Background: A link between inflammation and venous thromboembolism (VTE) in COVID-19 disease has been suggested pathophysiologically and clinically. The aim of this study was to investigate the association between inflammation and disease outcomes in adult hospitalized COVID-19 patients with VTE. Methods: This was a retrospective observational study, including quantitative and qualitative data collected from COVID-19 patients hospitalized at the Infectious Diseases Unit (IDU) of the University Hospital of Ioannina, from 1 March 2020 to 31 May 2022. Venous thromboembolism was defined as a diagnosis of pulmonary embolism (PE) and/or vascular tree-in-bud in the lungs. The burden of disease, assessed by computed tomography of the lungs (CTBoD), was quantified as the percentage (%) of the affected lung parenchyma. The study outcomes were defined as death, intubation, and length of hospital stay (LoS). A chi-squared test and univariate logistic regression analyses were performed in IBM SPSS 28.0. Results: After propensity score matching, the final study cohort included 532 patients. VTE was found in 11.2% of the total population. In patients with VTE, we found that lymphocytopenia and a high neutrophil/lymphocyte ratio were associated with an increased risk of intubation and death, respectively. Similarly, CTBoD > 50% was associated with a higher risk of intubation and death in this group of patients. The triglyceride–glucose (TyG) index was also linked to worse outcomes. Conclusions: Inflammatory indices were associated with VTE. Lymphocytopenia and an increased neutrophil-to-lymphocyte ratio negatively impacted the disease’s prognosis and outcomes. Whether these indices unfavorably affect outcomes in COVID-19-associated VTE must be further evaluated.

In cases of SARS-CoV-2 hospitalization, despite low bacterial co-infection rates, antimicrobial use may be disproportionately high. Our aim was to quantify such usage in COVID-19 patients and identify factors linked to increased antibiotic use. We retrospectively studied patients with SARS-CoV-2 infection who were hospitalized at our institution during the pandemic. In the initial two waves of the pandemic, antimicrobial use was notably high (89% in the first wave and 92% in the second), but it decreased in subsequent waves. Elevated procalcitonin (>0.5 μg/mL) and C-reactive protein (>100 mg/L) levels were linked to antibiotic usage, while prior vaccination reduced antibiotic incidence. Antimicrobial use decreased in the pandemic, suggesting enhanced comprehension of SARS-CoV-2′s natural course. Additionally, it was correlated with heightened SARS-CoV-2 severity, elevated procalcitonin, and C-reactive protein levels.

The gut–liver axis is central to the systemic complications of liver cirrhosis, but it is usually described as a linear cascade in which barrier failure releases microbial products that activate a downstream immune response. This review proposes instead a four-compartment framework, in which the epithelial/barrier, innate immune, adaptive effector, and stromal–endothelial compartments—the last including the gut–vascular barrier—are treated as reciprocally interacting nodes, and pathological bacterial translocation is treated as both an input to and an output of the network rather than as its endpoint. Applying this framework across the stages of cirrhosis, we examine how tight-junction disassembly, mucus-layer thinning, Paneth-cell dysfunction and reduced secretory IgA, together with dysbiosis and small-intestinal bacterial overgrowth, permit translocation; how translocated bacteria and pathogen-associated molecular patterns activate all four compartments; and how the resulting cytokine circuits further degrade the barrier, generating feed-forward loops that underlie cirrhosis-associated immune dysfunction and chronic systemic inflammation. We relate these circuits to spontaneous bacterial peritonitis, hepatic encephalopathy, aggravated portal hypertension, and acute-on-chronic liver failure, distinguishing throughout between mechanisms demonstrated in humans and those inferred from animal or in vitro models. We identified evidence through structured searches of PubMed/MEDLINE, Embase, and Web of Science, and report it according to the SANRA checklist. Framed as a network, biomarkers become compartment-specific reporters, and barrier-, microbiome-, and immune-directed therapies become interventions at defined nodes and edges—a view that clarifies both their rationale and the current limits of the evidence.