Sepsis is a critical condition resulting from the excessive activation of the inflammatory/immune system in response to an infection, with high mortality if treatment is not administered promptly. One of the many possible complications of sepsis is liver dysfunction with consequent cholestasis. The aim of this paper is to review the main mechanisms involved in the development of cholestasis in sepsis. Cholestasis in a septic patient must raise the suspicion that it is the consequence of the septic condition and limit the laborious attempts of finding a hepatic or biliary disease. Prompt antibiotic administration when sepsis is suspected is essential and may improve liver enzymes. Cholestasis is a syndrome with a variety of etiologies, among which sepsis is frequently overlooked, despite a number of studies and case reports in the literature demonstrating not only the association between sepsis and cholestasis but also the role of cholestasis as a prognostic factor for sepsis‐induced death.

As presepsin levels increase with kidney dysfunction (KD), our aim was to establish cutoff points for presepsin adapted to the level of KD in order to avoid bacterial infection overdiagnosis, antibiotic overprescription, and risk of bacterial resistance. This is a unicenter retrospective study, which included all patients admitted on an emergency basis to 2 departments of a teaching hospital during a 2-year interval to whom presepsin level was determined at the emergency department prior to admission. Serum creatinine (sCrt) was employed to estimate the severity of KD using 3 thresholds (1.5, 2, and 4 mg/dL) resulting in 4 degrees of severity: KD_1, KD_2, KD_3, KD_4. There is an ascending exponential relationship between presepsin and sCrt: presepsin = 600.03e^0.212sCrt. Presepsin levels are significantly different between the patients with KD_1, KD_2, KD_3, and KD_4. In the receiver operating characteristic curves exploring the usefulness of presepsin in sepsis diagnosis, the area under the curve was satisfactory for KD_1 (0.78), KD_2 (0.78), and KD_3 (0.82), but unacceptably low for KD_4 (0.59), while the optimal cutoff points were (depending on the computational method) 700/ 982, 588/ 1125, 1065, and 2260 pg/mL for KD_1, KD_2, KD_3, and KD_4 respectively. The threshold for abnormal presepsin should be about 600, 1000, and 1300 pg/mL in patients with KD_1, KD_2, and KD_3, respectively. In patients with KD_4, presepsin has a poor discriminating power for sepsis diagnosis. If, notwithstanding, it is used for this purpose, the cutoff point should be at least at 2200.

A complex interplay of factors reflecting the general biological, cardiovascular, neurological, renal, and metabolic status of patients influences the outcome of thrombolysis in stroke patients. This is a retrospective cohort observational study aimed to determine the importance of kidney dysfunction among these factors. Data (demographic, lifestyle, physical examination, laboratory, imaging, including metabolic and cardiovascular risk factors and comorbidities, neurological scores, and outcomes) of all stroke patients who underwent thrombolysis have been registered since January 1, 2016, in an online database. A total of 296 patients registered until December 31, 2020, were included in the study. The National Institutes of Health Stroke Scale, modified Rankin scale, Barthel index, percentage of hemorrhagic transformation, and in hospital death were used to evaluate the neurological status and outcomes of the patients. Regression analysis, Mann–Whitney test, Fisher exact test, logistic regression, and multivariate analysis were used for statistical analysis. Kidney dysfunction, as reflected by the estimated glomerular filtration rate, was associated with in hospital death and all but one of the neurological scores. Other risk factors most frequently associated with neurological scores were age, international normalized ratio, and cognitive decline. Multivariate analysis revealed estimated glomerular filtration rate (as determined by chronic kidney disease-EPI equation) as a determinant for all but one of these scores, and as the most important determinant for most of them, except for those reflecting the pre-intervention neurological status of the patient. Kidney dysfunction seems to be the most important determinant of the outcome of thrombolysed stroke patients, a result obtained by no other study.

Background: The serum levels of presepsin correlate with parameters indicating cholestasis in sepsis; however, the probability and significance of this association remain uncertain. We aimed to ascertain whether infection, as signaled by presepsin levels, is the primary determinant of elevated biliary parameters in sepsis. Methods: A unicenter, retrospective study included 396 COVID-free emergency-admitted patients, in which presepsin level was determined. Presepsin, neutrophil count, leukocyte count, C reactive protein, and fibrinogen evaluated the septic/inflammatory state. The statistically significant factors associated with cholestasis, ALT, and AST were analyzed by Fisher’s exact test and Spearman regression with Bonferroni’s correction. Results: Presepsin emerged as the most likely variable correlated with all cholestasis markers: alkaline phosphatase (p = 7 × 10⁻⁸), gamma-glutamyl transferase (p = 5 × 10⁻¹⁰), and conjugated bilirubin (p = 4 × 10⁻¹⁵). Thrombocyte count, C reactive protein, age, creatinine, urea, lactate, and blood pressure, were associated with only one or two of these markers. Conclusions: In a sepsis setting, the increase in cholestasis-related parameters is associated with presepsin with a higher probability than hemodynamic, inflammatory, or coagulation-related variables. Determining this robust link between sepsis and cholestasis could eliminate unnecessary imaging procedures in critically ill patients, enabling clinicians to focus efforts on addressing the primary infectious cause.

It is already known that Coronavirus disease 2019 (COVID-19) may lead to various degrees and forms of lung parenchyma damage, but some cases take a strikingly severe course that is difficult to manage. We report the case of a 62-year old male, non-obese, non-smoker, and non-diabetic, who presented with fever, chills, and shortness of breath. The infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was diagnosed by real-time Polymerase Chain Reaction. Although the patient had been vaccinated with 2 doses of Pfizer-BioNTech COVID-19 vaccine 7 months earlier and had no risk factors for a severe outcome, serial computed tomography (CT) scan revealed lung involvement progressively extending from an initial 30% to 40% to almost 100% 2.5 months later. The spectrum of lung lesions included at first only ground-glass opacities and some tiny emphysema bullae, but later also bronchiectasis, pulmonary fibrosis, and large emphysema bullae as post-COVID-19 pulmonary sequelae. For fear of severe evolution of superimposed bacterial infection (Clostridoides difficile enterocolits and possibly bacterial pneumonia) the administration of corticosteroids was intermittent. Massive right pneumothorax secondary to bulla rupture, possibly favored by the indispensable high flow oxygen therapy, led to respiratory failure compounded by hemodynamic instability, and ultimately to the patient’s final demise. COVID-19 pneumonia may cause severe lung parenchyma damage which requires long-term supplemental oxygen therapy. Beneficial or even lifesaving as it might be, high flow oxygen therapy may nonetheless have deleterious effects too, including the development of bullae that may rupture engendering pneumothorax. Corticosteroid treatment should probably be pursued despite superimposed bacterial infection to limit the viral induced damage to lung parenchyma.

Introduction: Chronic kidney disease (CKD) induces changes in the myocardium known to influence morbidity and mortality, most severe in patients with end stage renal disease. Objectives: The working hypothesis was that in patients on chronic hemodialysis the prevalence of left ventricular diastolic dysfunction is correlated with the inflammatory, oxidative, metabolic, nutritional, and atherosclerotic status. Patients and Methods: An observational study was performed on 51 patients (age 59.76 ± 13.24 years) on hemodialysis treatment. Transthoracic cardiac ultrasound was conducted to evaluate LVDD. The burden of cardiac and arterial atherosclerosis was evaluated by cardiac ultrasound (aortic and mitral valve calcifications), vascular ultrasound (carotid and femoral atheroma plaques, common carotid intima-media thickness), and by abdominal radiography (aortic calcification score). Demographic and anthropometric parameters were determined. Blood samples were used to determine laboratory parameters reflecting the inflammatory, oxidative, and metabolic/nutrition status. Results: LVDD is positively correlated with the serum level of C-reactive protein (CRP) (P=0.04), the total antioxidant capacity of the serum (P=0.04), the presence (P=0.022) and number (P=0.04) of femoral plaques, the aortic calcification score (P=0.02), aortic valve stenosis (P=0.037), aortic annulus calcifications (P=0.02) and mitral valve calcifications (P=0.041). After the removal of the main confounder, degenerative aortic stenosis, only the associations with serum total antioxidant capacity (P=0.04) and aortic calcification score (P= 0.02) maintain their statistical significance. Conclusion: LVDD is positively correlated with inflammation and oxidative stress markers and with the severity of aortic calcification.