To measure hepatic steatosis (HS) in hospitalized COVID-19 patients using unenhanced chest computed tomography (CT) imaging and to evaluate the relationship between disease severity and prognosis in adult patients.This retrospective study included 152 consecutive hospitalized COVID-19 patients with a positive reverse transcriptase polymerase chain reaction (RT-PCR) test. The COVID-19 Reporting and Data System (CO-RADS) and the chest CT score were evaluated. HS measurements were performed based on CT images using a single region of interest placed on the right liver lobe (segments V-VII). HS was defined as a liver attenuation value <40 Hounsfield units. Data were collected and compared with the patients' prognostic parameters.Of the 152 inpatients, 137 patients (90.1%) had a CT score ≥3 and 109 patients (71.7%) had a CO-RADS score ≥4, 43 (28.2%) had HS. All patients with HS (100%) and 94/109 (86.2%) patients without HS had a CT score ≥3. There was a statistically significant difference between the two groups in terms of chest CT score (p=0.006). There was no statistically significant difference between the two groups in terms of CO-RADS score (p=0.291). The median CRP levels were significantly increased in patients with HS compared to patients without HS (p=0.023). There was no significant difference in ICU hospitalization and mortality due to the presence of HS (p>0.05).The current study revealed significantly higher chest CT scores in COVID-19 patients with HS measured on CT compared to those without HS. Opportunistic use of CT images for the detection of HS can be considered as an adjunctive tool in the risk analysis of COVID-19 patients hospitalized due to COVID-19 pneumonia.The severity of COVID-19 disease is increased in hospitalized patients with hepatosteatosis compared to patients with a normal liver. Density measurements for the evaluation of HS using opportunistic CT applications can be considered as an adjunctive tool in the prognostic evaluation of hospitalized patients with COVID-19 pneumonia. · Parlak AE, Erdem Toslak İ, Turkoglu Selcuk N. Can Opportunistic Use of Computed Tomography Help Reveal the Association Between Hepatic Steatosis and Disease Severity in Hospitalized COVID-19 Patients?. Rofo 2025; 197: 648-656.

Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) binds to Angiotensin Converting Enzyme - 2 (ACE2) receptor targeting various organs including liver. Liver injury is a common feature of SARS-CoV-2 acute infection. A few studies have also described chronic hepatic alterations in patients with previous COVID-19. We hypothesize that steatosis seen in COVID-19 patients reflects their metabolic profile and is not caused by persistent inflammation sustained by SARS-CoV-2.

We conducted a prospective study to evaluate long-term changes in liver function and structure in patients hospitalized for COVID-19. Patients without a prior known hepatic disease with mild to moderate COVID-19 were enrolled during hospitalization and reevaluated during a follow-up visit at a medium 16 months. Complete blood panels with metabolic profile, BMI, alcohol consumption and physical activity were compared between baseline and follow-up. Specific ultrasound scans were obtained during hospital stay and at follow-up to quantify steatosis using Steatoscore2.0.

Among 55 eligible patients, 33 were included in the analysis and only 3 (9 %) had a new diagnosis of steatosis at follow-up. Steatoscore2.0 did not change significantly from baseline to follow-up (1.7 vs 1.73, p = 0.348), while changes occurred in body mass index and physical activity estimated by IPAQ questionnaire (26.3 vs 26.6 kg/m2, p = 0.005; 540 vs. 480, p = 0.015, respectively). There was a statistically significant increase in total cholesterol (144.5 vs 187.0 mg/dl, p = 0.003) and low-density lipoprotein-cholesterol (73.8 vs 113.9 mg/dl, p = 0.003). Inflammatory markers normalized at follow-up, including C-reactive protein (41.1 vs. 0.8 mg/L, p < 0.001), and ferritin (410.0 vs. 91.0 ng/dl, p < 0.001). Four patients had a 3-time rise in liver transaminase levels at baseline, and this was not confirmed at follow-up. Change in Steatoscore2.0 correlated significantly with Triglyceride-glucose index as a surrogate of insulin resistance.

In our study, long term functional and structural changes were not observed in patients with previous SARS-CoV-2 infection. There was a significant deterioration of metabolic profile post COVID-19.

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.

This study investigated the consistency of the FIB-4, APRI, and GPR indices in assessing significant liver fibrosis and cirrhosis in patients with Coronavirus Disease 2019(COVID-19) who also suffer from various liver diseases, providing references for the clinical selection and application for non-invasive assessment methods.

The study evaluated 744 COVID-19 patients with coexisting liver diseases: 508 cases with non-alcoholic fatty liver disease (NAFLD), 158 cases with chronic hepatitis B (CHB), and 78 cases with a combination of both ailments. FIB-4, APRI, and GPR were employed to assess significant liver fibrosis and cirrhosis. Concordance among the methods was determined using Kappa analysis, and receiver operating characteristic (ROC) curves helped identify the optimal cutoff values for each index.

For COVID-19 patients with NAFLD, Kappa values for significant liver fibrosis were 0.81, 0.90, 0.80, and 0.79, and for cirrhosis, they were 0.88, 0.97,0.88, and 0.88, respectively (all p < 0.05). Among those with CHB, Kappa values were 0.81, 0.81, 0.83, and 0.75 for fibrosis, and0.87, 0.91, 0.88, and 0.92 for cirrhosis (all p < 0.05). In patients with coexisting liver diseases, the values were 0.87, 0.86, 0.86, and 0.78 for fibrosis, and 0.67, 0.69, 0.54, and 0.81for cirrhosis (all p < 0.05). Linear trend analysis revealed significant relationships between FIB-4 values, APRI values, GPR values, and the severity of COVID-19 (χ2 trend: 15.205,35.114, and 13.973, respectively, all p < 0.001), between FIB-4 values and APRI values and the coronavirus negative conversion time (all p < 0.05) in COVID-19 with NAFLD, and between FIB-4 values and GPR values and the coronavirus negative conversion time in patients with COVID-19 with CHB(all p < 0.05).

Using the current cutoff values, the non-invasive assessments demonstrated almost perfect consistency in evaluating significant liver fibrosis and cirrhosis in COVID-19 patients with liver diseases, though FIB-4 and GPR showed moderate consistency in cirrhosis evaluation in patients with coexisting liver conditions. Moreover, it also indicated that increased liver fibrosis correlates with more severe COVID-19 and prolonged coronavirus negative conversion time.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters host cells via the angiotensin-converting enzyme 2 (ACE2) receptor. Mounting evidence has indicated the presence of hepatic SARS-CoV-2 infection and liver injury in patients with coronavirus disease 2019 (COVID-19). Understanding the mechanisms of hepatic SARS-CoV-2 infection is crucial for addressing COVID-19-related liver pathology and developing targeted therapies. This editorial discusses the significance of ACE2 in hepatic SARS-CoV-2 infection, drawing on the research by Jacobs et al. Their findings indicate that hepatic ACE2 expression, frequency of hepatic SARS-CoV-2 infection, and severity of liver injury are elevated in patients with pre-existing chronic liver diseases. These data suggest that hepatic ACE2 could be a promising therapeutic target for COVID-19.

Background/Objectives: Fatty liver disease (FLD), particularly non-alcoholic fatty liver disease (NAFLD), is a growing global health concern that underscores the need for effective dietary management strategies. With over 25% of patients seeking dietary advice through platforms like YouTube, the quality and reliability of this information remain critical. However, the disparity in educational value and engagement metrics between professional and non-professional content remains underexplored. This study evaluates YouTube's role in disseminating dietary advice for FLD management, focusing on content reliability, engagement metrics, and the educational value of videos. Methods: This cross-sectional study systematically analyzed 183 YouTube videos on FLD and dietary advice. Videos were selected based on relevance, English language, and non-promotional content. Scoring systems, including DISCERN, Global Quality Score (GQS), and the Video Information and Quality Index (VIQI), were employed to assess reliability, quality, and educational value. Engagement metrics such as views, likes, dislikes, and interaction rates were analyzed across uploader categories, including healthcare professionals, patients, and undefined sources. Results: Videos uploaded by healthcare professionals demonstrated significantly higher DISCERN scores (4.2 ± 0.8) and GQS ratings (4.1 ± 0.6) compared to patient-generated content (DISCERN: 2.8 ± 0.9; GQS: 3.0 ± 0.7). However, patient-generated videos achieved higher engagement rates, with median views reaching 340,000 (IQR: 15,000-1,000,000) compared to 450,050 (IQR: 23,000-1,800,000) for professional videos. Nutritional recommendations spanned diverse approaches, including low-carb diets, Mediterranean diets, and guidance to avoid processed foods and sugars. A significant proportion of videos lacked evidence-based content, particularly among non-professional uploads. Conclusions: YouTube represents a widely accessed but inconsistent source of dietary advice for FLD. While healthcare professional videos exhibit higher reliability and educational value, patient-generated content achieves broader engagement, revealing a critical gap in trusted, accessible dietary guidance. These findings highlight the need for clinicians and content creators to collaborate in curating and disseminating evidence-based content, ensuring patients receive accurate, actionable advice for managing FLD.

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.

Metabolic dysfunction-associated steatotic liver disease (MASLD) patients are at an elevated risk of developing severe coronavirus disease 2019 (COVID-19). The objective of this study was to assess antibody responses and safety profiles six months after the third dose of the inactivated acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine in MASLD patients.

This study included MASLD patients and healthy volunteers without a history of SARS-CoV-2 infection. Blood samples were collected six months after receiving the third dose of the inactivated vaccine to measure the levels of neutralizing antibodies (NAbs) and anti-spike IgG antibodies against SARS-CoV-2.

A total of 335 participants (214 MASLD patients and 121 healthy volunteers) were enrolled. The seroprevalence of NAb was 61.7% (132 of 214) in MASLD patients and 74.4% (90 of 121) in healthy volunteers, which was a significant difference (p = 0.018). Statistically significant differences in IgG seroprevalence were also observed between MASLD patients and healthy volunteers (p = 0.004). Multivariate analysis demonstrated that the severity of MASLD (OR, 2.97; 95% CI, 1.32-6.68; p = 0.009) and age (OR, 1.03; 95% CI, 1.01-1.06; p = 0.004) were independent risk factors for NAb negativity in MASLD patients. Moderate/severe MASLD patients had a lower NAb seroprevalence than mild MASLD patients (45.0% vs. 65.5%, p = 0.016).

Lower antibody responses were observed in MASLD patients six months after their third dose of the inactivated vaccine than in healthy volunteers, providing further assistance in monitoring patients who are more vulnerable to hypo-responsiveness to SARS-CoV-2 vaccines.

The incidence of hepatic abnormalities has been notably higher following the coronavirus disease 2019 (COVID-19) infection, attributed to the virus's entry into cells via angiotensin-converting enzyme 2 (ACE2) surface expression. The gastrointestinal tract's significant ACE2 expression, alongside a lesser degree in the biliary epithelium, has been implicated in gastrointestinal symptoms and liver injury.

The aim of this study was to determine whether specific ultrasonographic findings in the liver correlate with acute increases in liver function tests (LFTs) among hospitalized patients.

A retrospective analysis was conducted on hospitalized COVID-19 patients at Hazem Mebaireek General Hospital in Qatar, from March 1, 2020, to June 30, 2020. The study focused on patients who experienced acute increases in LFTs, excluding those with chronic liver disease. Ultrasound imaging and patient records were reviewed to gather data.

Out of 223 ultrasound studies of COVID-19 patients, 158 met the inclusion criteria. The majority were male, with a mean age of 47.76 ± 13.76 years. Ultrasound results showed 43.7% normal liver parenchyma, while 56.3% exhibited nonspecific abnormalities such as diffuse liver hyperechogenicity (39.2%), enlargement with diffuse hyperechogenicity (12.7%), and other findings (4.4%). The biliary tree was predominantly normal (96.2%), with 3.8% showing abnormalities, including intrahepatic (2.5%) and extrahepatic (1.3%) dilatation. Gallbladder evaluations were normal in 60.1% of cases, with 39.9% showing abnormalities like stones (6.3%), stones with sludge (13.3%), polyps (6.3%), wall thickening (1.9%), and other conditions (12%). A significant correlation was found between abnormal liver parenchyma findings and elevated levels of bilirubin (total and direct) and alkaline phosphatase, with p-values < 0.05. Only aspartate aminotransferase levels showed a significant correlation with biliary tree abnormalities.

The most common ultrasonographic finding associated with acute increases in LFTs among hospitalized COVID-19 patients was diffuse liver hyperechogenicity, with or without enlargement. These findings suggest a nonspecific yet significant association with liver function anomalies in the context of COVID-19.

Limited data are currently available regarding the cellular immune response to a live attenuated hepatitis A virus (HAV) vaccine, especially in children with obesity. The objective of this retrospective cohort study was to compare the activation of antigen-specific interferon (IFN)-γ+ T cells in obese children and adolescents with healthy individuals before and after immunization with a single dose of live attenuated HAV vaccine.

Blood samples were obtained from the 2021 study by Dumrisilp et al. investigating the immunogenicity of the live attenuated hepatitis A vaccine in children and young adults. Prior to enrollment, all 212 subjects had never received any HAV vaccine and tested negative for anti-HAV antibodies. The participants were vaccinated with a freeze-dried, live attenuated HAV vaccine of the H2 strain. In this study, we analyzed the stored peripheral blood mononuclear cells (PBMCs) obtained from a subgroup of 30 obese subjects and 30 normal-weight healthy controls of the same age and sex. PBMCs were collected before and 8-9 weeks after HAV vaccination for further analysis. These cells were stimulated with a recombinant antigen derived from HAV-VP3, and the immune response was evaluated using the IFN-γ enzyme-linked immunospot (ELISpot) assay.

The between-group analysis indicated that the T-cell response of obese participants was comparable to that of normal-weight controls both before and after vaccination. The change in IFN-γ production from before to after vaccination in the obese group was not significantly different from that of the control group. Additionally, in the obese group, no correlation was found between IFN-γ production and clinical characteristics such as sex, body mass index, waist circumference, and acanthosis nigricans.

Testing for cellular immune response provides a comprehensive understanding of the overall immune response to vaccination. This study, the first to explore this significant aspect, suggests that obesity does not affect the short-term cellular immune response to live attenuated HAV vaccination.

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.

Increased liver fibrosis scores (LFS), such as fibrosis-4 index (FIB-4) or non-alcoholic fatty liver disease fibrosis score (NFS), and fatty liver are known risk factors for severe coronavirus disease 2019 (COVID-19). The purpose of this study was to identify the best scores, which predict the prognosis of COVID-19.

Participants comprised consecutive Japanese COVID-19 patients admitted to our hospital between February 14, 2020, and April 14, 2021. Multivariate logistic regression analysis was performed to evaluate the relationships between LFS (FIB-4, NFS, aspartate aminotransferase-to-platelet ratio index [APRI], BARD score, and hepatic steatosis index [HSI]) or fatty liver on computed tomography (CT), and severity of COVID-19.

Of the 415 patients (mean age, 59 years), 177 patients (42.7%) needed oxygen therapy, 90 patients (21.7%) worsened to severe COVID-19, and 45 patients (10.8%) died during admission. Multivariate logistic regression analysis showed that increased FIB-4 and NFS were risk factors for death, severe COVID-19, and oxygen demand; that increased BARD was a risk factor for severe COVID-19 and oxygen demand; and that increased APRI and HSI were not risk factors for any status of COVID-19. Furthermore, increased NFS or BARD and fatty liver were independent risk factors for severe COVID-19 and oxygen demand.

This study showed that FIB-4 and NFS were the best liver fibrosis scores that predicted worse prognosis for COVID-19, and that increased NFS or BARD and fatty liver evident on CT represented independent risk factors for severe COVID-19 and oxygen demand.

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.

Hepatic sequelae are frequently reported in coronavirus disease 2019 cases and are correlated with increased disease severity. Therefore, a detailed exploration of host factors contributing to hepatic impairment and ultimately infection outcomes in patients is essential for improved clinical management. The causes of hepatic injury are not limited to drug-mediated toxicity or aberrant host inflammatory responses. Indeed, multiple studies report the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in liver autopsies and the susceptibility of explanted human hepatocytes to infection. In this review, we confirm that hepatic cells express an extensive range of factors implicated in SARS-CoV-2 entry. We also provide an overview of studies reporting evidence for direct infection of liver cell types and the infection-induced cell-intrinsic processes that likely contribute to hepatic impairment.

One significant challenge in addressing the coronavirus disease 2019 (COVID-19) pandemic is to grasp a comprehensive picture of its infectious mechanisms. We urgently need a consistent framework to capture the intricacies of its complicated viral infectious processes and diverse symptoms.

We systematized COVID-19 infectious processes through an ontological approach and provided a unified description framework of causal relationships from the early infectious stage to severe clinical manifestations based on the homeostasis imbalance process ontology (HoIP). HoIP covers a broad range of processes in the body, ranging from normal to abnormal. Moreover, our imbalance model enabled us to distinguish viral functional demands from immune defense processes, thereby supporting the development of new drugs, and our research demonstrates how ontological reasoning contributes to the identification of patients at severe risk.

The HoIP organises knowledge of COVID-19 infectious processes and related entities, such as molecules, drugs, and symptoms, with a consistent descriptive framework. HoIP is expected to harmonise the description of various heterogeneous processes and improve the interoperability of COVID-19 knowledge through the COVID-19 ontology harmonisation working group.

Background: Steatotic liver disease (SLD) has been linked to more exacerbated inflammatory responses in various scenarios. The relationship between SLD and COVID-19 prognosis remains unclear. Our aim was to investigate the impact of SLD on the outcome of COVID-19. Methods: Patients hospitalized with confirmed COVID-19 and who underwent laboratory tests and chest CT scans were included. SLD was assessed by measuring the attenuation coefficient on CT scans. The relationship between SLD, the severity of COVID-19 clinical presentation and in-hospital mortality were assessed. Results: A total of 610 patients were included (mean age 62 ± 16 years, 64% male). The prevalence of SLD was 30%, and the overall in-hospital mortality rate was 19%. Patients with SLD were younger (58 ± 13 vs. 64 ± 16 years, p < 0.001) and had a higher BMI (32 ± 5 vs. 28 ± 4 kg/m2, p = 0.014). Admission AST values were higher in patients with SLD (82 ± 339 vs. 50 ± 37, p = 0.02), while D-dimer (1112 ± 2147 vs. 1959 ± 8509, p = 0.07), C-reactive protein (12 ± 9 vs. 11 ± 8, p = 0.27), ALT (67 ± 163 vs. 47 ± 90, p = 0.11), ALP (83 ± 52 vs. 102 ± 125, p = 0.27), and GGT (123 ± 125 vs. 104 ± 146, p = 0.61) did not significantly differ compared to patients without SLD. No difference was observed regarding lung parenchyma involvement >50% (20% vs. 17%, p = 0.25), hospital length of stay (14 ± 19 vs. 16 ± 23 days, p = 0.20), hemodialysis support (14% vs. 16%, p = 0.57), use of mechanical ventilation (20% vs. 20%, p = 0.96), and in-hospital mortality (17% vs. 20%, p = 0.40) when comparing patients with and without SLD. Conclusions: SLD showed no significant association with morbidity and mortality in patients with COVID-19.

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.

Coronavirus disease 2019 (COVID-19) has had a significant impact on global health and healthcare systems. This retrospective study aimed to assess the association between biochemical parameters and outcomes in COVID-19 patients in Jazan, Saudi Arabia.

After establishing the inclusion criteria and obtaining ethical approval, data from 156 reverse transcriptase-polymerase chain reaction (RT-PCR)-confirmed COVID-19 patients were collected from electronic medical records from a general hospital in Samtah, Jazan, from April 2020 to October 2021. The collected data included patient demographics and liver, kidney, heart, and electrolyte function marker levels. Descriptive, inferential, and principal component analyses were conducted.

Survival rates varied according to age and body mass index (BMI). Statistical analysis demonstrated that the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), sodium (Na), potassium (K), blood urea nitrogen (BUN), creatinine (Cr), creatine kinase (CK), CK myocardial band (MB), and lactate dehydrogenase (LDH) were significantly higher (P < 0.05) than the reference values, as assessed using the one-sample t-test. Principal component analysis (PCA) also revealed an underlying pattern in the variation of these biochemical markers. These findings suggest that certain biochemical parameters may serve as useful indicators for monitoring the condition of COVID-19 patients.

This retrospective study in Jazan, Saudi Arabia highlights the association between biochemical parameters and outcomes in COVID-19 patients. Elevated levels of markers of liver, kidney, heart, and electrolyte function suggest organ damage and dysregulation. The pattern identified through PCA provides insights into disease severity. Monitoring these parameters may serve as valuable indicators for assessing COVID-19 patients. Further research is needed to validate these findings, explore their potential for personalized treatment strategies, and improve patient outcomes during the ongoing pandemic.

Metabolic dysfunction-associated steatotic liver disease (MASLD), formally known as nonalcoholic fatty liver disease, is the most common chronic liver disease in the United States. Patients with MASLD have been reported to be at a higher risk of developing severe coronavirus disease 2019 (COVID-19) and death. However, most studies are single-center studies, and nationwide data in the United States is lacking.

To study the influence of MASLD on COVID-19 hospitalizations during the initial phase of the pandemic.

We retrospectively analyzed the 2020 National Inpatient Sample (NIS) database to identify primary COVID-19 hospitalizations based on an underlying diagnosis of MASLD. A matched comparison cohort of COVID-19 hospitalizations without MASLD was identified from NIS after 1: N propensity score matching based on gender, race, and comorbidities, including hypertension, heart failure, diabetes, and cirrhosis. The primary outcomes included inpatient mortality, length of stay, and hospitalization costs. Secondary outcomes included the prevalence of systemic complications.

A total of 2210 hospitalizations with MASLD were matched to 2210 hospitalizations without MASLD, with a good comorbidity balance. Overall, there was a higher prevalence of severe disease with more intensive care unit admissions (9.5% vs 7.2%, P = 0.007), mechanical ventilation (7.2% vs 5.7%, P = 0.03), and septic shock (5.2% vs 2.7%, P <0.001) in the MASLD cohort than in the non-MASLD cohort. However, there was no difference in mortality (8.6% vs 10%, P = 0.49), length of stay (5 d vs 5 d, P = 0.25), and hospitalization costs (42081.5 $ vs 38614$, P = 0.15) between the MASLD and non-MASLD cohorts.

The presence of MAFLD with or without liver cirrhosis was not associated with increased mortality in COVID-19 hospitalizations; however, there was an increased incidence of severe COVID-19 infection. This data (2020) predates the availability of COVID-19 vaccines, and many MASLD patients have since been vaccinated. It will be interesting to see if these trends are present in the subsequent years of the pandemic.

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are potential risk factors for severe pneumonia and other infections. Available data on the role of NAFLD/NASH in worsening outcomes for COVID-19 are controversial and might be confounded by comorbidities.

We used the PINC AI™ Healthcare Data Special Release (PHD-SR) to identify patients with COVID-19 (ICD-10) at approximately 900 hospitals in the United States. We performed exact matching (age, gender, and ethnicity) for patients with or without NAFLD/NASH, adjusting for demographics (admission type, region) and comorbidities (e.g., obesity, diabetes) through inverse probability of treatment weighting and then analysed hospitalisation-related outcomes.

Among 513 623 patients with SARS-CoV-2 (COVID-19), we identified 14 667 with NAFLD/NASH who could be matched to 14 667 controls. Mean age was 57.6 (±14.9) years, 50.8% were females and 43.7% were non-Hispanic whites. After matching, baseline characteristics (e.g., age, ethnicity, and gender) and comorbidities (e.g., hypertension, obesity, diabetes, and cardiovascular disease) were well balanced (standard difference (SD) <.10), except for cirrhosis and malignancies. Patients with COVID-19 and NAFLD/NASH had higher FIB-4 scores, a significantly longer hospital length of stay (LOS) and intensive care LOS than controls (9.4 vs. 8.3 days, and 10.4 vs. 9.3, respectively), even after adjusting for cirrhosis and malignancies. Patients with COVID-19 and NAFLD/NASH also had significantly higher risk of needing invasive mandatory ventilation (IMV) (odds ratio 1.0727; 95% CI 1.0095-1.1400). Other outcomes were similar in both groups.

In this large real-world cohort of patients hospitalised for COVID-19 in the United States, NAFLD/NASH were obesity-independent risk factors for complicated disease courses.

SARS-CoV-2 causes varied gastrointestinal symptoms. Cirrhosis patients face higher mortality rates from it, especially those with decompensated cirrhosis. This study examines SARS-CoV-2's impact on decompensation in previously compensated cirrhotic patients.

We analyzed the Global Collaborative Network, comprising 98 healthcare organizations across sixteen countries, using TriNetX's deidentified research database. Compensated cirrhosis patients were split into two groups: one with SARS-CoV-2-positive patients and another testing negative. Using a 1:1 propensity score matching model based on baseline characteristics and comorbidities, we created comparable cohorts. We then assessed decompensation, mortality, and GI bleed at 1 and 3 months.

Out of 252,631 identified compensated cirrhosis patients, 27.3% (69,057) tested SARS-CoV-2-positive, while 72.6% (183,574) remained negative. Post PSM, 61,963 patients were in each group. SARS-CoV-2-positive patients showed significantly higher decompensation rates (4.4% vs. 1.9% at 1 month; 6% vs. 2.6% overall). Rates of complications, like ascites, SBP, HE, and HRS, increased notably. Mortality (2.5% vs. 1.7% at 1 month; 3.6% vs. 2.7% at 3 months) and GI bleed (1.3% vs. 0.9% at 1 month; 1.9% vs. 1.2% at 3 months) were also elevated in SARS-CoV-2 patients.

SARS-CoV-2 increases decompensation over 2-fold in compensated cirrhosis patients and raises mortality and increases rates of complications at 1 and 3 months.

Background: The effectiveness of the novel oral antiviral agents, nirmatrelvir plus ritonavir and molnupiravir, in treating COVID-19 in patients with nonalcoholic fatty liver disease is unclear. Objective: To assess the effectiveness of novel oral antiviral agents against COVID-19 among patients with nonalcoholic fatty liver diseases. Methods: This retrospective cohort study used the TriNetX Research Network to identify non-hospitalized patients with COVID-19 and nonalcoholic fatty liver disease between 1 January 2022, and 30 June 2023. Propensity score matching was used to form two matched cohorts treated with or without nirmatrelvir-ritonavir or molnupiravir. Results: In the two matched cohorts of 6,358 patients each, the use of novel oral antiviral agents was associated with a significantly lower risk of all-cause emergency department visits, hospitalization, or mortality (6.59% versus 8.24%; hazard ratio [HR], 0.80; 95% confidence interval [CI], 0.70-0.91). The novel antiviral group had a significantly lower risk of all-cause emergency department visits (HR, 0.85; 95% CI, 0.74-0.99). Additionally, the incidence of hospitalization was significantly lower in the oral antiviral group than in the control group (HR, 0.71; 95% CI, 0.55-0.90). There were no deaths in the oral antiviral group but 12 deaths in the control group. Conclusion: Novel oral antiviral agents are beneficial for treating COVID-19 in patients with nonalcoholic fatty liver disease.

The novel disease produced by SARS-CoV-2 mainly harms the respiratory tract, but it has shown the capacity to affect multiple organs. Epidemiologic evidence supports the relationship between Coronavirus Disease 2019 (COVID-19) and pancreatic and hepatic injury development, identified by alterations in these organ function markers. In this regard, it is important to ascertain how the current prevalence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) might affect COVID-19 evolution and complications. Although it is not clear how SARS-CoV-2 affects both the pancreas and the liver, a multiplicity of potential pathophysiological mechanisms seem to be implicated; among them, a direct viral-induced injury to the organ involving liver and pancreas ACE2 expression. Additionally, immune system dysregulation, coagulopathies, and drugs used to treat the disease could be key for developing complications associated with the patient's clinical decline. This review aims to provide an overview of the available epidemiologic evidence regarding developing liver and pancreatic alterations in patients with COVID-19, as well as the possible role that NAFLD/NASH might play in the pathophysiological mechanisms underlying some of the complications associated with COVID-19. This review employed a comprehensive search on PubMed using relevant keywords and filters. From the initial 126 articles, those aligning with the research target were selected and evaluated for their methodologies, findings, and conclusions. It sheds light on the potential pathophysiological mechanisms underlying this relationship. As a result, it emphasises the importance of monitoring pancreatic and hepatic function in individuals affected by COVID-19.

This study investigates the intricate interplay between Metabolic-associated Fatty Liver Disease (MAFLD) and COVID-19, exploring the impact of MAFLD on disease severity, outcomes, and the efficacy of the antiviral agent Paxlovid (nirmatrelvir/ritonavir). MAFLD, affecting a quarter of the global population, emerges as a potential risk factor for severe COVID-19, yet the underlying pathophysiological mechanisms remain elusive. This study focuses on the clinical significance of Paxlovid, the first orally bioavailable antiviral agent granted Emergency Use Authorization in the United States. Notably, outcomes from phase II/III trials exhibit an 88% relative risk reduction in COVID-19-associated hospitalization or mortality among high-risk patients. Despite conflicting data on the association between MAFLD and COVID-19 severity, this research strives to bridge the gap by evaluating the effectiveness of Paxlovid in MAFLD patients with COVID-19, addressing the scarcity of relevant studies.

Abnormal liver function was frequently observed in nonalcoholic fatty liver disease (NAFLD) patients infected with SARS-CoV-2. Our aim was to explore the effect of SARS-CoV-2 inactivated vaccines on liver function abnormality among NAFLD patients with COVID-19.

The multi-center retrospective cohort included 517 NAFLD patients with COVID-19 from 1 April to 30 June 2022. Participants who received 2 doses of the vaccine (n = 274) were propensity score matched (PSM) with 243 unvaccinated controls. The primary outcome was liver function abnormality and the secondary outcome was viral shedding duration. Logistic and Cox regression models were used to calculate the odds ratio (OR) and hazard ratio (HR) for the outcomes. Sensitivity analysis was conducted to assess robustness.

PSM identified 171 pairs of vaccinated and unvaccinated patients. Liver function abnormality was less frequent in the vaccinated group (adjusted OR, 0.556 [95% CI (confidence interval), 0.356-0.869], p = 0.010). Additionally, the vaccinated group demonstrated a lower incidence of abnormal bilirubin levels (total bilirubin: adjusted OR, 0.223 [95% CI, 0.072-0.690], p = 0.009; direct bilirubin: adjusted OR, 0.175 [95% CI, 0.080-0.384], p < 0.001) and shorter viral shedding duration (adjusted HR, 0.798 [95% CI, 0.641-0.994], p = 0.044) than the unvaccinated group. Further subgroup analysis revealed similar results, while the sensitivity analyses indicated consistent findings.

SARS-CoV-2 vaccination in patients with NAFLD may reduce the risk of liver dysfunction during COVID-19. Furthermore, vaccination demonstrated beneficial effects on viral shedding in the NAFLD population.

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To investigate the performance of a novel radiological-metabolic scoring (RM-S) system to predict mortality and intensive care unit (ICU) requirements among COVID-19 patients and to compare performance with the chest computed-tomography severity-scoring (C-CT-SS). The RMS was created from scoring systems such as visual coronary-artery-calcification scoring (V-CAC-S), hepatic-steatosis scoring (HS-S) and pancreatic-steatosis scoring (PS-S).

Between May 2021 and January 2022, 397 patients with COVID-19 were included in this retrospective cohort study. All demographic, clinical and laboratory data and chest CT images of patients were retrospectively reviewed. RM-S, V-CAC-S, HS-S, PS-S and C-CT-SS scores were calculated, and their performance in predicting mortality and ICU requirement were evaluated by univariate and multivariable analyses.

A total of 32 (8.1%) patients died, and 77 (19.4%) patients required ICU admission. Mortality and ICU admission were both associated with older age (p < 0.001). Sex distribution was similar in the deceased vs. survivor and ICU vs. non-ICU comparisons (p = 0.974 and p = 0.626, respectively). Multiple logistic regression revealed that mortality was independently associated with having a C-CT-SS score of ≥ 14 (p < 0.001) and severe RM-S category (p = 0.010), while ICU requirement was independently associated with having a C-CT-SS score of ≥ 14 (p < 0.001) and severe V-CAC-S category (p = 0.010).

RM-S, C-CT-SS, and V-CAC-S are useful tools that can be used to predict patients with poor prognoses for COVID-19. Long-term prospective follow-up of patients with high RM-S scores can be useful for predicting long COVID.

Metabolic dysfunction-associated fatty liver disease is a crucial global health concern. Studies have shown that metabolic dysfunction-associated fatty liver disease patients are at higher risk of severe coronavirus disease 2019. However, there are no precise measures of the correlation between the degree of metabolic dysfunction-associated fatty liver disease fibrosis and coronavirus disease 2019 severity. This study evaluated the association between metabolic dysfunction-associated fatty liver disease with varying degrees of fibrosis and coronavirus disease 2019 prognosis.

All hospitalized coronavirus disease 2019 patients who had liver steatosis as determined by computed tomography scan were included. Metabolic dysfunction-associated fatty liver disease was diagnosed in accordance with international consensus criteria. Liver fibrosis was assessed using the nonalcoholic fatty liver disease fibrosis score, FIB-4 and FIB-8 indexes. Coronavirus disease 2019 severity was defined using World Health Organization criteria. Logistic regression was used to determine the associations between varying degrees of fibrosis and the severity of coronavirus disease 2019.

A total of 996 confirmed hospitalized coronavirus disease 2019 cases with complete data were reviewed; of these, 296 (29.7%) cases of metabolic dysfunction-associated fatty liver disease were diagnosed. Metabolic dysfunction-associated fatty liver disease patients with any fibrotic state had more severe coronavirus disease 2019 than nonmetabolic dysfunction-associated fatty liver disease patients (adjusted odds ratio 1.912, 95% CI 1.363-2.684; P < .05). Multiple logistic regression analysis showed that metabolic dysfunction-associated fatty liver disease patients with significant fibrosis according to the FIB-8 score were more likely to have severe coronavirus disease 2019 (adjusted odds ratio 5.458, 95% CI 1.481-20.110; P < .05).

The presence of metabolic dysfunction-associated fatty liver disease in hospitalized coronavirus disease 2019 patients strongly correlated with the severity of coronavirus disease 2019. The hepatic FIB-8 index appears to provide the best prognostic value among the fibrosis scores in metabolic dysfunction-associated fatty liver disease patients with coronavirus disease 2019.

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.

The COVID-19 pandemic has had a profound impact on global health, necessitating a comprehensive understanding of its diverse manifestations. Cholangiopathy, a condition characterized by biliary dysfunction, has emerged as a significant complication in COVID-19 patients. In this review, we report the epidemiology of COVID-19, describe the hepatotropism of SARS-CoV-2, and present the histopathology of acute liver injury (ALI) in COVID-19. Additionally, we explore the relationship between pre-existing chronic liver disease and COVID-19, shedding light on the increased susceptibility of these individuals to develop cholangiopathy. Through an in-depth analysis of cholangiopathy in COVID-19 patients, we elucidate its clinical manifestations, diagnostic criteria, and underlying pathogenesis involving inflammation, immune dysregulation, and vascular changes. Furthermore, we provide a summary of studies investigating post-COVID-19 cholangiopathy, highlighting the long-term effects and potential management strategies for this condition, and discussing opportunities for intervention, including therapeutic targets, diagnostic advancements, supportive care, and future research needs.

Patients with COVID-19 and metabolic-dysfunction associated fatty liver disease (MAFLD) appear to be at higher risk for severe manifestations, especially in the youngest decades. Our aim was to examine whether patients with MAFLD and/or with increased liver fibrosis scores (FIB-4) are at risk for severe COVID-19 illness, using a machine learning (ML) model. Six hundred and seventy two patients were enrolled for SARS-CoV-2 pneumonia between February 2020 and May 2021. Steatosis was detected by ultrasound or computed tomography (CT). ML model valuated the risks of both in-hospital death and prolonged hospitalizations (> 28 days), considering MAFLD, blood hepatic profile (HP), and FIB-4 score. 49.6% had MAFLD. The accuracy in predicting in-hospital death was 0.709 for the HP alone and 0.721 for HP + FIB-4; in the 55-75 age subgroup, 0.842/0.855; in the MAFLD subgroup, 0.739/ 0.772; in the MAFLD 55-75 years, 0.825/0.833. Similar results were obtained when considering the accuracy in predicting prolonged hospitalization. In our cohort of COVID-19 patients, the presence of a worse HP and a higher FIB-4 correlated with a higher risk of death and prolonged hospitalization, regardless of the presence of MAFLD. These findings could improve the clinical risk stratification of patients diagnosed with SARS-CoV-2 pneumonia.

SARS-CoV-2 infection may affect the liver in healthy individuals but also influences the course of COVID-19 in patients with chronic liver disease (CLD). As described in healthy individuals, a strong SARS-CoV-2-specific adaptive immune response is important for the outcome of COVID-19, however, knowledge on the adaptive immune response in CLD is limited.Here, we review the clinical and immunological features of SARS-CoV-2 infection in individuals with CLD. Acute liver injury occurs in many cases of SARS-CoV-2 infection and may be induced by multiple factors, such as cytokines, direct viral infection or toxic effects of COVID-19 drugs. In individuals with CLD, SARS-CoV-2 infection may have a more severe course and promote decompensation and particularly in patients with cirrhosis. Compared with healthy individuals, the SARS-CoV-2-specific adaptive immune responses is impaired in patients with CLD after both, natural infection and vaccination but improves at least partially after booster vaccination.Following SARS-CoV-2 vaccination, rare cases of acute vaccine-induced liver injury and the development of autoimmune-like hepatitis have been reported. However, the concomitant elevation of liver enzymes is reversible under steroid treatment.

It is estimated that around 30% of the population living in Western countries has metabolic dysfunction-associated steatotic liver disease (MASLD), a spectrum of pathology (not attributed to alcohol/substance intake) initiated by steatosis and progression toward inflammation and irreversible fibrosis metabolic dysfunction-associated steatohepatitis (MASH). With inflammation being a key component of the transition to MASH, it raises the question of whether the ongoing COVID-19 pandemic, which has notoriously induced hyperinflammatory states, may influence the progression of MASLD. Specifically, it remains unclear if the potential chronic sequelae of COVID-19 in patients who recovered from it may increase the predisposition for MASH. Since MASH maintains a high risk for hepatocellular carcinoma, liver failure, and the need for a liver transplant, the potential additive effects of COVID-19 could prove critical to study. Thus, the objective of this study was to conduct a literature review to examine if COVID-19 could have chronic sequelae that affect the progression of MASLD pathogenesis. It was hypothesized that severe cases of COVID-19 could induce systemic inflammation, metabolic changes, and lasting gut microbiome alterations that lead to inflammatory and fibrotic changes in the liver, similar to those seen in MASH. A scoping review of the literature was conducted utilizing the PubMed database. Studies that examined hepatobiliary pathology, gut microbiome, systemic inflammation, metabolic changes, drug-induced liver injury (DILI), and hypoxia seen in COVID-19 were included. Human studies of adult cohorts, animal models, and in vitro experiments were included. Genetic components of MASLD were not examined. Exclusion criteria also encompassed any studies not referencing the hepatobiliary, gastrointestinal tract, portal system, or systemic circulation. Findings indicated a frequent trend of elevated liver enzymes, mild steatosis, Kupffer cell hyperplasia, and hepatobiliary congestion. It was found that direct cytopathic effects on hepatocytes were unlikely, but the direct viral insult of cholangiocytes was a potential complication. High serum levels of IL-1, TNF-a, and MCP-1, in COVID-19 were found as potential risk factors for MASH development. Hypoxia, altered lipid metabolism, and iatrogenic DILI were also proposed as potential precipitators of MASH development. Notably, lasting changes in gut microbiome were also frequently observed and correlated closely with those seen in MASH.

The COVID-19 outbreak has had severe consequences for global public health, medical communities, and the socioeconomic status of a considerable number of countries. The emergence of COVID-19 has also significantly impacted the world of liver transplantation (LT). Studies from transplantation centers around the world have shown that LTs during the COVID-19 pandemic have been restricted because of the high risk of serious COVID-19 infection in this population. According to the Centers for Disease Control and Prevention, patients with liver disease are considered at higher risk for severe COVID-19 infection. In March 2020, the American Association for the Study of Liver Diseases recommended that LT should be limited to emergency cases. The COVID-19 treatment guidelines published by the National Institutes of Health are being constantly updated according to new epidemiology trends and treatment regimens. Immunocompromised patients have a higher risk of developing severe disease or death from COVID-19 compared with the general population. In this review, we summarize the available evidence regarding treatment guidelines and considerations for the evaluation and management of LT candidates and recipients in the era of COVID-19. In addition, we present data regarding COVID-19 among LT patients in our local transplantation center.

Metabolic-associated fatty liver disease (MAFLD) and its potential impact on the severity of COVID-19 have gained significant attention during the pandemic. This review aimed to explore the genetic determinants associated with MAFLD, previously recognized as non-alcoholic fatty liver disease (NAFLD), and their potential influence on COVID-19 outcomes. Various genetic polymorphisms, including PNPLA3 (rs738409), GCKR (rs780094), TM6SF2 (rs58542926), and LYPLAL1 (rs12137855), have been investigated in relation to MAFLD susceptibility and progression. Genome-wide association studies and meta-analyses have revealed associations between these genetic variants and MAFLD risk, as well as their effects on lipid metabolism, glucose regulation, and liver function. Furthermore, emerging evidence suggests a possible connection between these MAFLD-associated polymorphisms and the severity of COVID-19. Studies exploring the association between indicated genetic variants and COVID-19 outcomes have shown conflicting results. Some studies observed a potential protective effect of certain variants against severe COVID-19, while others reported no significant associations. This review highlights the importance of understanding the genetic determinants of MAFLD and its potential implications for COVID-19 outcomes. Further research is needed to elucidate the precise mechanisms linking these genetic variants to disease severity and to develop gene profiling tools for the early prediction of COVID-19 outcomes. If confirmed as determinants of disease severity, these genetic polymorphisms could aid in the identification of high-risk individuals and in improving the management of COVID-19.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) enters the respiratory tract, where it infects the alveoli epithelial lining. However, patients have sequelae that extend well beyond the alveoli into the pulmonary vasculature and, perhaps, beyond to the brain and other organs. Because of the dynamic events within blood vessels, histology does not report platelet and neutrophil behavior. Because of the rapid nontranscriptional response of these cells, neither single-cell RNA sequencing nor proteomics report robustly on their critical behaviors. We used intravital microscopy in level-3 containment to examine the pathogenesis of SARS-CoV-2 within 3 organs in mice expressing human angiotensin converting enzyme 2 (ACE-2) ubiquitously (CAG-AC-70) or on epithelium (K18-promoter). Using a neon-green SARS-CoV-2, we observed both the epithelium and endothelium infected in AC70 mice but only the epithelium in K18 mice. There were increased neutrophils in the microcirculation but not in the alveoli of the lungs of AC70 mice. Platelets formed large aggregates in the pulmonary capillaries. Despite only neurons being infected within the brain, profound neutrophil adhesion forming the nidus of large platelet aggregates were observed in the cerebral microcirculation, with many nonperfused microvessels. Neutrophils breached the brain endothelial layer associated with a significant disruption of the blood-brain-barrier. Despite ubiquitous ACE-2 expression, CAG-AC-70 mice had very small increases in blood cytokine, no increase in thrombin, no infected circulating cells, and no liver involvement suggesting limited systemic effects. In summary, our imaging of SARS-CoV-2-infected mice gave direct evidence that there is a significant perturbation locally in the lung and brain microcirculation induced by local viral infection leading to increased local inflammation and thrombosis in these organs.

The COVID-19 pandemic has resulted in significant worldwide morbidity and mortality. In this review, we examine the intricate relationships between COVID-19 and liver diseases. While respiratory manifestations of COVID-19 are well known, its impact and consequences in patients with liver diseases remain an area of ongoing investigation. COVID-19 can induce liver injury through various mechanisms and is associated with higher mortality in individuals with preexisting chronic liver disease. Mortality increases with the severity of chronic liver disease and the level of care required. The outcomes in patients with autoimmune hepatitis remain unclear, whereas liver transplant recipients are more likely to experience symptomatic COVID-19 but have comparable outcomes to the general population. Despite suboptimal immunological response, COVID-19 vaccinations are safe and effective in liver disease, although cases of autoimmune hepatitis-like syndrome have been reported. In conclusion, COVID-19 has significant implications in liver diseases; early recognition and treatments are important for improving patient outcomes.

The global spread of severe acute respiratory syndrome coronavirus 2, responsible for coronavirus disease 2019 (COVID-19), poses a significant risk to public health. Beyond the respiratory issues initially associated with the condition, severe cases of COVID-19 can also lead to complications in other organs, including the liver. Patients with severe COVID-19 may exhibit various clinical signs of liver dysfunction, ranging from minor elevations in liver enzymes without symptoms to more serious cases of impaired liver function. Liver damage is more commonly observed in patients with severe or critical forms of the disease.

To present the research landscape on COVID-19 and liver dysfunction while also offering valuable insights into the prominent areas of interest within this particular domain.

On 18 February 2023, Scopus was utilised to conduct a comprehensive exploration of the relationship between COVID-19 and the liver dysfunction. The investigation encompassed the period from 1 January 2020 to 31 December 2022. Primary sources were meticulously examined and organised in a Microsoft Excel 2013 spreadsheet, categorised by journal, institution, funding agency, country and citation type. VOSviewer version 1.6.18 was employed to explore the prominent topics and knowledge network related to the subject.

There were 2336 publications on COVID-19 and liver dysfunction analysed in this study, of which 558 were published in 2020, 891 in 2021 and 887 in 2022. Researchers from 111 different countries participated in the retrieved documents. The United States contributed the most studies, with 497 documents, representing 21.28% of the total, followed by China with 393 documents (16.82%) and Italy with 255 documents (10.92%). In the context of research related to COVID-19 and the liver, co-occurrence analysis identified three distinct clusters of topics: (1) 'COVID-19 vaccines in liver transplant recipients'; (2) 'liver function tests as a predictor of the severity and clinical outcomes in hospitalised patients'; and (3) 'care of patients with liver disease during the COVID-19 pandemic'.

This bibliometric study provides a comprehensive overview of liver-related publications in COVID-19 research over the past 3 years. This study highlights the significant contributions of high-income nations, particularly the United States, China, and Italy, to the production of liver-related scholarly literature in this field. Most of the articles focused on liver dysfunction in patients with COVID-19 and the implications of the virus for gastroenterologists and hepatologists.

Background and Objective: The association of non-alcoholic fatty liver disease (NAFLD) and metabolic-associated fatty liver disease (MAFLD) with intensive care unit (ICU) admissions and the need for mechanical ventilation and disease severity in COVID-19 patients. Material and Methods: A systematic literature review was conducted on the databases: Cochrane, Embase, PubMed, ScienceDirect, and the Web of Science from January 2019 to June 2022. Studies evaluating MAFLD using laboratory methods, non-invasive imaging, or liver biopsy were included. The study protocol was registered in PROSPERO (ID CRD42022313259), and PRISMA guidelines were followed. The NIH quality assessment tool was used for quality assessment. RevMan version 5.3 software was used for pooled analysis. A sensitivity analysis was performed to assess the result's stability. Results: A total of 37,974 patients from 17 studies were assessed for the association between MAFLD and ICU admission. A total of 3396 COVID-19 patients required ICU admission: 1236 (20.41%) in the MAFLD group and 2160 (6.77%) in the non-MAFLD group. The odds ratio was 1.86 for ICU admission, p = 0.007, and a (95% CI) of [1.18-2.91]. A total of 37,166 patients from 13 studies were included in the need for invasive mechanical ventilation analysis. A total of 1676 patients required mechanical ventilation: 805 in the MAFLD group (14.20% of all MAFLD patients) and 871 patients in the non-MAFLD group (2.76% of all non-MAFLD patients). The odds ratio was 2.05, p = 0.02, and a (95% CI) of [1.12-3.74]. A total of 5286 patients from 14 studies were included in the COVID-19 disease severity analysis. Severe COVID-19 was seen in 1623 patients, with 33.17% (901/2716) of MAFLD patients and 28.09% (722/2570) of non-MAFLD patients having severe disease. The odds ratio was 1.59 for disease severity, p = 0.010, and a (95% CI) of [1.12-2.26]. Conclusions: Our meta-analysis suggests that there are significantly increased odds of ICU admissions, a need for invasive mechanical ventilation, and disease severity in MAFLD patients who acquire COVID-19.

Convergence of the two pandemics: metabolic syndrome and COVID-19 over last two years has posed unprecedented challenges to individuals as well as healthcare systems. Epidemiological data suggest a close association between metabolic syndrome and COVID-19 while variety of possible pathogenic connections have been proposed while some have been proven. Despite the evidence of high risk for adverse COVID-19 outcomes in people with metabolic syndrome, little is known about the differences in efficacy and safety among people with metabolic syndrome and without. It is important to recognize that among people with metabolic syndrome This review summarizes the current knowledge and epidemiological evidence on the association between metabolic syndrome and adverse COVID-19 outcomes, pathogenic interrelationships, management considerations for acute COVID-19 and post-COVID sequalae and sustaining care of people living with metabolic syndrome with appraisal of evidence and gaps in knowledge.

In late 2019, the world was shaken by the COVID-19 pandemic. Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection became one of the main causes of illness and hospitalization worldwide, especially in subjects with metabolic comorbidities such as obesity, diabetes, or liver disease. This scenario crosses with the metabolic liver disorders' "pandemic", caused by the exponential spreading of non-alcoholic fatty liver disease, which is now the most prevalent cause of chronic liver disease (CLD). The aim of this review is to analyze the key factors of the relationship between COVID-19 and the spectrum of fatty liver disorders (FLD), in terms of molecular mechanisms and clinical presentation which can predict a more severe course of the infection. In addition, this review will face the change in management of FLD during pandemics, with a central role of telemedicine, and the role of other interventions in preventing and treating severe infection in these subjects.