likelihood of cardiac recovery. Patients who recovered showed better ventricular function at discharge, as well as reduced systemic inflammation and renal dysfunction. These findings highlight the importance of early identification of predictors of myocardial recovery to optimize management and therapeutic decision making in this high-risk population. Full article

Background: Postoperative wound complications following total joint arthroplasty (TJA) significantly impact patient outcomes and healthcare costs. Reliable preoperative biomarkers for identifying patients at increased risk are critical for optimizing patient management and reducing complication rates. This study evaluated the predictive utility of the C-reactive protein to albumin ratio (CAR) and the prognostic nutritional index (PNI) for periprosthetic joint infection (PJI) and postoperative wound complications in patients undergoing total hip arthroplasty (THA) and total knee arthroplasty (TKA). Methods: We retrospectively studied patients who underwent primary THA and TKA in our department from March 2019 to April 2024. The study included a total of 842 patients (568 knees and 274 hips). Preoperative blood samples were assessed for serum CRP, albumin, and total lymphocyte count, facilitating the calculation of CAR and PNI values. Patient outcomes were monitored, identifying PJI and aseptic wound complications such as persistent wound drainage, hematoma, seroma, skin erosion, and wound dehiscence within 2 weeks post-surgery. Results: The average follow-up time for patients was 39.2 months (range 13–73 months). PJI was significantly linked with elevated admission CAR and diminished PNI ratio (p < 0.001 and p < 0.001). ROC analysis demonstrated optimal predictive cut-off values for CAR at 3.1 (Area under curve [AUC]: 0.92, specificity 97.4%, sensitivity 92.3%) and PNI at 49.4 (AUC: 0.93, specificity 94.7%, sensitivity 91.7%). Furthermore, both CAR (Odds ratio [OR]: 3.84, 95% confidence interval [CI]: 1.6–9.1, p = 0.002) and PNI (OR: 21.8, 95% CI: 9–48.6, p < 0.001) were identified as two independent risk factors associated with the development of PJI following THA or TKA. Further subgroup analysis revealed distinct predictive thresholds for CAR and PNI according to surgical procedure type (TKA and THA), enhancing diagnostic accuracy. Conclusions: Preoperative admission elevated CAR and decreased PNI effectively predict PJI and postoperative wound complications in THA and TKA, supporting their utility as simple, cost-effective biomarkers in clinical practice. Incorporating CAR and PNI evaluations into preoperative assessments can enhance patient stratification and preventive strategies, thus mitigating risks and improving surgical outcomes. Full article

Background/Objectives: Sepsis is a high-mortality syndrome characterized by organ dysfunction resulting from a dysregulated host response to infection. This study aimed to evaluate the potential of growth differentiation factor 15 (GDF15), a stress-inducible cytokine, as a biomarker in patients diagnosed with urosepsis. Methods: A total of 13 patients diagnosed with urosepsis, based on an increase of ≥2 points in the Sequential Organ Failure Assessment (SOFA) score and positive urine culture, were included in the study. Daily blood samples were collected from patients for 10 days, and serum levels of GDF15, procalcitonin (PCT), and presepsin (P-SEP) were measured by ELISA. C-reactive protein (CRP), blood urea nitrogen (BUN), serum creatinine, estimated glomerular filtration rate (eGFR), hemoglobin, and neutrophil, lymphocyte, and platelet counts were determined using autoanalyzers. Temporal changes were analyzed using the Friedman test, and correlations were analyzed using Spearman’s test. Results: GDF15 levels began to decrease from Day 3, with a significant decline observed from Day 7 compared to Day 1 (p < 0.001). Similar decreasing trends were observed in CRP and PCT levels, whereas presepsin levels did not exhibit significant changes. Significant positive correlations were identified between GDF15 and CRP (r = 0.65, p = 0.015), BUN (r = 0.57, p = 0.041), and creatinine (r = 0.62, p = 0.024), and a significant negative correlation was observed with eGFR (r = −0.62, p = 0.024). No significant correlation was found between GDF15 and presepsin (p > 0.05). Conclusions: GDF15 is a biomarker sensitive to the resolution phase of inflammation and organ dysfunction in sepsis, demonstrating significant temporal changes. It holds potential as an indicator for monitoring clinical progression and assessing prognosis. Full article

Background. Type 2 diabetes mellitus (T2D) and moderate-to-severe obstructive sleep apnea (OSA) commonly coexist and exacerbate poor glycemic control, systemic inflammation, and diminished quality of life (QoL). Although continuous positive airway pressure (CPAP) therapy has demonstrated metabolic and anti-inflammatory benefits, its real-world impact in Bulgarian outpatient settings—where CPAP costs are borne entirely by patients—has not been characterized. Objectives. To evaluate the effects of six months of CPAP therapy on glycemic control (hemoglobin A₁c [HbA₁c]), systemic inflammation (high-sensitivity C-reactive protein [hsCRP]), body mass index (BMI), lipid profile (low-density lipoprotein [LDL]), QoL (Short Form 36 Physical Component Summary [SF-36 PCS] and Mental Component Summary [SF-36 MCS]), and survival among Bulgarian outpatients with T2D and moderate-to-severe OSA. Methods. In this prospective, multicenter cohort study conducted from January 2022 to July 2023, 142 adults with established T2D and OSA (apnea–hypopnea index [AHI] ≥ 15) were enrolled at three outpatient centers in Bulgaria. Fifty-five patients elected to purchase and use home-based CPAP (intervention group), while 87 declined CPAP—either because of cost or personal preference—and continued standard medical care without CPAP (control group). All participants underwent thorough outpatient evaluations at baseline (month 0) and at six months, including measurement of HbA₁c, hsCRP, BMI, fasting lipid profile (LDL), and patient-reported QoL, via the SF-36 Health Survey. Survival was tracked throughout follow-up. Results. After six months, the CPAP group experienced a significant reduction in HbA₁c from a median of 8.2% (IQR 7.5–9.5%) to 7.7% (6.7–8.7%), p < 0.001, whereas the control group’s HbA₁c decreased modestly from a median of 8.6% (IQR 7.9–9.4%) to 8.3% (7.6–9.1%); p < 0.001), with a significant between-group difference at follow-up (p = 0.005). High-sensitivity CRP in the CPAP arm fell from a median of 2.34 mg/L (IQR 1.81–3.41) to 1.45 mg/L (IQR 1.25–2.20), p < 0.001, while remaining unchanged in controls (p = 0.847). BMI in the CPAP group declined significantly from 28.6 kg/m², IQR 26.6–30.6 to 28 kg/m², IQR 25.6–29.2 (p < 0.001), compared to no significant change in controls (median 28.9 kg/m²), p = 0.599. LDL decreased in the CPAP group from a median of 3.60 mmol/L (IQR 3.03–3.89) to 3.22 mmol/L (IQR 2.68–3.48), p < 0.001, with no significant reduction in controls (p = 0.843). Within the CPAP arm, both SF-36 PCS and SF-36 MCS scores improved significantly from baseline (p < 0.001 for each), although between-group differences at six months did not reach statistical significance (PCS: 48 ± 10 vs. 46 ± 9, p = 0.098; MCS: 46, IQR 40–54 vs. 46, IQR 39–53, p = 0.291). All-cause mortality during follow-up included 2 events in the CPAP group and 11 events in the control group (log-rank p = 0.071). Conclusions. In Bulgarian outpatients with T2D and moderate-to-severe OSA, six months of CPAP therapy significantly improved glycemic control, reduced systemic inflammation, lowered BMI and LDL, and enhanced QoL, with a non-significant trend toward reduced mortality. These findings underscore the importance of integrating CPAP into multidisciplinary management despite financial barriers. Full article

Background: Atherosclerosis is a chronic inflammatory condition that underlies both cardiovascular and cerebrovascular complications. Emerging evidence suggests that COVID-19 may play a role in its progression. Purpose: The aim of the study was to evaluate the potential impact of SARS-CoV-2 infection on the development of atherosclerosis. Patients and Methods: Common carotid artery (CCA) intima media thickness (IMT) was measured by ultrasonography twice, 12–18 months apart, in a cohort of 92 patients (47 with COVID-19 and 45 controls). Clinical data were collected from medical histories, physical examinations, and laboratory findings. Results: Baseline IMT values were comparable between the study groups (0.85 mm vs. 0.78 mm). However, the COVID-19 group exhibited a significantly greater increase in IMT over time, with a median change of 0.13 mm compared to 0.05 mm in the controls (p = 0.018). Furthermore, 69.2% of COVID-19 patients exceeded the median IMT progression threshold compared to 36% in the control group (p = 0.017). An elevated level of C-reactive protein (CRP) and a higher triglyceride (Tg)-to-High-Density Lipoprotein Cholesterol (HDL) ratio were significantly associated with increased IMT in the COVID-19 group. Age and heart rate were identified as significant predictors of IMT progression across both groups. Conclusions: COVID-19 may accelerate the progression of subclinical atherosclerosis. The strong associations of CRP and the TG/HDL ratio with IMT highlight the potential roles of chronic inflammation and metabolic dysregulation in driving these vascular changes. Further large-scale, multicenter studies are needed to elucidate the underlying mechanisms, confirm these observations, and guide targeted preventive and therapeutic strategies for individuals with an increased cardiovascular and cerebrovascular risk. Full article

Inflammation and congestion are key pathophysiological processes in heart failure (HF). Our aim was to evaluate the potential modulatory effect of carbohydrate antigen 125 (CA125) on inflammation, assessed by high-sensitivity C-reactive protein (hs-CRP). We analyzed a cohort of 4043 consecutive patients in whom hs-CRP and CA125 levels were measured during a hospitalization for acute HF. Multivariate Cox regression models were applied to assess the association between the biomarkers and all-cause mortality and death/HF rehospitalization at 6 months. In multivariable analysis, a significant interaction between hs-CRP and CA125 was observed for both outcomes (p-value for interaction = 0.036 and <0.001, respectively). hs-CRP was significantly associated with an increased risk of death (HR = 1.27; 95% CI 1.16–1.41; p < 0.001) and death/HF rehospitalization (HR = 1.18; 95% CI 1.09–1.28; p < 0.001) if CA125 > 35 U/mL. In contrast, hs-CRP was not predictive of events when CA125 ≤ 35 U/mL. In conclusion, in patients with acute HF, the association between hs-CRP and clinical outcomes was modulated by CA125 levels. hs-CRP was associated with a higher risk of events only in patients with elevated CA125. These findings support a potential modulatory and amplifying role for CA125 in the inflammatory response in HF. Full article

To characterize changes in markers of oxidative stress for the clinical evaluation of patients with long COVID, we assessed oxidative stress and antioxidant activity based on serum samples from patients who visited our clinic between May and November 2024. Seventy-seven patients with long COVID (41 [53%] females and 36 [47%] males; median age, 44 years) were included. Median [interquartile range] serum levels of diacron-reactive oxygen metabolites (d-ROM; CARR Unit), biological antioxidant potential (BAP; μmol/L), and oxidative stress index (OSI) were 533.8 [454.9–627.6], 2385.8 [2169.2–2558.1] and 2.0 [1.7–2.5], respectively. Levels of d-ROMs (579.8 vs. 462.2) and OSI (2.3 vs. 1.8), but not BAP (2403.4 vs. 2352.6), were significantly higher in females than in males. OSI levels positively correlated with age and body mass index, whereas BAP levels negatively correlated with these parameters. d-ROM and OSI levels were significantly associated with inflammatory markers, including C-reactive protein (CRP) and fibrinogen, whereas BAP levels were inversely correlated with CRP and ferritin levels. Notably, serum free thyroxine levels were negatively correlated with d-ROMs and OSI, whereas cortisol levels were positively correlated with d-ROMs. Among long COVID symptoms, patients reporting brain fog exhibited significantly higher OSI levels (2.2 vs. 1.8), particularly among females (d-ROMs: 625.6 vs. 513.0; OSI: 2.4 vs. 2.0). The optimal OSI cut-off values were determined to be 1.32 for distinguishing long COVID from healthy controls and 1.92 for identifying brain fog among patients with long COVID. These findings suggest that oxidative stress markers may serve as indicators for the presence or prediction of psycho-neurological symptoms associated with long COVID in a gender-dependent manner. Full article

Statins, primarily prescribed for their lipid-lowering effects, have garnered significant attention for their potent anti-inflammatory effects. This review explores the underlying molecular pathways and clinical relevance of statins’ anti-inflammatory actions, extending beyond cardiovascular disease management to chronic inflammatory conditions and oncological applications. The lipid-lowering effect of statins stems from their ability to suppress HMG-CoA reductase, a crucial enzyme in cholesterol synthesis; however, their pleiotropic effects include modulation of critical inflammatory pathways such as the inhibition of NF-κB signalling, a reduction in pro-inflammatory cytokine production, and enhancement of endothelial function. We delve into the molecular pathways influenced by statins, including their effects on inflammatory mediators like C-reactive protein (CRP), interleukins (IL-6, IL-1β), and tumour necrosis factor-alpha (TNF-α). Clinical evidence supporting the efficacy of statins in managing chronic inflammatory diseases, such as rheumatoid arthritis, chronic obstructive pulmonary disease, diabetes, and osteoarthritis, is critically reviewed. Additionally, we investigate the emerging role of statins in oncology, examining their impact on inflammation-driven carcinogenesis, tumour microenvironment modulation, and cancer progression. Despite their broad therapeutic potential, the safety profile of statins, particularly concerning adverse effects such as myopathy, hepatotoxicity, and potential diabetes risk, is discussed. Controversies surrounding the extent of their anti-inflammatory benefits and the variability in patient responses are also addressed. This review consolidates the current literature, elucidating the biochemical mechanisms underlying the anti-inflammatory properties of statins and evaluating their clinical applications and associated controversies. Future research directions are identified, including the development of novel statin analogues with enhanced anti-inflammatory effects and the investigation of new therapeutic indications in inflammatory diseases and cancer. By providing an in-depth analysis, this review underscores the expanding therapeutic scope of statins and advocates for their integration into broader clinical strategies for the management of inflammation and cancer. Full article

Background/Objectives: Chronic exercise training reduces markers of systemic inflammation; however, less is known about how to optimize this adaptation using nutrition. Dairy products, especially fermented ones, like Greek yogurt (GY), contain anti-inflammatory constituents. This secondary analysis aimed to examine the influence of post-exercise GY consumption vs. an isoenergetic carbohydrate pudding (CP; control) on markers of systemic inflammation during an exercise training intervention. Methods: Thirty healthy young males completed 12 weeks of resistance and plyometric exercise training and were randomized to consume GY (n = 15) or CP (n = 15). Rested/fasted blood samples were acquired at baseline, and weeks 1 and 12, and inflammatory biomarkers (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-6, IL-1 receptor antagonist [IL-1ra], IL-1Beta [IL-1β], IL-10, and C-reactive protein [CRP]) were measured. Linear mixed models were run on the absolute concentrations, and linear regressions were performed on the absolute change (baseline to week 12), allowing us to account for important covariates. Results: In both groups, CRP (pro) and IL-1ra (anti) increased at week 1 vs. baseline and week 12, while IL-1β (pro) decreased at week 12 vs. baseline (main time effects). We observed significant interactions for IL-6, TNF-α, and the TNF-α/IL-10 ratio, indicating that at week 12, IL-6 (pro) was lower in GY, whereas TNF-α and TNF-α/IL-10 (both pro-inflammatory) were higher in CP vs. week 1 and baseline, respectively. Additionally, within our linear regression models, higher baseline concentrations of IL-1ra (anti), IL-10 (anti) and CRP (pro) predicted greater change over the intervention. Conclusions: These results indicate that our intervention benefited circulating inflammatory markers, and GY supplementation may enhance these effects. Full article

Background: Metabolic syndrome (MS) and obstructive sleep apnea (OSA) frequently coexist, exacerbating systemic inflammation, oxidative stress, and metabolic dysregulation. This study evaluates the effects of dietary and probiotic interventions, compared to a non-intervention control group, on metabolic, hemodynamic, and neurochemical parameters, with a specific focus on the neurotransmitters GABA and glutamate. Methods: In a prospective randomized study (2020–2023), 120 patients with coexisting MS and OSA were assigned to three groups: control (n = 36), diet therapy (n = 42), and diet therapy combined with probiotics (n = 42). Interventions lasted six months and included personalized dietary plans and probiotic supplementation. Outcome measures included BMI, visceral fat, HOMA index, lipid profile, oxygen saturation, and urinary GABA and glutamate levels. Unsupervised K-means clustering and principal component analysis (PCA) were applied to identify phenotypic response patterns based on delta values. Results: Diet therapy led to significant reductions in BMI (−15.7%, p = 0.001), visceral fat (−17.3%, p = 0.001), triglycerides (−14.6%, p = 0.003), uric acid (−9.5%, p = 0.011), and C-reactive protein (CRP) (−21.4%, p = 0.007). The combined intervention group exhibited further improvements in visceral fat (−22.8%, p = 0.001), glutamate (−18.2%, p = 0.002), and GABA levels (+19.5%, p = 0.001). Oxygen saturation improved across all groups, with the greatest increase in the probiotics group (+2.3%). Clustering analysis revealed three distinct response phenotypes—strong, moderate, and non-responders—highlighting inter-individual variability in treatment efficacy. Conclusions: Personalized dietary interventions, especially when paired with probiotics, effectively improve metabolic, inflammatory, and neurochemical profiles in patients with MS and OSA. Integrating clustering algorithms enables phenotype-specific stratification, offering a step toward precision lifestyle medicine. Future studies should explore long-term outcomes and refine microbiota-targeted approaches to optimize intervention efficacy. Full article

Background and Objectives: Obstructive sleep apnea (OSA) represents an increasing public health concern, closely linked with cardiovascular, metabolic, and neurocognitive disorders, as well as impaired quality of life. The complex pathophysiology of OSA involves upper airway dysfunction, oxidative stress, and inflammation, with endothelial dysfunction considered central to its associated comorbidities. Despite notable advances in OSA research, the biological mechanisms driving these complications remain insufficiently understood. The present study aimed to examine the associations between redox status, proinflammatory biomarkers, and the gene expression of full-length receptor for advanced glycation end products (flRAGE) and transforming growth factor beta 1 (TGF-β1) in relation to the presence and severity of OSA. Materials and Methods: The study cohort comprised 125 participants with diagnosed OSA and 42 controls without evidence of OSA. General and clinical characteristics were recorded for all participants. Laboratory analyses included the assessment of redox and inflammatory markers in serum and plasma, while flRAGE and TGF-β1 messenger ribonucleic acids (mRNA) were quantified in peripheral blood mononuclear cells. Results: Patients with OSA demonstrated elevated oxidative stress and inflammation, characterized by increased total antioxidant status (TAS) and C-reactive protein CRP levels, together with reduced concentrations of soluble RAGE (sRAGE). The severity of OSA, indicated by the apnea-hypopnea index, increases total oxidative status (TOS) and TGF-β1 mRNA, while sRAGE decreases. The sRAGE–ROS-related factor was negatively associated with OSA, whereas the redox status factor showed a positive association. TOS was independently and positively correlated with OSA severity. Conclusions: Individuals with OSA exhibit a state of enhanced oxidative stress and inflammation. Increasing severity of OSA was associated with rising TOS and TGF-β1 mRNA expression, accompanied by declining sRAGE concentrations. A combined redox–inflammatory biomarker profile was found to be associated with both the presence and severity of OSA. Full article

Background: Inflammation and nutritional status are known to affect outcomes in patients with chronic obstructive pulmonary disease (COPD). However, their prognostic relevance in critically ill COPD patients remains unclear. This study investigated whether C-reactive protein (CRP), serum albumin, and the CRP/albumin ratio (CAR) were associated with in-hospital mortality in ICU patients with COPD. Methods: We conducted a retrospective cohort study using data from the MIMIC-IV database. Adult ICU patients with a diagnosis of COPD were included. We analyzed CRP, albumin, CAR, glucose, lactate, and creatinine. The primary outcome was in-hospital mortality. Multivariable logistic regression was used to identify variables that were independently associated with in-hospital mortality. Subgroup analyses stratified by age and sex were performed. Results: We included 1000 ICU patients with COPD. In-hospital mortality was 19.6%. In univariate analyses, glucose, creatinine, and lactate levels were significantly higher in non-survivors. In multivariable models, only elevated creatinine (OR 1.60, 95% CI 1.01–2.53) remained independently associated with mortality, while glucose was no longer statistically significant. CRP, albumin, and CAR were not significantly associated with in-hospital mortality. Subgroup analyses showed consistent results across age and sex strata. Conclusion: In critically ill COPD patients, glucose and creatinine levels upon ICU admission were independently associated with in-hospital mortality, whereas inflammation- and nutrition-related markers, such as CRP, albumin, and CAR, were not. However, given that albumin is heavily influenced by systemic inflammation, it cannot serve as a standalone nutritional marker in the ICU setting. Composite nutritional scores such as the Nutritional Risk Screening (NRS-2002) or the Global Leadership Initiative on Malnutrition (GLIM), which were not available in the MIMIC-IV database, may provide more accurate assessments. These findings highlight the need for integrated risk models incorporating metabolic and renal parameters for early prognostication. Full article