Gastrointestinal (GI) manifestations have been reported as the most extra-pulmonary manifestations of coronavirus disease 2019 (COVID-19). Recognizing the various manifestations, especially as presenting symptoms of COVID-19 is of great importance. We aimed to investigate the GI and hepatic manifestations of COVID - 19 in children, determining the factors associated with the disease severity and prognosis related to GI symptoms.

In this retrospective study, children aged 1-month to 16-years who were admitted to Afzalipour Hospital in Kerman, Iran. for a period of one year (from October 2020 to October 2021) with the diagnosis of COVID-19 were included. The comparison of clinical symptoms and laboratory variables in the appendectomy and non-appendectomy groups were evaluated. Patients' information was extracted from the patient's medical record and analyzed in SPSS statistical. software.

A total of 163 patients (107 boy and 56 girls) with mean age of 4.35 ± 3.86 (range 0.08 to 16) years were included. The most frequent GI symptoms at the time of admission were watery diarrhea (46.6%), vomiting (45.4%), and abdominal pain (32.5%). There was no significant relationship between clinical symptoms and laboratory variables in the appendectomy and non-appendectomy groups, but the severity of COVID-19 was significantly associated with appendicitis (P = 0.03). There was no statistically significant relationship between liver enzyme levels and disease severity and pediatric intensive care unit admission.

Although most COVID-19 patients present with GI manifestations, we could not determine the relationship between GI and hepatic manifestations and disease severity in this study.

Not applicable.

COVID-19 severity affects liver damage. The utilization of various anti-COVID-19 drugs in non-severe cases related to liver impairment in the short term seemed intriguing.

To assess the dynamic course of liver injury in mild to moderate COVID-19 patients within 10 days of admission and identify risk variables, including medication linkage.

This prospective cohort study of 300 newly diagnosed mild to moderate COVID-19 cases between September 2021 and October 2022. Tertiary center hospitel, field hospital, or cohort ward admissions were made. Patient demographics and treatment were recorded. The drug, liver injury (LI) dynamics, and clinical course were evaluated.

Hospitel/field hospital (188) and cohort wards (112) had 300 individuals. One hundred fifteen participants had liver damage. Favipiravir (45 %), remdesivir (17.4 %), molnupiravir (11.3 %), Andrographis paniculata (ADG) (8.7 %), and favipiravir plus ivermectin (7.7 %) were given to most LI group (n = 104). The baseline AST/ALT levels of 68 (65.4 %) treated patients were abnormal. Favipiravir, remdesivir, and favipiravir + ivermectin increased mean AST/ALT in participants with normal baseline AST/ALT (p = 0.001, 0.003, and 0.016, respectively), but not molnupiravir or Andrographis paniculata. Transaminase levels climbed in untreated patients independent of baseline. The ground-glass imaging pattern was linked to mild LI. Most subjects had transaminase declines after 10 days. Preexisting liver disease did not increase the likelihood of in-hospital LI.

In the real world, a less-than-critical level of liver damage was reported in mild to moderate COVID-19 that allows clinicians to administer a variety of standard medications during short periods of hospital stay.

The global pandemic of novel coronavirus pneumonia (COVID-19) has resulted in millions of deaths over the past three years. As one of the most commonly affected extra-pulmonary organs, numerous studies have reported varying degrees of liver injury in a significant proportion of patients with COVID-19, particularly in severe and critically ill patients. Early prediction of liver dysfunction in hospitalized patients would facilitate the clinical management of COVID-19 and improve clinical prognosis, but reliable and valid predictive models are still lacking.MethodsWe collected data from 286 patients with RT-PCR confirmed COVID-19 admitted to various ICUs from the case system. These patients were randomly divided into a training cohort (50%) and a validation cohort (50%). In the training cohort, we first used ROC curves to measure the predictive efficiency of each of the variables for the development of liver damage during hospitalization in patients with COVID-19, followed by LASSO regression analysis to screen the variables for predictive models and logistic regression analysis to identify relevant risk factors. A nomogram based on these variables was created following the above model. Finally, the efficiency of the prediction models in the training and validation cohorts was assessed using AUC, consistency index (C index), calibration curves and Decision Curve Analysis.ResultsOut of a total of 80 parameters for COVID-19 patients admitted to the ICUs, 10 were determined to be significantly associated with the occurrence of liver dysfunction during hospitalization. Based on these predictors, further prediction models were used to construct and develop a nomogram that was offered for practical clinical application. The C-index of the column line graphs for the training and validation cohorts was 0.956 and 0.844 respectively. in addition, the calibration curves for the model showed a high degree of agreement between the predicted and actual incidence of liver dysfunction in patients with COVID-19.ConclusionBy developing a predictive model and associated nomogram, we predicted the incidence of liver dysfunction during hospitalization in patients with COVID-19 in the ICU. The model's predictive performance was determined in both the training and validation cohorts, contributing to the clinical management of COVID-19.

Highly active antiretroviral therapy (HAART), consisting of three or more antiretroviral drugs, is recommended for patients with HIV infection. HAART effectively reduces HIV RNA levels, lowers the risk of opportunistic infections, and improves immune function and survival rates. However, it is also associated with an increased risk of liver injury in HIV-infected individuals. This review aims to summarize the mechanisms underlying HAART-induced liver injury. A comprehensive search was conducted in PubMed and EMBASE using keywords such as "Antiretroviral/ARV drugs and drug-induced liver injury (DILI)," "HAART and DILI," "Antiretroviral therapy and DILI," and "HIV infection and DILI." Relevant papers published before March 2024 were included. Experimental studies have demonstrated that zidovudine and efavirenz can cause structural alterations in mitochondria, impair the respiratory chain, generate free radicals, and deplete mitochondrial DNA, leading to oxidative and endoplasmic reticulum stress, as well as the accumulation of advanced glycation end products in liver tissue. Zidovudine disrupts lipid homeostasis by increasing fatty acid synthesis and reducing metabolism. Efavirenz and its metabolite, 8-hydroxyefavirenz, induce hepatocellular death and activate proapoptotic markers through c-Jun N-terminal kinase signaling. Additionally, lamivudine has been shown to induce liver injury and oxidative stress in rats. Clinically, approximately 50% of HIV patients on HAART regimens containing non-nucleoside reverse transcriptase inhibitors experience mild to moderate liver injury. HAART regimens that include efavirenz, lamivudine, and tenofovir impair glucose and lipid homeostasis in rats, highlighting the need for caution in HIV patients with fatty liver disease. Patients with viral hepatitis coinfection, those taking antitubercular drugs or cotrimoxazole, and those on nevirapine-containing regimens are at particularly high risk. Regular monitoring of liver function is essential to prevent liver damage associated with HAART in HIV-infected patients. While HAART significantly improves survival rates in HIV patients, it also poses a considerable risk of liver injury, necessitating careful monitoring and management.

Acute kidney injury (AKI) and acute liver injury (ALI) were associated with poor outcomes during hospitalization, respectively. However, the clinical outcome of AKI combined with ALI (AKI-ALI) remains unknown. The current study aimed to describe AKI-ALI's incidences, risk factors, and outcomes.

The study population included patients aged 18-99 years with enough serum creatinine and liver testing hospitalized at 19 medical centers throughout China between 2000 and 2021. AKI was defined by Kidney Disease Improving Global Outcomes and ALI was defined by the change of liver enzymes based on Asia Pacific Association of Study of Liver consensus guidelines. Cox proportional hazard model was used to identify risk factors for AKI-ALI, and a time-dependent Cox proportional hazard regression model was used to estimate the association between AKI-ALI and in-hospital mortality.

Among the 18,461 patients with AKI, 1689 (9.1%) combined with ALI. Male patients or those who have used nonsteroidal anti-inflammatory drugs or vasopressors, and who have heart failure or shock, with higher AST or GGT values, were associated with an increased risk of AKI-ALI. Compared with AKI-nonALI, patients with AKI-ALI were at higher risk of in-hospitalized mortality (hazard ratio [HR] 1.76, 95% confidence interval [CI] 1.54, 2.00). In addition, a stronger association between AKI-ALI and in-hospital mortality was found in those with lower AKI grades (p for interaction = 0.037).

ALI was not uncommon among patients with AKI, especially in patients who used vasopressors and had shock. This study highlights the association between AKI-ALI and a significantly increased risk of mortality. It suggests that dynamic monitoring of liver function is essential, particularly in patients with AST and GGT exceeding the normal upper limit, to improve the in-hospital prognosis of AKI patients.

The association and interaction between SARS-CoV-2 (COVID-19) infection and irritable bowel syndrome (IBS) has not been adequately explored. We sought to determine whether a mechanistic relationship exists and whether vaccination against COVID-19 plays a role in this relationship.

Using the Veterans Affairs (VA) electronic healthcare database, we obtained a random sample of veterans in October 2022 for this cross-sectional study. Demographic characteristics of the participants (e.g., age, sex, race), prior COVID infection, COVID vaccination status, and IBS diagnosis were extracted from the VA medical records. Univariate and multivariate logistic regression analyses were performed to determine potential associations between the listed factors and IBS diagnosis.

A total of 9,112 veterans were analyzed. In univariate analysis, race, COVID infection, and vaccination were significantly associated with IBS. In multivariate regression analysis, only the effects of COVID infection and vaccination were statistically significant. The odds ratios for development of IBS among veterans with COVID infection versus those without was 1.94 (95% CI: 1.53-2.45), and for vaccinated versus unvaccinated, was 1.49 (95% CI: 1.18-1.89). Further analysis showed that vaccinated veterans who did not contract COVID infection had a lower risk of developing IBS compared to unvaccinated veterans who contracted COVID.

The results of this study suggest that veterans with COVID infection are almost twice as likely to develop IBS compared to those who have never had COVID infection. Vaccinated veterans have a lower risk of contracting COVID and subsequently, a diminished chance of developing IBS. Overall, vaccination of veterans with protection against COVID diminishes the risk of IBS development.

COVID-19 disease has spread rapidly worldwide, causing high mortality. Accessible biomarkers capable of early identification of patients at risk of severe form are needed in clinical practice. The aim of the study was to determine the biological markers that predict a critical condition.

Retrospective study including patients with confirmed COVID-19 hospitalized between September 2020 and June 2021. The primary endpoint was progression to critical status within 7 days from admission. We defined two groups:Critical group: Patients who developed a critical condition or died or transferred to the ICU before or at 7 th day.Non-critical group: Patients who remained in non-critical respiratory status until 7 th day or discharged before or at 7 th day.

Our study included 456 patients, with a sex ratio of 1.32 and an average age of 62 years. At the 7 th day of hospitalization, 115 (25.2%) patients were in the critical group and 341 (74.8%) patients were in the non-critical group. The univariate logistic regression indicated that laboratory findings between non-critical and critical groups showed that C-reactive protein (CRP) (p=0.047), D-Dimer (p=0.011), creatinine (0.026), creatine kinase (p=0.039), lactate dehydrogenase (p=0.04), and troponin (p=0.001) were all higher among patients in critical group. However, lymphocyte (p<0.001) and platelet (p<0.001) counts were significantly lower among the critical group. Multivariate logistic regression model, identified four independent risk factors: lymphopenia (OR=2.771, 95%CI=1.482-5.181, p=0.001), Neutrophil to Lymphocyte Ratio (NLR) (OR=2.286, 95%CI=1.461-3.578, p<0.001), thrombocytopenia (OR=1.944, 95%CI=1.092-3.459, p=0.024), and CRP>71.5 (OR=1.598, 95% CI=1.042-2.45, p=0.032) were associated to critical group.

Our results show the predictive value of lymphopenia, thrombocytopenia, high NLR and CRP levels to evaluate the prognosis of COVID-19 pneumonia. A prognostic score could be proposed for guiding clinical care and improving patient outcomes.

The aim was to investigate how different hepatic injury (HI) definitions used in the same study population change incidence and mortality rates and which would best diagnose secondary HI.

Single-centre retrospective observational cohort study.

Tertiary hospital ICU, ANKARA, Turkey.

Four hundred seventy-eight adult patients were included in the study.

None.

Three definitions of HI were compared. Taking the SOFA hepatic criteria (SOFA: Total bilirubin (TBL) > 1.2 mg/dl) as the gold standard, sensitivity, specificity, positive and negative predictive values, and accuracy of the modified 2017 definition by the American College of Gastroenterology (ACG) and the 2019 European Association for the Study of the Liver (EASL) were calculated.

Incidence rates ranged from 10% to 45% according to the definition (p < 0.005), while mortality rates ranged from 38% to 57%. When the SOFA1.2 (TBL > 1.2 definition was taken as the gold standard, the diagnostic value of the ACG definition was high, and HI was found to be an independent risk factor that increased mortality four times.

According to this study's results, the incidence and mortality rates of secondary HI vary greatly depending on the definition used. A definition that includes minimal increases in ALT, AST, and TBL predicts mortality with reasonable incidence rates.

There is a demand for additional data regarding the impact of coronavirus disease 2019 (COVID-19) on the pediatric population. This study sought to determine the clinical and epidemiological features of pediatric COVID-19 in Iran.

A retrospective study was performed to assess medical records of children with COVID-19 admitted to Abuzar Hospital in Ahvaz (Iran). Their clinical and demographic data were recorded.

In this study, 600 medical records of pediatric COVID-19 patients were evaluated. Over 50% of them were boys. Mild, moderate, and severe manifestations of COVID-19 were identified in 250, 200, and 150 children, respectively. Patients with severe or moderate COVID-19 had substantially higher levels of various inflammatory markers (C-reactive protein (CRP), fibrinogen, and d-dimer), alanine transaminase (ALT), creatine kinase (CPK), blood urea nitrogen (BUN), neutrophils, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), creatinine (Cr), bilirubin, and gamma-glutamyl transferase (GGT) compared to children with mild COVID-19 (p < 0.001); they also had lower levels of lymphocytes, hemoglobin (Hb), and vitamin D than patients with mild COVID-19 (p < 0.001). In addition, children with severe or moderate COVID-19 had a notably higher incidence of fever or dry cough and longer hospital stays than those with mild COVID-19 (p < 0.001). The prevalence of malnutrition and anemia in patients was 50.6% and 31.5%, respectively. A significant proportion of children who were underweight and stunted experienced moderate to severe COVID-19. Furthermore, there was a considerably higher prevalence of malnutrition, anemia, and vitamin D insufficiency, or deficiency in children with moderate-to-severe COVID-19 compared to patients with mild COVID-19 (p < 0.001).

The outcomes of this study revealed a significantly higher prevalence of malnutrition, anemia, vitamin D insufficiency or deficiency, elevated liver and kidney function test results, and increased inflammatory markers in children with moderate to severe COVID-19 compared to those with mild COVID-19.

This review explores the mechanisms, diagnostic approaches, and management strategies for COVID-19-induced liver injury, with a focus on its impact on patients with pre-existing liver conditions, liver cancer, and those undergoing liver transplantation.

A comprehensive literature review included studies on clinical manifestations of liver injury due to COVID-19. Key areas examined were direct viral effects, drug-induced liver injury, cytokine storms, and impacts on individuals with chronic liver diseases, liver transplants, and the role of vaccination. Data were collected from clinical trials, observational studies, case reports, and review literature.

COVID-19 can cause a spectrum of liver injuries, from mild enzyme elevations to severe hepatic dysfunction. Injury mechanisms include direct viral invasion, immune response alterations, drug toxicity, and hypoxia-reperfusion injury. Patients with chronic liver conditions (such as alcohol-related liver disease, nonalcoholic fatty liver disease, cirrhosis, and hepatocellular carcinoma) face increased risks of severe outcomes. The pandemic has worsened pre-existing liver conditions, disrupted cancer treatments, and complicated liver transplantation. Vaccination remains crucial for reducing severe disease, particularly in chronic liver patients and transplant recipients. Telemedicine has been beneficial in managing patients and reducing cross-infection risks.

This review discusses the importance of improved diagnostic methods and management strategies for liver injury caused by COVID-19. It emphasizes the need for close monitoring and customized treatment for high-risk groups, advocating for future research to explore long-term effects, novel therapies, and evidence-based approaches to improve liver health during and after the pandemic.

In this mini review, we explore the complex network of inflammatory reactions incited by SARS-CoV-2 infection, which extends its reach well beyond the respiratory domain to influence various organ systems. Synthesizing existing literature, it elucidates how the hyperinflammation observed in COVID-19 patients affects multiple organ systems leading to physiological impairments that can persist over long after the resolution of infection. By exploring the systemic manifestations of this inflammatory cascade, from acute respiratory distress syndrome (ARDS) to renal impairment and neurological sequelae, the review highlights the profound interplay between inflammation and organ dysfunction. By synthesizing recent research and clinical observations, this mini review aims to provide an overview of the systemic interactions and complications associated with COVID-19, underscoring the need for an integrated approach to treatment and management. Understanding these systemic effects is crucial for improving patient outcomes and preparing for future public health challenges.

Clinical practice showed that many patients with SARS-CoV-2 infection presented with long COVID syndrome in digestive system. We sought to investigate the factor affecting the incidence of long COVID syndrome in digestive system.

Patients with SARS-CoV-2 infection diagnosed at two centers of Zhongshan Hospital and one center of Shanghai Pudong Hospital from March 01, 2022 to May 31, 2022 were enrolled, collected in the hospital database, and followed up until March 30, 2023. The primary outcome of the study was the occurrence of post-acute sequelae of COVID-19 in the digestive system (long COVID syndrome). Modified Poisson regression was used to calculate the relative risk (RR). This cohort study included 494 patients with SARS-CoV-2 infection, 144 (29.1 %) patients developed liver function abnormality on admission. During the follow-up period, the primary study outcome occurred in 30 (20.8 %) of the group presenting with liver function abnormality on admission and in 20 (5.7 %) of the group without liver function abnormality on admission (adjusted, RR = 3.550, 95%CI: 2.099-6.006, P ≤ 0.001).

Our study suggests that patients with COVID-19 who experience liver function abnormality on admission have an increased risk of developing long COVID syndrome in the digestive system.

The emergence of the SARS-CoV-2 Omicron variant has posed a significant global public health challenge. Elucidating the laboratory profiles of individuals infected with this variant is crucial for assessing organ damage. This study aimed to investigate the variations in liver function tests and their correlation with demographic characteristics and inflammatory markers in patients with early Omicron variant infections.

A retrospective cohort study was conducted on 1133 mild or asymptomatic COVID-19 cases at Tianjin First Central Hospital. Data on age, gender, body mass index (BMI), and serum markers were collected and analyzed. Statistical analyses were performed using SPSS software, version 24.0.

Abnormal liver function parameters, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and total bilirubin (TBIL), were observed in 314 (27.71%) patients. "Hepatocellular type" was identified in 56 (4.94%) patients, "cholestatic type" in 185 (16.33%) patients, and "mixed type" in 73 (6.44%) patients. In the mixed group, we observed a pronounced elevation in the levels of ALT, AST, and GGT. Moreover, the hepatocellular group exhibited a statistically significant increase in AST and ALT concentrations relative to both the normal and cholestatic groups. Notably, the cholestatic group demonstrated a substantial increment in ALP levels. Males had a significantly higher prevalence of "abnormal liver enzyme markers" compared to females. Patients with "abnormal liver enzyme markers" exhibited significantly decreased immunoglobulin G (IgG) levels and elevated levels of inflammatory markers, including procalcitonin (PCT), interleukin-6 (IL6), as well as C-reactive protein (CRP) compared to normal group. Logistic regression analysis revealed that male gender and PCT levels were significantly associated with the risk of abnormal liver enzyme markers. Patients in hepatocellular group were likely accompanied with high CRP levels, whereas those in the cholestatic type were associated with high IL6 levels.

Early Omicron infection might cause liver stress response. Elevated liver enzyme marker levels were correlated with age, gender, inflammatory factors, and IgG.

Hemorrhagic fever with renal syndrome (HFRS) is a severe public health problem in Jiangxi province, China. Previous studies reported genetic variants of Orthohantavirus hantanense (Hantaan virus, HTNV) in rodents in this area. However, the relationship between HTNV variants and human infection needs to be confirmed. This study aimed to identify the HTNV variants in patients and to understand the clinical characteristics of HFRS caused by these variants.

Samples were collected from hospitalized suspected cases of HFRS during the acute phase. HFRS cases were confirmed using quantitative real-time RT-PCR. Peripheral blood mononuclear cells (PBMC) from patients with HFRS were inoculated into Vero-E6 cells for viral isolation. The genomic sequences of HTNV from patients were obtained by amplicon-based next-generation sequencing. A retrospective analysis was conducted on the clinical characteristics of the patients.

HTNV RNA was detected in 53 of 183 suspected HFRS patients. Thirteen HTNVs were isolated from 32 PBMCs of HFRS cases. Whole genome sequences of 14 HTNVs were obtained, including 13 isolates in cell culture from 13 patients, and one from plasma of the fatal case which was not isolated successfully in cell culture. Genetic analysis revealed that the HTNV sequence from the 14 patients showed significant variations in nucleotide and amino acid to the HTNV strains found in other areas. Fever (100%, 53/53), thrombocytopenia (100%, 53/53), increased serum aspartate aminotransferase (100%, 53/53), and increased lactate dehydrogenase (96.2%, 51/53) were the most common characteristics. Severe acute kidney injury was observed in 13.2% (7/53) of cases. Clinical symptoms, such as pain, petechiae, and gastrointestinal or respiratory symptoms were uncommon.

The HTNV genetic variants cause human infections in Jiangxi. The clinical symptoms of HFRS caused by the HTNV genetic variant during the acute phase are atypical. In addition to renal dysfunction, attention should be paid to the common liver injuries caused by these genetic variants.

Many studies have revealed a link between non-alcoholic fatty liver disease (NAFLD) and coronavirus disease 2019 (COVID-19), making understanding the relationship between these two conditions an absolute requirement.

To provide a qualitative synthesis on the currently present data evaluating COVID-19 and NAFLD.

This systematic review was conducted in accordance with the guidelines provided by preferred reporting items for systematic reviews and meta-analyses and the questionnaire utilized the population, intervention, comparison, and outcome framework. The search strategy was run on three separate databases, PubMed/MEDLINE, Scopus, and Cochrane Central, which were systematically searched from inception until March 2024 to select all relevant studies. In addition, ClinicalTrials.gov, Medrxiv.org, and Google Scholar were searched to identify grey literature.

After retrieval of 11 studies, a total of 39282 patients data were pooled. Mortality was found in 11.5% and 9.4% of people in NAFLD and non-NAFLD groups. In all, 23.2% of NAFLD patients and 22% of non-NAFLD admissions diagnosed with COVID-19 were admitted to the intensive care unit, with days of stay varying. Ventilatory support ranged from 5% to 40.5% in the NAFLD cohort and from 3.1% to 20% in the non-NAFLD cohort. The incidence of acute liver injury showed significance. Clinical improvement on days 7 and 14 between the two classifications was significant. Hospitalization stay ranged from 9.6 days to 18.8 days and 7.3 days to 16.4 days in the aforementioned cohorts respectively, with 73.3% and 76.3% of patients being discharged. Readmission rates varied.

Clinical outcomes except mortality consistently showed a worsening trend in patients with NAFLD and concomitant COVID-19. Further research in conducting prospective longitudinal studies is essential for a more powerful conclusion.

Since the start of the pandemic, considerable advancements have been made in our understanding of the effects of SARS-CoV-2 infection and the associated COVID-19 on the hepatic system. There is a broad range of clinical symptoms for COVID-19. It affects multiple systems and has a dominant lung illness depending on complications. The progression of COVID-19 in people with pre-existing chronic liver disease (CLD) has also been studied in large multinational groups. Notably, SARS-CoV-2 infection is associated with a higher risk of hepatic decompensation and death in patients with cirrhosis. In this review, the source, composition, mechanisms, transmission characteristics, clinical characteristics, therapy, and prevention of SARS-CoV-2 were clarified and discussed, as well as the evolution and variations of the virus. This review briefly discusses the causes and effects of SARS-CoV-2 infection in patients with CLD. As part of COVID-19, In addition, we assess the potential of liver biochemistry as a diagnostic tool examine the data on direct viral infection of liver cells, and investigate potential pathways driving SARS-CoV-2-related liver damage. Finally, we explore how the pandemic has had a significant impact on patient behaviors and hepatology services, which may increase the prevalence and severity of liver disease in the future. The topics encompassed in this review encompass the intricate relationships between SARS-CoV-2, liver health, and broader health management strategies, providing valuable insights for both current clinical practice and future research directions.

The acute manifestations of coronavirus disease 2019 (COVID-19) exhibit the hallmarks of sepsis-associated complications that reflect multiple organ failure. The inflammatory cytokine storm accompanied by an imbalance in the pro-inflammatory and anti-inflammatory host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to severe and critical septic shock. The sepsis signature in severely afflicted COVID-19 patients includes cellular reprogramming and organ dysfunction that leads to high mortality rates, emphasizing the importance of improved clinical care and advanced therapeutic interventions for sepsis associated with COVID-19. Phytochemicals of functional foods and nutraceutical importance have an incredible impact on the healthcare system, which includes the prevention and/or treatment of chronic diseases. Hence, in the present review, we aim to explore the pathogenesis of sepsis associated with COVID-19 that disrupts the physiological homeostasis of the body, resulting in severe organ damage. Furthermore, we have summarized the diverse pharmacological properties of some potent phytochemicals, which can be used as functional foods as well as nutraceuticals against sepsis-associated complications of SARS-CoV-2 infection. The phytochemicals explored in this article include quercetin, curcumin, luteolin, apigenin, resveratrol, and naringenin, which are the major phytoconstituents of our daily food intake. We have compiled the findings from various studies, including clinical trials in humans, to explore more into the therapeutic potential of each phytochemical against sepsis and COVID-19, which highlights their possible importance in sepsis-associated COVID-19 pathogenesis. We conclude that our review will open a new research avenue for exploring phytochemical-derived therapeutic agents for preventing or treating the life-threatening complications of sepsis associated with COVID-19.

Coronavirus disease 2019 (COVID-19) is characterized by an acute respiratory infection with multisystem involvement and the association of its severity to liver function abnormalities is not well characterized. The aim of this study was to assess the association between the severity of COVID-19 patients and liver function abnormalities. This retrospective study included adult patients with confirmed COVID-19, which were classified as non-severe or severe according to World Health Organization guidelines. Liver function test results were compared between the severity groups. A total of 339 patients were included of which 150 (44.25%) were severe cases. The male-to-female ratio was 0.9:1 and 3:2 in the non-severe and severe groups, respectively (p=0.031). Aspartate aminotransferase (AST), alanine transaminase (ALT), and total bilirubin levels and acute liver injury (ALI) incidence were significantly higher in the severe group compared to non-severe group (p<0.001, p<0.001, p=0.025, p=0.014, respectively). In contrast, albumin levels were significantly lower (p=0.001). Multivariate analysis showed that ALI was significantly associated with human immunodeficiency virus (HIV) infection (odds ratio (OR): 5.275; 95% confidence interval (CI): 1.165-23.890, p=0.031), hemoglobin level (OR: 1.214; 95%CI: 1.083-1.361, p=0.001), and hypoalbuminemia (OR: 2.627; 95%CI: 1.283-5.379, p=0.008). Pre-existing liver diseases were present in 6.5% of patients. No significant differences were observed between the groups based on COVID-19 severity and ALI presence. Liver function test abnormalities, including ALI, are more prevalent in patients with severe COVID-19 infection. HIV infection, high hemoglobin levels, and hypoalbuminemia may be potential risk factors for ALI.

COVID-19 is a novel coronavirus pneumonia, which is related to abnormal liver function. Thus, it is important to explore the occurrences and causes of abnormal liver function with COVID-19.

We chose 109 patients with COVID-19 in 2020 and studied the relationship between gender, age, basic diseases, antiviral drug treatment, disease classification, and abnormal liver function, and analyzed the causes of abnormal liver function in patients with COVID-19.

Among patients, 46 (42.20%) had abnormal liver function at admission; 37 (80.43%) had mild abnormal liver function; and 9 (19.57%) had severe liver function. Compared with other age groups, the abnormal rate of serum ALP in the group younger than 21 years old were the highest (P < 0.05). The abnormal rates and concentrations of serum ALT, AST and γ-GT in the male groups were higher than in female groups (P < 0.05), basic disease group were higher than those in the non-basic disease group (P < 0.05). Serum γ-GT concentration after 1 week of antiviral treatment was higher than that before treatment (P < 0.05). The abnormal rate of ALT and AST at discharge was lower than that after antiviral treatment for 1 week (P < 0.05). Serum TB and AST concentrations at discharge were lower than those before treatment (P < 0.05). Serum AST and γ-GT concentrations in severe/critical type group were higher than those in mild or ordinary type group (P < 0.05).

In this study, we found male sex, basic diseases, antiviral drugs, and severe/critical types are related to the occurrence of abnormal liver function in COVID-19 patients.

COVID-19 has affected millions worldwide, causing significant morbidity and mortality. While predominantly involving the respiratory tract, SARS-CoV-2 has also caused systemic illnesses involving other sites. Liver injury due to COVID-19 has been variably reported in observational studies. It has been postulated that liver damage may be due to direct damage by the SARS-CoV-2 virus or multifactorial secondary to hepatotoxic therapeutic options, as well as cytokine release syndrome and sepsis-induced multiorgan dysfunction. The approach to a COVID-19 patient with liver injury requires a thorough evaluation of the pattern of hepatocellular injury, along with the presence of underlying chronic liver disease and concurrent medications which may cause drug-induced liver injury. While studies have shown uneventful recovery in the majority of mildly affected patients, severe COVID-19 associated liver injury has been associated with higher mortality, prolonged hospitalization, and greater morbidity in survivors. Furthermore, its impact on long-term outcomes remains to be ascertained as recent studies report an association with metabolic-fatty liver disease. This present review provides insight into the subject by describing the postulated mechanism of liver injury, its impact in the presence of pre-existing liver disease, and its short- and long-term clinical implications.

Currently, SARS-CoV-2 is still spreading rapidly and globally. A large proportion of patients with COVID-19 developed liver injuries. The human-induced pluripotent stem cell (iPSC)-derived hepatocytes recapitulate primary human hepatocytes and have been widely used in studies of liver diseases.

To explore the susceptibility of hepatocytes to SARS-CoV-2, we differentiated iPSCs to functional hepatocytes and tried infecting them with different MOI (1, 0.1, 0.01) of SARS-CoV-2.

The iPSC-derived hepatocytes are highly susceptible to virus infection, even at 0.01 MOI. Other than the ancestral strain, iHeps also support the replication of SARS-CoV-2 variants including alpha, beta, theta, and delta. More interestingly, the ACE2 expression significantly upregulated after infection, suggesting a vicious cycle between virus infection and liver injury.

The iPSC-derived hepatocytes can support the replication of SARS-CoV-2, and this platform could be used to investigate the SARS-CoV-2 hepatotropism and hepatic pathogenic mechanisms.

DILI accounts for more than half of acute liver failure cases in the United States and is a major health care issue for the public worldwide. As investigative toxicology is playing an evolving role in the pharmaceutical industry, mechanistic insights into drug hepatotoxicity can facilitate drug development and clinical medication.

By integrating multisource datasets including gene expression profiles of rat livers from open TG-GATE database and DrugMatrix, drug labels from FDA Liver Toxicity Knowledge Base, and clinical reports from LiverTox, and with the employment of bioinformatic and computational tools, this study developed an approach to characterize and predict DILI based on the molecular understanding of the processes (toxicity pathways).

A panel of 11 pathways widely covering biological processes and stress responses was established using a training set of six positive and one negative DILI drugs from open TG-GATEs. An entropy weight method-based model was developed to weight responsive genes within a pathway, and an interpretable machine-learning (ML) model XGBoot-SHAP was trained to rank the importance of pathways to the panel activity. The panel activity was proven to differentiate between injured and noninjured sample points and characterize DILI manifestation using six training drugs. Next, the model was tested using an additional 89 drugs (61 positives + 28 negatives), and a precision of 86% and higher can be achieved.

This study provides a novel approach to mechanisms-driven prediction modeling, as well as big data integration for insights into pharmacology and other human biology areas.

Aptamers, as a kind of small-molecule nucleic acid, have attracted much attention since their discovery. Compared with biological reagents such as antibodies, aptamers have the advantages of small molecular weight, low immunogenicity, low cost, and easy modification. At present, aptamers are mainly used in disease biomarker discovery, disease diagnosis, treatment, and targeted drug delivery vectors. In the process of screening and optimizing aptamers, it is found that there are still many problems need to be solved such as the design of the library, optimization of screening conditions, the truncation of screened aptamer, and the stability and toxicity of the aptamer. In recent years, the incidence of liver-related diseases is increasing year by year and the treatment measures are relatively lacking, which has attracted the people's attention in the application of aptamers in liver diseases. This article mainly summarizes the research status of aptamers in disease diagnosis and treatment, especially focusing on the application of aptamers in liver diseases, showing the crucial significance of aptamers in the diagnosis and treatment of liver diseases, and the use of Discovery Studio software to find the binding target and sequence of aptamers, and explore their possible interaction sites.

The coronavirus disease 2019 (COVID-19) pandemic has caused changes in the global health system, causing significant setbacks in healthcare systems worldwide. This pandemic has also shown resilience, flexibility, and creativity in reacting to the tragedy. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection targets most of the respiratory tract, resulting in a severe sickness called acute respiratory distress syndrome that may be fatal in some individuals. Although the lung is the primary organ targeted by COVID-19 viruses, the clinical aspect of the disease is varied and ranges from asymptomatic to respiratory failure. However, due to an unorganized immune response and several affected mechanisms, the liver may also experience liver cell injury, ischemic liver dysfunction, and drug-induced liver injury, which can result in respiratory failure because of the immune system's disordered response and other compromised processes that can end in multisystem organ failure. Patients with liver cirrhosis or those who have impaired immune systems may be more likely than other groups to experience worse results from the SARS-CoV-2 infection. We thus intend to examine the pathogenesis, current therapy, and consequences of liver damage concerning COVID-19.

Blood is critical for health, supporting key functions like immunity and oxygen transport. While studies have found links between common blood clinical indicators and COVID-19, they cannot provide causal inference due to residual confounding and reverse causality. To identify indicators affecting COVID-19, we analyzed clinical data (n = 2,293, aged 18-65 years) from Guangzhou Medical University's first affiliated hospital (2022-present), identifying 34 significant indicators differentiating COVID-19 patients from healthy controls. Utilizing bidirectional Mendelian randomization analyses, integrating data from over 2.46 million participants from various large-scale studies, we established causal links for six blood indicators with COVID-19 risk, five of which is consistent with our observational findings. Specifically, elevated Troponin I and Platelet Distribution Width levels are linked with increased COVID-19 susceptibility, whereas higher Hematocrit, Hemoglobin, and Neutrophil counts confer a protective effect. Reverse MR analysis confirmed four blood biomarkers influenced by COVID-19, aligning with our observational data for three of them. Notably, COVID-19 exhibited a positive causal relationship with Troponin I (Tnl) and Serum Amyloid Protein A, while a negative association was observed with Plateletcrit. These findings may help identify high-risk individuals and provide further direction on the management of COVID-19.

Coronavirus disease 2019 (COVID-19) was an epidemic that effected human health caused by SARS-CoV-2 infection. All-trans retinoic acid (ATRA) has anti-inflammatory capability. In this article, we evaluated the effectiveness and revealed the molecular mechanism of ATRA for treating SARS-CoV-2 using deep learning, in vitro studies, multi-scale molecular modeling, and network pharmacology. The DeepDTA model suggested that ATRA would be effective against COVID-19. In vitro studies confirmed the antiviral activity of ATRA. Subsequently, multi-scale molecular modeling indicated that ATRA could binding to angiotensin converting enzyme 2 (ACE2), 3C-like protease (3CLpro), RNA dependent RNA polymerase (RdRp), helicase, and 3'-to-5' exonuclease by non-covalent interactions. Additionally, network pharmacology suggested that ATRA alleviated inflammatory response by regulating the IL-17 signaling pathway and binding with TNF, PTGS2, and MAPK1 directly. In summary, our findings provide the first evidence that ATRA suppresses the entry and replication of SARS-CoV-2, and regulates inflammatory response of host cells.

COVID-19 is an illness caused by the SARS-CoV-2 virus, a type of coronavirus initially identified in China in late 2019, emerging as the leading cause of death attributed to a single infectious agent worldwide. The COVID-19 pandemic poses a substantial challenge to global public health in the first quarter of this century. The rapid evolution of the pandemic and its intricate response have hindered the formulation of definitive conclusions, and it may take years to comprehend its long-term effects. Assessing the extent of organ damage beyond the lungs could guide physicians in the disease's severity or progression. Based on these characteristics, an earlier and more targeted approach can be initiated at the appropriate moment. The association between hepatic profile and mortality in COVID-19 patients is a subject of scientific interest, as SARS-CoV-2 infection can lead to hepatitis. In severe cases, it may induce sepsis-related liver injury, potentially culminating in hepatic failure.

The study's objective is to determine the prevalence of mortality in adult patients with elevated hepatic profile hospitalized due to SARS-CoV-2 infection. This cross-sectional, monocentric study was conducted at a healthcare institution in Bogotá, Colombia.

This study includes 91 patients with confirmed diagnoses of COVID-19, revealing a prevalence of hepatic profile alterations in 61.5% (n=56) of hospitalized patients. The mortality rate observed is 17.6% (n= 16), with an odds ratio (OR) of 12.4 (95% CI = 1.56-99.0) in patients with hepatic profile alterations.

This research underscores the importance of early detection of hepatic profile alterations in hospitalized patients with COVID-19. Not only are these alterations prevalent, but they are also potentially associated with an increased risk of mortality. These findings emphasize the necessity for further research to enhance strategies and prognostication for patients with COVID-19 in the future.

Objective  The four initial severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected pregnant women presenting at term gestation to our institution presented with transaminitis. Three of the four were diagnosed with intrahepatic cholestasis of pregnancy (IHCP). Growing evidence exists of an associated transaminitis in nonpregnant SARS-CoV-2 patients. However, there are limited data of hepatic involvement of SARS-CoV-2 in pregnancy, and no previous studies have assessed the association with IHCP in patients with coronavirus disease 2019 (COVID-19). Study Design  This was a retrospective, single-center case series of four consecutive pregnant women with a positive result for SARS-CoV-2 presenting with transaminitis in third trimester. Results  The clinical courses of four pregnant women with COVID-19 and transaminitis, three of four of whom were diagnosed with IHCP, are described. Testing for SARS-CoV-2 was done through a reverse transcription polymerase chain reaction test of a nasopharyngeal swab. Conclusion  As we await larger studies ascertaining the incidence of IHCP in SARS-CoV-2, this prevalence highlights the importance of diagnosing IHCP among women with COVID-19 as a potential etiology of transaminitis, as IHCP risks may be ameliorated with earlier delivery. Moreover, delineating a hepatobiliary association in pregnancy may provide further information about the mechanism of liver impairment in SARS-CoV-2 in all patients.

Causality assessment of suspected drug-induced liver injury (DILI) during metabolic dysfunction-associated steatohepatitis (MASH) clinical trials can be challenging, and liver biopsies are not routinely performed as part of this evaluation. While the field is moving away from liver biopsy as a diagnostic and prognostic tool, information not identified by non-invasive testing may be provided on histology.

To address the appropriate utilisation of liver biopsy as part of DILI causality assessment in this setting.

From 2020 to 2022, the Liver Forum convened a series of webinars on issues pertaining to liver biopsy during MASH trials. The Histology Working Group was formed to generate a series of consensus documents addressing these challenges. This manuscript focuses on liver biopsy as part of DILI causality assessment.

Expert opinion, guidance and recommendations on the role of liver biopsy as part of causality assessment of suspected DILI occurring during clinical trials for a drug(s) being developed for MASH are provided. Lessons learned from prior MASH programs are reviewed and gaps identified.

Although there are no pathognomonic features, histologic evaluation of suspected DILI during MASH clinical trials may alter patient management, define the pattern and severity of injury, detect findings that favour a diagnosis of DILI versus MASH progression, identify prognostic features, characterise the clinicopathological phenotype of DILI, and/or define lesions that influence decisions about trial discontinuation and further development of the drug.

Coronavirus disease 2019 (COVID-19), a global pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has posed a catastrophic threat to human health worldwide. Human stem cell-derived organoids serve as a promising platform for exploring SARS-CoV-2 infection. Several review articles have summarized the application of human organoids in COVID-19, but the research status and development trend of this field have seldom been systematically and comprehensively studied. In this review, we use bibliometric analysis method to identify the characteristics of organoid-based COVID-19 research. First, an annual trend of publications and citations, the most contributing countries or regions and organizations, co-citation analysis of references and sources and research hotspots are determined. Next, systematical summaries of organoid applications in investigating the pathology of SARS-CoV-2 infection, vaccine development and drug discovery, are provided. Lastly, the current challenges and future considerations of this field are discussed. The present study will provide an objective angle to identify the current trend and give novel insights for directing the future development of human organoid applications in SARS-CoV-2 infection.

High-flow nasal oxygen (HFNO) and prone positioning may improve outcomes of coronavirus disease 2019 (COVID-19) patients treated in the intensive care unit (ICU). The aim of this study was to describe outcomes following the timely application of HFNO and prone positioning in COVID-19 patients treated in a ward setting.

The study included 89 prospectively recruited subjects at the COVID-19 ward unit of the University Hospital of Heraklion, Greece, between March and December 2020.

Seventy-four (83%) of the 89 subjects in the study had severe COVID-19. Of those, 33 (45%) required HFNO treatment and prone positioning and 15 (45%) were transferred to the ICU, with 4 of them being intubated. Severe COVID-19 and HFNO needs were associated with an increased pneumonia severity index (PSI) score on admission and a worse PaO2/FiO2 ratio. In multivariate analysis, PSI was the only independent predictor of subsequent HFNO needs (OR=1.022). Overall intubation and mortality rates were 5.6% and 3.4%, respectively.

This study shows that for patients with severe COVID-19 hospitalized in medical wards, standard COVID-19 treatment, along with the timely utilization of HFNO and prone positioning, resulted in excellent outcomes with fewer ICU admission rates.

Historically, biological research has relied primarily on animal models. While this led to the understanding of numerous human biological processes, inherent species-specific differences make it difficult to answer certain liver-related developmental and disease-specific questions. The advent of 3D organoid models that are either derived from pluripotent stem cells or generated from healthy or diseased tissue-derived stem cells have made it possible to recapitulate the biological aspects of human organs. Organoid technology has been instrumental in understanding the disease mechanism and complements animal models. This review underscores the advances in organoid technology and specifically how liver organoids are used to better understand human-specific biological processes in development and disease. We also discuss advances made in the application of organoid models in drug screening and personalized medicine.

Liver function tests (LFTs) are elevated in >50% of hospitalized individuals infected with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), with increased enzyme levels correlating with a more severe COVID-19 course. Despite these observations, evaluations of viral presence within liver parenchyma and viral impact on liver function remain controversial.

Our work is a comprehensive immunopathological evaluation of liver tissue from 33 patients with severe, and ultimately fatal, cases of SARS-CoV-2 infection. Coupled with clinical data, we reveal the absence of SARS-CoV-2 infection in cholangiocytes and hepatocytes despite dramatic systemic viral presence. Critically, we identify significant focal viral sinusoidal aggregates in 2/33 patients and single viral RNA molecules circulating in the hepatic sinusoids of 15/33 patients. Utilizing co-immunofluorescence, focal viral liver aggregates in patients with COVID-19 were colocalized to platelet and fibrin clots, indicating the presence of virus-containing sinusoidal microthrombi. Furthermore, this patient cohort, from the initial months of the COVID-19 pandemic, demonstrates a general downtrend of LFTs over the course of the study timeline and serves as a remarkable historical time point of unattenuated viral replication within patients.

Together, our findings indicate that elevated LFTs found in our patient cohort are not due to direct viral parenchymal infection with SARS-CoV-2 but rather likely a consequence of systemic complications of COVID-19. This work aids in the clinical treatment considerations of patients with SARS-CoV-2 as therapies for these patients may be considered in terms of their direct drug hepatotoxity rather than worsening hepatic function due to direct infection.

Coronavirus Disease of 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients had varying clinical symptoms and disease severity (mild, moderate, severe, and critical). Several risk factors, including genetic polymorphisms, have been reported to be associated with disease risk and severity. This study aimed to investigate the association of two polymorphisms in the orosomucoid1-like 3 (ORMDL3) and a disintegrin and metalloprotease 33 (ADAM33) asthma-related genes with the severity of COVID-19.

The study included 116 COVID-19 patients with a positive polymerase chain reaction (PCR) test for the SARS-CoV-2 Delta variant. 58 patients with moderate symptoms, 28 patients with severe symptoms, and 30 outpatients with mild symptoms. Genotyping of rs7216389 in the ORMDL3 and rs2280091 in ADAM33 genes was performed by polymerase chain reaction-restriction fragment length polymorphism. Furthermore, records of patients were studied for hematological profiles and biochemical markers.

No significant association was found between rs7216389 and rs2280091 and the severity of COVID-19 between different groups of COVID-19 patients. The serum levels of RBC and neutrophil-to-lymphocyte ratio were significantly increased; the erythrocyte sedimentation rate (ESR), and Aspartate transaminase (SGOT) were significantly decreased during treatment in intensive care unit (ICU) patients. The serum levels of red blood cells, Platelets, Urea, Alkaline phosphatase, ESR, Alanine transaminase (SGPT), and SGOT were significantly increased during treatment in hospitalized patients. The serum levels of inflammatory factors, including C-reactive protein (CRP), D-dimer, and Ferritin at the time of admission, were significantly higher in patients admitted to the ICU patients compared to the other group of patients.

The two polymorphisms studied in this research are not suitable markers for predicting the severity of COVID-19. However, there are significant differences in the amounts of some blood factors in different groups of COVID-19 patients (P < 0.05) and these factors can be used as a marker for the disease severity prediction.

Using a large dataset, we evaluated prevalence and severity of alterations in liver enzymes in COVID-19 and association with patient-centred outcomes.

We included hospitalized patients with confirmed or suspected SARS-CoV-2 infection from the International Severe Acute Respiratory and emerging Infection Consortium (ISARIC) database. Key exposure was baseline liver enzymes (AST, ALT, bilirubin). Patients were assigned Liver Injury Classification score based on 3 components of enzymes at admission: Normal; Stage I) Liver injury: any component between 1-3x upper limit of normal (ULN); Stage II) Severe liver injury: any component ≥3x ULN. Outcomes were hospital mortality, utilization of selected resources, complications, and durations of hospital and ICU stay. Analyses used logistic regression with associations expressed as adjusted odds ratios (OR) with 95% confidence intervals (CI).

Of 17,531 included patients, 46.2% (8099) and 8.2% (1430) of patients had stage 1 and 2 liver injury respectively. Compared to normal, stages 1 and 2 were associated with higher odds of mortality (OR 1.53 [1.37-1.71]; OR 2.50 [2.10-2.96]), ICU admission (OR 1.63 [1.48-1.79]; OR 1.90 [1.62-2.23]), and invasive mechanical ventilation (OR 1.43 [1.27-1.70]; OR 1.95 (1.55-2.45). Stages 1 and 2 were also associated with higher odds of developing sepsis (OR 1.38 [1.27-1.50]; OR 1.46 [1.25-1.70]), acute kidney injury (OR 1.13 [1.00-1.27]; OR 1.59 [1.32-1.91]), and acute respiratory distress syndrome (OR 1.38 [1.22-1.55]; OR 1.80 [1.49-2.17]).

Liver enzyme abnormalities are common among COVID-19 patients and associated with worse outcomes.

Liver dysfunction was common in coronavirus disease 2019 (COVID-19), but its association with clinical features and poor prognosis has not been fully delineated. Our study aimed to determine the role of liver dysfunction in COVID-19 and understand the predictors for worse outcomes in patients with liver injury.

We conducted this multicenter, retrospective study in five designated hospitals for COVID-19 management. Laboratory-confirmed COVID-19 patients were enrolled and classified into the normal live function group and liver dysfunction group according to liver enzymes, bilirubin, and albumin on admission, respectively. Data of baseline, clinical manifestations, and outcomes were collected and compared in the paired groups.

Of the 649 included COVID-19 patients, 200 (30.8%), 69 (10.6%), and 267 (41.1%) patients had elevated liver enzymes, increased bilirubin, and low-level albumin, respectively. Fever, cough, and dyspnea were the most common symptoms and showed an increased proportion in the liver dysfunction group. Compared with patients in the normal liver function group, patients with liver dysfunction manifested decreased lymphocytes, higher level of leukocytes, neutrophils, inflammatory indicators, and cytokines, as well as more severe impairment in kidney function and myocardium. They were more likely to show bilateral involvement and more pulmonary lobes involved according to chest images. With increased proportion of patients who developed severe/critical conditions and needed mechanical ventilation and systemic glucocorticoid therapy, patients with liver dysfunction on admission showed significantly higher in-hospital mortality. Moreover, cardiac troponin I ≥1.5 ng/mL was identified as an independent mortality predictor in the elevated liver enzymes group.

Patients with liver dysfunction on admission had worse clinical manifestation, and resulted in higher rate of severe/critical type, receiving mechanical ventilation and in-hospital mortality.