scholarly journals Liver Injury in Patients with COVID-19 without Underlying Liver Disease

2022 ◽  
Vol 11 (2) ◽  
pp. 308
Author(s):  
Monika Pazgan-Simon ◽  
Sylwia Serafińska ◽  
Michał Kukla ◽  
Marta Kucharska ◽  
Jolanta Zuwała-Jagiełło ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Vascular Endothelial Cells ◽  
Signs And Symptoms ◽  
Liver Function Tests ◽  
Underlying Mechanism ◽  
Underlying Liver Disease ◽  
Pattern Of Injury ◽  
Laboratory Test Results ◽  
Type Pattern

SARS-CoV-2 shows a high affinity for the ACE-2 receptor, present on the epithelial cells of the upper and lower respiratory tract, within the intestine, kidneys, heart, testes, biliary epithelium, and—where it is particularly challenging—on vascular endothelial cells. Liver involvement is a rare manifestation of COVID-19. Material and Methods: We reviewed 450 patients admitted due to the fact of SARS-CoV-2 infection (COVID-19) including 88 with liver injury. Based on medical history and previous laboratory test results, we excluded cases of underlying liver disease. The analysis involved a clinical course of COVID-19 in patients without underlying liver disease as well as the type and course of liver injury. Results: Signs and symptoms of liver injury were present in 20% of patients, mostly presenting as a mixed-type pattern of injury with less common cases of standalone hepatocellular (parenchymal) or cholestatic injury. The liver injury symptoms resolved at the end of inpatient treatment in 20% of cases. Sixteen patients died with no cases where liver injury would be deemed a cause of death. Conclusions: (1) Liver injury secondary to COVID-19 was mild, and in in 20%, the signs and symptoms of liver injury resolved by the end of hospitalization. (2) It seems that liver injury in patients with COVID-19 was not associated with a higher risk of mortality. (3) The underlying mechanism of liver injury as well as its sequelae are not fully known. Therefore, caution and further monitoring are advised, especially in patients whose liver function tests have not returned to normal values.

scholarly journals Interaction of volatile organic compounds and underlying liver disease: a new paradigm for risk

2018 ◽  
Vol 399 (11) ◽  
pp. 1237-1248 ◽  
Author(s):  
Anna L. Lang ◽  
Juliane I. Beier
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Industrial Chemicals ◽  
New Paradigm ◽  
Alcoholic Fatty Liver ◽  
Underlying Liver Disease ◽  
Volatile Organic ◽  
Occupational Cohort ◽  
Alcoholic Fatty Liver Disease

Abstract Occupational and environmental exposures to industrial chemicals are known to cause hepatotoxicity and liver injury, in humans and in animal models. Historically, research has focused on severe acute liver injury (e.g. fulminant liver failure) or endstage diseases (e.g. cirrhosis and HCC). However, it has become recently recognized that toxicants can cause more subtle changes to the liver. For example, toxicant-associated steatohepatitis, characterized by hepatic steatosis, and inflammation, was recently recognized in an occupational cohort exposed to vinyl chloride. At high occupational levels, toxicants are sufficient to cause liver damage and disease even in healthy subjects with no comorbidities for liver injury. However, it is still largely unknown how exposure to toxicants initiate and possibly more importantly exacerbate liver disease, when combined with other factors, such as underlying non-alcoholic fatty liver disease caused by poor diet and/or obesity. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of toxicant-induced liver disease, rational targeted therapy can be developed to better predict risk, as well as to treat or prevent this disease. The purpose of this review is to summarize established and proposed mechanisms of volatile organic compound-induced liver injury and to highlight key signaling events known or hypothesized to mediate these effects.

scholarly journals Implications of Liver Injury in Risk-Stratification and Management of Patients with COVID-19

2020 ◽  
Author(s):  
Jiaofang Shao ◽  
Yuan Liang ◽  
Yan Li ◽  
Rong Ding ◽  
Mengyan Zhu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Cell Types ◽  
Test Results ◽  
Severity Of Disease ◽  
Liver Injuries ◽  
Laboratory Test Results ◽  
Score Model

Abstract BackgroundInfection with SARS-CoV-2 has been associated with liver dysfunction, aggravation of liver burden, and liver injury. This study aimed to assess the effects of liver injuries on the clinical outcomes of patients with COVID-19.MethodsA total of 1,564 patients with severe or critical COVID-19 from Huoshenshan Hospital, Wuhan, were enrolled. Chronic liver disease (CLD) was confirmed by consensus diagnostic criteria. Laboratory test results were compared between different groups. scRNA-seq data and bulk gene expression profiles were used to identify cell types associated with liver injury.ResultsA total of 10.98% of patients with severe or critical COVID-19 developed liver injury after admission that was associated with significantly higher rates of mortality (21.74%, p<0.001) and intensive care unit admission (26.71%, p<0.001). A pre-existing CLD was not associated with a higher risk. However, fatty liver disease and cirrhosis were associated with higher risks, supported by evidences from single cell and bulk transcriptome analysis that showed more TMPRSS2+ cells in these tissues. By generating a model, we were able to predict the risk and severity of liver injury during hospitalization.ConclusionWe demonstrate that liver injury occurring during therapy in patients with COVID-19 is significantly associated with the severity of disease and mortality, but the presence of CLD is not associated. We provide a risk-score model that can predict whether patients with COVID-19 will develop liver injury or proceed to higher risk stages during subsequent hospitalizations. These findings may prove beneficial for the clinical management of patients infected with SARS-CoV-2.

scholarly journals Liver injury in COVID-19: The current evidence

2020 ◽  
Vol 8 (5) ◽  
pp. 509-519 ◽  
Author(s):  
Saleh A Alqahtani ◽  
Jörn M Schattenberg
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Liver Function ◽  
Case Series ◽  
Current Evidence ◽  
Disease Course ◽  
Underlying Liver Disease ◽  
Hepatobiliary Complications ◽  
Novel Coronavirus ◽  
Work Up

Patients with novel coronavirus disease 2019 (COVID-19) experience various degrees of liver function abnormalities. Liver injury requires extensive work-up and continuous surveillance and can be multifactorial and heterogeneous in nature. In the context of COVID-19, clinicians will have to determine whether liver injury is related to an underlying liver disease, drugs used for the treatment of COVID-19, direct effect of the virus, or a complicated disease course. Recent studies proposed several theories on potential mechanisms of liver injury in these patients. This review summarizes current evidence related to hepatobiliary complications in COVID-19, provides an overview of the available case series and critically elucidates the proposed mechanisms and provides recommendations for clinicians.

scholarly journals Characteristics and outcomes of patients with COVID-19 and liver injury: a retrospective analysis and a multicenter experience

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Andrei Voiosu ◽  
Adina Roman ◽  
Ruxandra Pop ◽  
Alina Boeriu ◽  
Cristiana Popp ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Liver Function ◽  
Chronic Liver Disease ◽  
Liver Function Tests ◽  
Chronic Liver ◽  
Upper Limit ◽  
Function Tests ◽  
Elevated Liver Function Tests ◽  
Negative Outcome

Abstract Background and aims: Patients with COVID-19 frequently present abnormal elevated liver function tests of unknown clinical significance. We aimed to investigate the characteristics and factors influencing outcome in patients with confirmed SARS-CoV-2 infection and liver injury on admission. Methods: This is a retrospective observational study of patients hospitalized in two COVID units in Romania. Relevant data on clinical and laboratory parameters and medication administered during the admission were analyzed to identify predictors of a negative outcome. Patients with confirmed COVID-19 and liver function tests (LFTs) above the upper limit of normal were included in the analysis. Results: From 1,207 patients, we identified 134 patients (11%) with abnormal LFTs during hospitalization. The majority of patients had mildly elevated levels and a predominantly cholestatic pattern of liver injury. Patients who received lopinavir/ritonavir were more likely to have increased ALAT levels (p<0.0001). Sixteen patients had pre-existing chronic liver disease, and they were more likely to suffer from severe COVID-19 (p=0.009) and have a negative outcome (p<0.001), but on multivariate analysis, only the severity of COVID-19 was predictive of death (OR 69.9; 95% CI 6.4-761.4). Conclusions: Mild liver injury is relatively common in COVID-19 and possibly influenced by medication. Patients with chronic liver disease are at high risk for negative outcome, but the severity of the infection is the only predictor of death.

S-adenosylmethionine and proliferation: new pathways, new targets

2008 ◽  
Vol 36 (5) ◽  
pp. 848-852 ◽  
Author(s):  
Nuria Martínez-López ◽  
Marta Varela-Rey ◽  
Usue Ariz ◽  
Nieves Embade ◽  
Mercedes Vazquez-Chantada ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Underlying Liver Disease ◽  
New Findings ◽  
Wide Range ◽  
The Common ◽  
Low Levels ◽  
Amp Activated Protein Kinase ◽  
Hepatocyte Growth ◽  
Growth Abnormalities

SAMe (S-adenosylmethionine) is the main methyl donor group in the cell. MAT (methionine adenosyltransferase) is the unique enzyme responsible for the synthesis of SAMe from methionine and ATP, and SAMe is the common point between the three principal metabolic pathways: polyamines, transmethylation and transsulfuration that converge into the methionine cycle. SAMe is now also considered a key regulator of metabolism, proliferation, differentiation, apoptosis and cell death. Recent results show a new signalling pathway implicated in the proliferation of the hepatocyte, where AMPK (AMP-activated protein kinase) and HuR, modulated by SAMe, take place in HGF (hepatocyte growth factor)-mediated cell growth. Abnormalities in methionine metabolism occur in several animal models of alcoholic liver injury, and it is also altered in patients with liver disease. Both high and low levels of SAMe predispose to liver injury. In this regard, knockout mouse models have been developed for the enzymes responsible for SAMe synthesis and catabolism, MAT1A and GNMT (glycine N-methyltransferase) respectively. These knockout mice develop steatosis and HCC (hepatocellular carcinoma), and both models closely replicate the pathologies of human disease, which makes them extremely useful to elucidate the mechanism underlying liver disease. These new findings open a wide range of possibilities to discover novel targets for clinical applications.

scholarly journals Ademetionine in patients with liver disease: a review

2019 ◽  
Vol 7 (6) ◽  
pp. 2482 ◽  
Author(s):  
Sanjiv Saigal ◽  
Dharmesh Kapoor ◽  
Dyotona Sen Roy
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Alcoholic Liver Disease ◽  
Biochemical Markers ◽  
Fatty Liver Disease ◽  
Signs And Symptoms ◽  
Drug Induced ◽  
Alcoholic Fatty Liver ◽  
Drug Induced Liver Injury ◽  
Alcoholic Fatty Liver Disease

The aim of the present review is to have an in-depth analysis of the published scientific literature relating to the clinical use of ademetionine in various etiologies of liver disease. Literature search was performed using electronic databases like Pubmed/Medline/others to identify studies on ademetionine in patients with intrahepatic cholestasis, alcoholic liver disease, non-alcoholic fatty liver disease, drug induced liver injury and viral hepatitis. Ademetionine has been studied in various etiologies of liver disease with varying dosing and durations. In patients with chronic and alcoholic liver disease, ademetionine was found to be beneficial in improving liver enzyme levels, increasing glutathione levels, improving signs and symptoms of fatigue, pruritus and jaundice. Positive effects of ademetionine therapy have also been documented in multiple studies in patients with non-alcoholic fatty liver disease, with improvements observed in triglyceride, total cholesterol, alanine transaminase and asprtate transaminase levels and ultrasound grading of fatty change. In patients with drug induced liver injury, improvements were observed in liver biochemical markers and symptoms such as pruritus, fatigue and jaundice. Ademetionine has also been studied in patients with viral hepatitis with improvement in laboratory markers and signs and symptoms. Published data suggest that there is clinical evidence to substantiate the use of ademetionine across indications. Its use has resulted in sustained improvement in biochemical markers; signs and symptoms of liver disease has been observed in both acute and chronic liver disease. Further data is warranted through clinical studies to focus on specific end points of therapy areas, in existing and new indications.

scholarly journals Protective functions of ZO-2/Tjp2 expressed in hepatocytes and cholangiocytes against liver injury and cholestasis

2019 ◽  
Author(s):  
Jianliang Xu ◽  
P. Jaya P. Kausalya ◽  
Noémi Van Hul ◽  
Matias J. Caldez ◽  
Shiyi Xu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Mouse Liver ◽  
Liver Function Tests ◽  
Protective Role ◽  
Detoxification Enzymes ◽  
Cholestatic Liver Disease ◽  
Missense Mutations ◽  
Expression Levels ◽  
Underlying Mechanisms

BACKGROUND & AIMSTight junctions (TJs) establish tissue barriers that maintain osmotic homeostasis and, in the liver, isolate bile flow from the blood circulation. ZO-2/Tjp2 is a scaffold protein that tethers TJ transmembrane proteins to the actin cytoskeleton. Missense mutations in Tjp2 have recently been shown to cause progressive cholestatic liver disease in humans. However, the underlying mechanisms still remain elusive. To study the role of Tjp2 in cholestatic liver disease, we generated and characterized mice lacking Tjp2 in hepatocytes, cholangiocytes, or both.METHODSTjp2 was inactivated in the mouse liver (both in hepatocytes and cholangiocytes) or hepatocytes or cholangiocytes only. Liver function tests were carried out by biochemical analysis of plasma and liver samples and liver tissue was evaluated by immunohistochemistry and histology. The mice were also subjected to cholic acid (CA) diet to assess their susceptibility to liver insults.RESULTSDeletion of Tjp2 in the mouse liver did not result in apparent changes in TJ structure and composition, but lead to progressive cholestasis with lower expression levels of the bile acid (BA) transporter ABCB11/Bsep and the detoxification enzyme Cyp2b10. Feeding a CA diet that is well tolerated by control mice caused severe cholestasis and necrotic liver injury in mice lacking hepatic Tjp2. Administration of a CAR agonist, TCPOBOP, protected these mice from CA induced injury by enhancing the expression of the detoxifying enzyme Cyp2b10 in hepatocytes. Mice lacking Tjp2 in only hepatocytes or in only cholangiocytes showed less severe CA diet induced liver injury.CONCLUSIONLoss of Tjp2 from hepatocytes and cholangiocytes both contribute to progressive cholestatic liver disease and higher susceptibility to liver injury. In hepatocytes, Tjp2 exerts a protective role by regulating expression levels of BA transporters and detoxification enzymes. The mice may provide a new animal model for cholestatic liver disease linked to Tjp2 mutations in humans.

Terbinafine used safely in autoimmune hepatitis for treatment of tinea corporis

2021 ◽  
Vol 14 (5) ◽  
pp. e243143
Author(s):  
Jessica Elizabeth Ferguson ◽  
Megan Prouty
Keyword(s):  
Liver Disease ◽  
Patient Education ◽  
Liver Function ◽  
Autoimmune Hepatitis ◽  
Signs And Symptoms ◽  
Liver Function Tests ◽  
Tinea Corporis ◽  
Function Tests ◽  
First Case ◽  
Oral Terbinafine

Terbinafine is often considered contraindicated in those with liver disease, as one of the known side effects is hepatotoxicity. We report the first case documenting the safe use of oral terbinafine in a 77-year-old woman with stable autoimmune hepatitis presenting with extensive tinea corporis. Precautions were carried out to minimise the risk of worsening hepatotoxicity, including consultation with the patient’s hepatologist, limiting terbinafine exposure to less than 6 weeks, monitoring of liver function tests, and patient education. The patient’s fungal infection cleared without any signs or symptoms of worsening liver disease. The rash had not recurred 6 months after treatment. When terbinafine must be used in a patient with pre-existing liver disease, we recommend considering a short course of oral terbinafine after consultation with their hepatologist, obtaining baseline liver function tests with consideration of further monitoring during treatment course, and patient education on the signs and symptoms of liver injury.

scholarly journals Obesity, Visceral Fat, and NAFLD: Querying the Role of Adipokines in the Progression of Nonalcoholic Fatty Liver Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
M. S. Mirza
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Underlying Mechanism ◽  
Critical Event ◽  
Nonalcoholic Fatty Liver ◽  
Reactive Protein ◽  
The Metabolic Syndrome

Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of clinicopathologic conditions ranging from steatosis alone to nonalcoholic steatohepatitis (NASH), with varying risks for progression to cirrhosis and hepatocellular carcinoma. There is mounting evidence that NAFLD not only complicates obesity, but also perpetuates its metabolic consequences. Critical event that leads to progressive liver injury in NAFLD is unknown. Obesity reflects a generalized proinflammatory state with its increased inflammatory markers like C reactive protein, IL-6, IL-8, IL-10, PAI-1, TNF-α, and hepatocyte growth factor. The elevated production of these adipokines is increasingly considered to be important in the development of diseases linked to obesity and the metabolic syndrome. Disordered cytokine production is likely to play a role in the pathogenesis of NAFLD. There is no effective treatment for NAFLD, though weight loss may halt disease progression and revert histological changes, the underlying mechanism remaining elusive. All stages of the disease pathway from prevention, early identification/diagnosis, and treatment require an understanding of the pathogenesis of liver injury in NAFLD.

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