Coronavirus disease-19 (COVID-19) continues to be a health threat worldwide. Increased blood lactate is common in intensive care unit (ICU) patients; however, its association with outcomes in ICU COVID-19 patients remains currently unexplored. In this retrospective, observational study we assessed whether lactate is associated with outcomes in COVID-19 patients. Blood lactate was measured on ICU admission and thereafter daily up to day 14 in 45 patients with confirmed COVID-19 pneumonia. Acute physiology and chronic health evaluation (APACHE II) was calculated on ICU admission, and sequential organ failure assessment (SOFA) score was assessed on admission and every second day. The cohort was divided into survivors and non-survivors based on 28-day ICU mortality (24.4%). Cox regression analysis revealed that maximum lactate on admission was independently related to 28-day ICU mortality with time in the presence of APACHE II (RR = 2.45, p = 0.008). Lactate’s area under the curve for detecting 28-day ICU mortality was 0.77 (p = 0.008). Mixed model analysis showed that mean daily lactate levels were higher in non-survivors (p < 0.0001); the model applied on SOFA scores showed a similar time pattern. Thus, initial blood lactate was an independent outcome predictor in COVID-19 ICU patients. The time course of lactate mirrors organ dysfunction and is associated with poor clinical outcomes.

Group 1 of PAH patients encompasses patients with a diverse underlying etiological condition, having histological modifications that can affect gas exchange across the alveolar-capillary membrane, as reflected by decreased DLCO. Values of DLCO did not identify the exact reason for their decrease, but they can provide insights into the underlying pathobiology and prognosis of PAH patients. Our aim was to explore whether PAH patients with low DLCO constitute a different subpopulation and describe their characteristics and response to treatment. A total of 69 PAH patients were studied retrospectively and divided into two groups: group 1: DLCO ≥ 45% and group 2: DLCO < 45%. IPAH and PAH-CTD mainly constituted our population. The proportion of IPAH to PAH-CTD was almost the same between the two groups. Patients in group 2 were older (66.83 ± 11.61 vs. 59.27 ± 111.90, p = 0.035), mostly male (47.5% vs. 11.5% p = 0.008), and ever smokers (59% vs. 22%, p = 0.049). They mainly had WHO-FC III (68% vs. 32%) and had received more advanced therapy (40% on triple combination therapy vs. 16%). The two groups had similar mean PAP (group 1 = 32 (22.00–38.00) vs. group 2 = 35 (28.50–48.50) mmHg), while PVR was higher in group 2 (6.49 (4.10–9.52) vs. 3.61 (2.95–5.22) WU). In group 2, neither IPAH nor PAH-CTD patients improved WHO-FC, 6MWD, or NT-proBNP after treatment. In our center, PAH patients with low DLCO had some distinct clinical characteristics, such as poor prognosis and poor treatment response to vasodilatory therapy. Understanding the role of DLCO in both phenotyping PAH patients and in treatment response would be useful in guiding therapeutic approaches, especially now that new therapeutic targets are involved in PAH treatment.

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.

Group of PAH patients encompasses patients with a diverse underlying aetiological condition, having histological modifications that can affect gas exchange across the alveolar-capillary membrane as it is reflected by decreased DLCO. DLCO values did not identify the exact reason of its decrease, but can provide insights into the underlying pathobiology and prognosis of PAH patients. Our aim was to explore if PAH patients with low DLCO constitute a different subpopulation and describe their characteristics and response to treatment. 69 PAH patients were studied retrospectively and divided into group1: DLCO≥45% and group2: DLCO< 45%. IPAH and PAH-CTD constituted mainly our population. The proportion of IPAH and PAH-CTD was almost the same. Patients in group 2 were older (66.83± 11.61 vs 59.27±111.90, p=0.035), more often male (47.5% vs 11.5% p=0.008) and ever smokers (59% vs 22%, p=0.049). They had mainly WHO-FC III ((68%) vs 32%) and have received more advanced therapy (40% on triple combination therapy vs 16%). The two groups had the same mean PAP (group1=32 (22.00-38.00) vs group2=35 (28.50-48.50) mmHg) and PVR was higher in group 2 (6.49(4.10-9.52) vs 3.61 (2.95-5.22) WU). In group 2 neither IPAH nor PAH-CTD patients did improve WHO-FC, 6MWD, or NT-proBNP after treatment. In our centre PAH patients with low DLCO have some distinct clinical characteristics. poor prognosis and treatment response in vasodilatory therapy. Understanding the role of DLCO in phenotyping PAH patient and in treatment response would be useful in guide therapeutic approaches, especially now that new therapeutic targets are involved in the PAH treatment.

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.

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.