SARS-CoV-2 infection might cause a critical disease, and patients’ follow-up is based on multiple parameters. Oxidative stress is one of the key factors in the pathogenesis of COVID-19 suggesting that its level could be a prognostic marker. Therefore, we elucidated the predictive value of the serum non-enzymatic total antioxidant capacity (TAC) and that of the newly introduced TAC/lymphocyte ratio in COVID-19. We included 61 COVID-19 (n = 27 ward, n = 34 intensive care unit, ICU) patients and 29 controls in our study. Serum TAC on admission was measured by an enhanced chemiluminescence (ECL) microplate assay previously validated by our research group. TAC levels were higher (p < 0.01) in ICU (median: 407.88 µmol/L) than in ward patients (315.44 µmol/L) and controls (296.60 µmol/L). Besides the classical parameters, both the TAC/lymphocyte ratio and TAC had significant predictive values regarding the severity (AUC-ROC for the TAC/lymphocyte ratio: 0.811; for TAC: 0.728) and acute kidney injury (AUC-ROC for the TAC/lymphocyte ratio: 0.747; for TAC: 0.733) in COVID-19. Moreover, the TAC/lymphocyte ratio had significant predictive value regarding mortality (AUC-ROC: 0.752). Serum TAC and the TAC/lymphocyte ratio might offer valuable information regarding the severity of COVID-19. TAC measured by our ECL microplate assay serves as a promising marker for the prediction of systemic inflammatory diseases.

Long-COVID syndrome is associated with high healthcare costs, but its pathophysiology is not yet fully understood. Inflammation, renal impairment or disturbance of the NO system emerge as potential pathogenetic factors. We aimed to investigate the relationship between symptoms of long-COVID syndrome and serum levels of cystatin-c (CYSC), orosomucoid (ORM), l-arginine, symmetric dimethylarginine (SDMA) and asymmetric dimethylarginine (ADMA). A total of 114 patients suffering from long-COVID syndrome were included in this observational cohort study. We found that serum CYSC was independently associated with the anti-spike immunoglobulin (S-Ig) serum level (OR: 5.377, 95% CI: 1.822–12.361; p = 0.02), while serum ORM (OR: 9.670 (95% CI: 1.34–9.93; p = 0.025) independently predicted fatigue in patients with long-COVID syndrome, both measured at baseline visit. Additionally, the serum CYSC concentrations measured at the baseline visit showed a positive correlation with the serum SDMA levels. The severity of abdominal and muscle pain indicated by patients at the baseline visit showed a negative correlation with the serum level of L-arginine. In summary, serum CYSC may indicate subclinical renal impairment, while serum ORM is associated with fatigue in long-COVID syndrome. The potential role of l-arginine in alleviating pain requires further studies.

The pathophysiology and consequences of early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (aSAH) remain incompletely understood. This study aims to investigate the role of orosomucoid (ORM) in aSAH, its potential as a marker for assessing the extent of EBI-induced damage, and its correlation with delayed cerebral ischemia (DCI) and functional recovery over a 3-month period. We collected serum specimens 72 h post-aSAH to measure ORM levels. The study included 151 aSAH patients and 105 healthy subjects. The serum ORM levels within the patient cohort significantly exceeded those in the control group (p < 0.001). The ORM value showed significant correlation with the admission WFNS (p < 0.0001) and mFS scores (p < 0.05). Substantially elevated serum ORM levels at 72 h post-aSAH were detected among patients experiencing DCI, as well as those with poor functional outcomes after 3 months (p = 0.009 and p < 0.001). Binary logistic regression analyses revealed that serum ORM at 72 h post-SAH was independently associated with DCI and 3-month functional outcome after adjusting for confounders. The early stage events of aSAH influence the level of ORM. ORM serves as a marker for assessing the extent of damage during EBI and is linked to the occurrence of DCI as well as unfavorable long-term functional outcomes.

A major complication of sepsis is the development of acute kidney injury (AKI). In case of acute tubular damage, Gc-globulin, a known serum sepsis marker is increasingly filtrated into the urine therefore, urinary Gc-globulin (u-Gc) levels may predict septic AKI. We developed and validated a competitive fluorescence ELISA method for u-Gc measurement. Serum and urine samples from septic patients were collected in three consecutive days (T1, T2, T3) and data were compared to controls. Intra- and interassay imprecisions were CV < 14% and CV < 20%, respectively, with a recovery close to 100%. Controls and septic patients differed (p < 0.001) in their u-Gc/u-creatinine levels at admission (T1, median: 0.51 vs. 79.1 µg/mmol), T2 (median: 0.51 vs. 57.8 µg/mmol) and T3 (median: 0.51 vs. 55.6 µg/mmol). Septic patients with AKI expressed higher u-Gc/u-creatinine values than those without AKI at T1 (median: 23.6 vs. 136.5 µg/mmol, p < 0.01) and T3 (median: 34.4 vs. 75.8 µg/mmol, p < 0.05). AKI-2 stage patients exhibited more increased u-Gc/u-creatinine levels at T1 (median: 207.1 vs. 53.3 µg/mmol, p < 0.05) than AKI-1 stage individuals. Moderate correlations (p < 0.001) were observed between u-Gc/u-creatinine and se-urea, se-creatinine, se-hsCRP, WBC, u-total protein, u-albumin, u-orosomucoid/u-creatinine, and u-Cystatin C/u-creatinine levels. U-Gc testing may have a predictive value for AKI in septic patients.

Background/Objectives: Sepsis is a life-threatening syndrome characterized by a dysregulated host response to infection, commonly accompanied by hypoalbuminemia (<30 g/L serum albumin level), associated with excessive production of reactive oxygen and nitrogen species, leading to oxidative stress, endothelial dysfunction, and organ injury. Low serum albumin reflects increased vascular permeability, reduced hepatic synthesis, and enhanced proteolysis. It also indicates the loss of albumin’s antioxidant and anti-inflammatory functions beyond oncotic regulation. Hypoalbuminemia may exacerbate this by reducing plasma antioxidant capacity and free radical scavenging, supporting interest in albumin supplementation as a potential therapeutic strategy. Methods: This prospective, randomized study investigated the effects of 3-day albumin administration in ICU patients (n = 38) with sepsis and hypoalbuminemia by assessing changes in oxidative stress and inflammatory markers. Results: Albumin supplementation increased serum albumin (p < 0.001) and was associated with higher total antioxidant capacity (Day 3 p = 0.045; Day 5 p = 0.004), glutathione levels (Day 3 p = 0.003; Day 5 p = 0.008), and protein sulfhydryl groups (Day 3–5 p = 0.004). Albumin-treated patients showed increased urinary concentration of the oxidative stress–related tyrosine isomers ortho- and meta-tyrosine (p = 0.004 and p = 0.001, respectively). Catalase activity and myeloperoxidase, procalcitonin, and IL-1β levels did not differ between groups, while IL-6 declined over time (p = 0.029). Conclusions: Based on our results, in septic patients with hypoalbuminemia, short-term albumin supplementation seems to restore serum albumin and improve systemic redox status, as evidenced by increased total antioxidant capacity, glutathione, and protein sulfhydryl levels. However, albumin supplementation did not significantly affect systemic inflammatory markers or cytokine dynamics. Albumin appears to act primarily by modulating oxidative stress, supporting its role as an adjunctive therapy to restore redox homeostasis in sepsis.

Background: The actin-binding protein Flightless-I (Flii) has not been quantified in the human serum yet. We aimed to determine serum Flii levels in healthy individuals and to investigate Flii as a potential marker in patients with sepsis focusing on diagnosis, organ failures, and short-term mortality. Methods: A total of 30 controls and 64 septic and 22 non-septic patients were enrolled in this follow-up study. Serum Flii levels were quantified by using the capillary electrophoresis-based Simple Western™ system with chemiluminescent detection. The assay was calibrated by applying dilution series of a purified recombinant human Flii standard and a parallel internal standard. Results: Flii levels of healthy controls were found between 3.5 and 8.8 mg/L, while septic and non-septic patients showed significantly lower values (p < 0.001). First-day Flii could differentiate sepsis from the non-septic inflammatory state (AUC: 0.667; p < 0.05) and indicated acute respiratory distress syndrome (ARDS) among septic patients (AUC: 0.686; p < 0.05). Furthermore, a combination of Flii and other sepsis markers seemed to offer an improved diagnostic performance (sepsis vs. non-sepsis, AUC of Flii + gelsolin (GSN) + Gc-globulin + procalcitonin: 0.974; p < 0.001 and ARDS vs. non-ARDS, AUC of Flii + GSN + presepsin: 0.776; p < 0.001) compared with single markers even in the prediction of 14-day mortality (AUC of Flii + GSN + Gc-globulin: 0.76; p < 0.001). Conclusions: We adapted a properly precise and reproducible automated Western blot method to determine concentrations of Flii in human serum. Our results revealed the relationship between Flii and sepsis; however, Flii alone did not appear to be a prominent sepsis marker. When combined with other biomarkers, measurement of serum Flightless-I may provide additional value supporting patient care.