Endothelin-1 (ET-1) is a potent vasoconstrictor produced by endothelial cells and cleared from circulating blood mainly in the pulmonary vasculature. In a healthy pulmonary circulation, the rate of local production of ET-1 is less than its rate of clearance. In the present study, we aimed to investigate whether the abnormal pulmonary circulatory handling of ET-1 relates to poor clinical outcomes in patients with coronavirus disease 2019 (COVID-19)-induced acute respiratory distress syndrome (ARDS). To this end, central venous and systemic arterial ET-1 plasma levels were simultaneously measured on Days 1 and 3 following ICU admission in mechanically ventilated COVID-19 patients with ARDS (COVID-19 ARDS, N = 18). Central venous and systemic arterial ET-1 plasma levels were also measured in two distinct SARS-CoV-2-negative mechanically ventilated critically ill patient groups, matched for age, sex, and critical illness severity, with ARDS (non-COVID-19 ARDS, N = 14) or without ARDS (non-COVID-19 non-ARDS, N = 20). Upon ICU admission, COVID-19-induced ARDS patients had higher systemic arterial and central venous ET-1 levels compared to the non-COVID-19 ARDS and non-COVID-19 non-ARDS patients (p < 0.05), yet a normal systemic arterial:central venous (A:V) ET-1 ratio [0.63 (0.49–1.02)], suggesting that pulmonary ET-1 clearance is intact in these patients. On the other hand, the non-COVID-19 ARDS patients demonstrated abnormal ET-1 handling [A:V ET-1 ratio 1.06 (0.93–1.20)], while the non-COVID-19 non-ARDS group showed normal ET-1 handling [0.79 (0.52–1.11)]. On Day 3, the A:V ratio in all three groups was <1. When the COVID-19 ARDS patients were divided based on 28-day ICU mortality, while their systemic arterial and central venous levels did not differ, the A:V ET-1 ratio was statistically significantly higher upon ICU admission in the non-survivors [0.95 (0.78–1.34)] compared to the survivors [0.57 (0.48–0.92), p = 0.027]. Our results highlight the potential importance of ET-1 as both a biomarker and a therapeutic target in critically ill COVID-19 patients. The elevated A:V ET-1 ratio in non-survivors suggests that the early disruption of pulmonary ET-1 handling may be a key marker of poor prognosis.

The outbreak of the new coronavirus strain SARS-CoV-2 (COVID-19) highlighted the need for appropriate feeding practices among critically ill patients admitted to the intensive care unit (ICU). This study aimed to describe feeding practices of intubated COVID-19 patients during their second week of hospitalization in the First Department of Critical Care Medicine, Evaggelismos General Hospital, and evaluate potential associations with all cause 30-day mortality, length of hospital stay, and duration of mechanical ventilation. We enrolled adult intubated COVID-19 patients admitted to the ICU between September 2020 and July 2021 and prospectively monitored until their hospital discharge. Of the 162 patients analyzed (52.8% men, 51.6% overweight/obese, mean age 63.2 ± 11.9 years), 27.2% of patients used parenteral nutrition, while the rest were fed enterally. By 30 days, 34.2% of the patients in the parenteral group had died compared to 32.7% of the patients in the enteral group (relative risk (RR) for the group receiving enteral nutrition = 0.97, 95% confidence interval = 0.88–1.06, p = 0.120). Those in the enteral group demonstrated a lower duration of hospital stay (RR = 0.91, 95% CI = 0.85-0.97, p = 0.036) as well as mechanical ventilation support (RR = 0.94, 95% CI = 0.89–0.99, p = 0.043). Enteral feeding during second week of ICU hospitalization may be associated with a shorter duration of hospitalization and stay in mechanical ventilation support among critically ill intubated patients with COVID-19.

Endothelin-1 (ET-1) is a potent vasoconstrictor produced by endothelial cells and cleared from circulating blood mainly in the pulmonary vasculature. In a healthy pulmonary circulation, the rate of local production of ET-1 is less than its rate of clearance. In the present study we aimed to investigate whether abnormal pulmonary circulatory handling of ET-1 relates to poor clinical outcomes in patients with COVID-19-induced ARDS. Plasma ET-1 levels were measured in 18 mechanically ventilated COVID-19-induced ARDS patients, with simultaneous central venous and systemic arterial blood sampling on Days 1 and 3 following ICU admission. Two age- and sex-matched non-COVID-19 control groups were also used [mechanically ventilated non-COVID-19 critically ill and ARDS patients]. On ICU admission, COVID-19-induced ARDS patients had higher systemic arterial and venous ET-1 levels compared to non-COVID-19 ARDS and critically ill patients (p< 0.05). The arterial:venous (A:V) ET-1 ratio was higher in the non-COVID-19 ARDS patients [1.06 (0.93-1.20)] compared to the other two groups (p< 0.05). The A:V ratio was 0.63 (0.49-1.02) in the COVID-19-induced ARDS patients and 0.79 (0.52-1.11) in the non-COVID-19 critically ill patients. On Day 3, the A:V ratio in all three groups was < 1. The COVID-19 patient group was then divided based on 28-day ICU mortality. Although arterial and venous levels did not differ, the A:V ratio was statistically significantly higher on ICU admission in the non-survivors [0.95 (0.78-1.34)] vs 0.57 (0.48-0.92), p= 0.027]. Measurement of ET-1 clearance via A:V plasma ET-1 levels on ICU admission may assist in predicting outcomes in COVID-19 critically ill patients.

Adipose tissue has emerged as a pivotal endocrine organ, secreting bioactive proteins termed adipokines that regulate metabolic and immune processes across multiple organ systems. In the context of sepsis and critical illness, conditions defined by a dysregulated host response to infection with life-threatening organ dysfunction, the role of novel adipokines has attracted considerable research interest. This review focuses on three novel adipokines, chemerin, vaspin (SERPINA12), and omentin-1 (intelectin-1). We will discuss current in vitro, in vivo experimental animal models, and clinical evidence, emphasizing their biology, mechanisms of action, and potential as diagnostic and prognostic biomarkers in critically ill patients. All three adipokines are elevated in sepsis compared with healthy controls and correlate with established severity scores, including APACHE II and SOFA. Chemerin and omentin-1 have both been independently associated with 28-day mortality in prospective cohort studies. Vaspin exhibits robust cardioprotective effects in murine sepsis models via inhibition of kallikrein 7 (KLK7) and attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI) both in vitro and in vivo. Omentin-1 suppresses LPS-induced macrophage activation through TLR4/MyD88/NF-κB inhibition in vitro and protects against LPS-induced ALI in murine models. Despite these promising findings, substantial methodological heterogeneity and limited large-scale clinical data currently preclude clinical implementation. Future research that standardizes assays, expands to multicenter cohorts, and investigates therapeutic modulation of these pathways is urgently needed.

Adipose tissue has emerged as a pivotal endocrine organ, secreting bioactive proteins termed adipokines that regulate metabolic and immune processes across multiple organ systems. In the context of sepsis and critical illness, conditions defined by a dysregulated host response to infection with life-threatening organ dysfunction, the role of novel adipokines has attracted considerable research interest. This review focuses on three novel adipokines: chemerin, vaspin (SERPINA12), and omentin-1 (intelectin-1). We will discuss current in vitro, in vivo experimental animal models, and clinical evidence, emphasizing their biology, mechanisms of action, and potential as diagnostic and prognostic biomarkers in critically ill patients. All three adipokines are elevated in sepsis compared with healthy controls and correlate with established severity scores, including APACHE II and SOFA. Chemerin and omentin-1 have both been independently associated with 28-day mortality in prospective cohort studies. Vaspin exhibits robust cardioprotective effects in murine sepsis models via inhibition of kallikrein 7 (KLK7) and attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI) both in vitro and in vivo. Omentin-1 suppresses LPS-induced macrophage activation through TLR4/MyD88/NF-κB inhibition in vitro and protects against LPS-induced ALI in murine models. Despite these promising findings, substantial methodological heterogeneity and limited large-scale clinical data currently preclude clinical implementation. Future research that standardizes assays, expands to multicenter cohorts, and investigates therapeutic modulation of these pathways is urgently needed.

Background/Objectives: Adipokines are candidate biomarkers in critical illness due to their roles in immunity and metabolism, both profoundly altered in sepsis. Omentin-1, vaspin, and chemerin have been studied in selected septic cohorts, but not concurrently in a heterogeneous ICU population including both septic and non-septic patients. Methods: Prospective observational cohort of 200 consecutive ICU patients with 28-day follow-up. Biomarkers were measured by ELISA within 24 h of admission. Analyses included Mann–Whitney U tests, Spearman correlations, ROC curves, and logistic regression with APACHE II and SOFA as comparators. Results: Vaspin was significantly higher in septic versus non-septic patients (406.4 [190.0–799.6] vs. 275.8 [101.8–559.8] pg/mL; p = 0.009). Omentin-1 was elevated in 28-day non-survivors (34.4 [22.5–56.1] vs. 25.1 [15.0–48.4] ng/mL; p = 0.037; AUROC 0.599), but lost significance after APACHE II adjustment (p = 0.295). Chemerin trended lower in non-survivors (p = 0.099); in septic patients, it correlated inversely with SOFA (r = −0.43) and lactate (r = −0.40), both p < 0.001. IL-6 and IL-10 were higher in non-survivors; IL-10 predicted 28-day mortality (AUROC 0.783), comparable to APACHE II (0.785). Conclusions: Vaspin distinguishes sepsis in mixed ICU populations. Omentin-1 shows a severity-driven association with mortality that does not survive APACHE II adjustment (AUROC 0.599, poor standalone discrimination), while chemerin inversely tracks hypoperfusion markers in septic patients, suggesting a potential counter-regulatory role requiring mechanistic confirmation. Individually, these adipokines do not add prognostic value beyond established severity scores, but their biological orthogonality to classical cytokines warrants exploration in multi-marker panel studies.