COVID-19 is a complex disease that can lead to fatal respiratory failure with extrapulmonary complications, either as a direct result of viral invasion in multiple organs or secondary to oxygen supply shortage. Liver is susceptible to many viral pathogens, and due to its versatile functions in the body, it is of great interest to determine how hepatocytes may interact with SARS-CoV-2 in COVID-19 patients. Liver injury is a major cause of death, and SARS-CoV-2 is suspected to contribute significantly to hepatopathy. Owing to the lack of knowledge in this field, further research is required to address these ambiguities. Therefore, we aimed to provide a comprehensive insight into host-virus interactions, underlying mechanisms, and associated risk factors by collecting results from epidemiological analyses and relevant laboratory experiments. Backed by an avalanche of recent studies, our findings support that liver injury is a sequela of severe COVID-19, and certain pre-existing liver conditions can also intensify the morbidity of SARS-CoV-2 infection in synergy. Notably, age, sex, lifestyle, dietary habits, coinfection, and particular drug regimens play a decisive role in the final outcome and prognosis as well. Taken together, our goal was to unravel these complexities concerning the development of novel diagnostic, prophylactic, and therapeutic approaches with a focus on prioritizing high-risk groups.
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http://dx.doi.org/10.1186/s12985-024-02332-y | DOI Listing |
Clin Nutr
December 2024
Department of Urology, Affiliated Hospital of Qingdao University, Qingdao, China. Electronic address:
Named after the Greek term for "hard fat", stearic acid has gradually entered people's field of vision. As an important component of various physiological cellular functions, stearic acid plays a regulatory role in diverse aspects of energy metabolism and signal transduction. Its applications range from serving as a bodily energy source to participating in endogenous biosynthesis.
View Article and Find Full Text PDFBest Pract Res Clin Gastroenterol
December 2024
Department of Anesthesiology and Critical Care, Hospital of the University of Pennsylvania, Philadelphia, PA, 19104, USA.
Acute liver failure (ALF) is defined as the loss of hepatic function in conjunction with hepatic encephalopathy and coagulopathy. There is histological evidence of profound hepatocyte damage. If it is not aggressively managed, ALF can be fatal within a few days.
View Article and Find Full Text PDFBest Pract Res Clin Gastroenterol
December 2024
Aster Integrated Liver Care, Aster Medcity, Kochi, India.
Acute liver failure (ALF) is a rare and dynamic syndrome occurring as a sequela of severe acute liver injury (ALI). Its mortality ranges from 50% to 75% based on the aetiology, patients age and severity of encephalopathy at admission. With improvement in intensive care techniques, transplant-free survival in ALF has improved over time.
View Article and Find Full Text PDFRev Esp Anestesiol Reanim (Engl Ed)
December 2024
Departamento de Farmacia, Clínica Universidad de Navarra, Pamplona, Universidad de Navarra, Spain.
Introduction: The independent association of vancomycin with Acute Kidney Injury (AKI) in the critically ill patient with sepsis or septic Shock is controversial. The aim of this study was to evaluate the incidence of AKI in a cohort of patients with sepsis or septic Shock with an adequate and strict monitoring of vancomycin, guided by the area under the concentration-time curve in relation to the minimum inhibitory concentration (AUC/MIC ratio).
Material And Methods: Retrospective cohort study on 106 patients admitted to the ICU with a diagnosis of sepsis or septic shock with vancomycin treatment, consecutively from January 2017 to December 2019.
Ecotoxicol Environ Saf
December 2024
Department of Pharmacy, Chaohu Hospital of Anhui Medical University, China. Electronic address:
This study investigates the protective effect of ginsenoside Rg1 against manganese (Mn)-induced hepatotoxicity, highlighting its role as a PPAR-γ activator and its impact on TLR4/MyD88/MAPK pathway. Manganese induces liver damage through mechanisms involving oxidative stress and inflammation. Rg1, a principal bioactive compound of ginseng, significantly alleviates Mn-induced liver injury.
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