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1.
World J Gastroenterol ; 28(11): 1102-1112, 2022 Mar 21.
Article in English | MEDLINE | ID: covidwho-1780095

ABSTRACT

Coronavirus disease 2019 (COVID-19) is, at present, one of the most relevant global health problems. In the literature hepatic alterations have been described in COVID-19 patients, and they are mainly represented by worsening of underlying chronic liver disease leading to hepatic decompensation and liver failure with higher mortality. Several potential mechanisms used by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to cause liver damage have been hypothesized. COVID-19 primary liver injury is less common than secondary liver injury. Most of the available data demonstrate how liver damage in SARS-CoV-2 infection is likely due to systemic inflammation, and it is less likely mediated by a cytopathic effect directed on liver cells. Moreover, liver alterations could be caused by hypoxic injury and drugs (antibiotics and non-steroidal anti-inflammatory drugs, remdesivir, tocilizumab, tofacitinib and dexamethasone). SARS-CoV-2 infection can induce multiple vascular district atherothrombosis by affecting simultaneously cerebral, coronary and peripheral vascular beds. Data in the literature highlight how the virus triggers an exaggerated immune response, which added to the cytopathic effect of the virus can induce endothelial damage and a prothrombotic dysregulation of hemostasis. This leads to a higher incidence of symptomatic and confirmed venous thrombosis and of pulmonary embolisms, especially in central, lobar or segmental pulmonary arteries, in COVID-19. There are currently fewer data for arterial thrombosis, while myocardial injury was identified in 7%-17% of patients hospitalized with SARS-CoV-2 infection and 22%-31% in the intensive care unit setting. Available data also revealed a higher occurrence of stroke and more serious forms of peripheral arterial disease in COVID-19 patients. Hemostasis dysregulation is observed during the COVID-19 course. Lower platelet count, mildly increased prothrombin time and increased D-dimer are typical laboratory features of patients with severe SARS-CoV-2 infection, described as "COVID-19 associated coagulopathy." These alterations are correlated to poor outcomes. Moreover, patients with severe SARS-CoV-2 infection are characterized by high levels of von Willebrand factor with subsequent ADAMTS13 deficiency and impaired fibrinolysis. Platelet hyperreactivity, hypercoagulability and hypofibrinolysis during SARS-CoV-2 infection induce a pathological state named as "immuno-thromboinflammation." Finally, liver dysfunction and coagulopathy are often observed at the same time in patients with COVID-19. The hypothesis that liver dysfunction could be mediated by microvascular thrombosis has been supported by post-mortem findings and extensive vascular portal and sinusoidal thrombosis observation. Other evidence has shown a correlation between coagulation and liver damage in COVID-19, underlined by the transaminase association with coagulopathy, identified through laboratory markers such as prothrombin time, international normalized ratio, fibrinogen, D-dimer, fibrin/fibrinogen degradation products and platelet count. Other possible mechanisms like immunogenesis of COVID-19 damage or massive pericyte activation with consequent vessel wall fibrosis have been suggested.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Liver Diseases , Thrombosis , COVID-19/complications , Fibrinogen , Humans , Liver Diseases/epidemiology , Liver Diseases/etiology , SARS-CoV-2
2.
Nat Rev Gastroenterol Hepatol ; 19(5): 277-278, 2022 May.
Article in English | MEDLINE | ID: covidwho-1751723
3.
World J Gastroenterol ; 28(6): 683-688, 2022 Feb 14.
Article in English | MEDLINE | ID: covidwho-1715852

ABSTRACT

The intra and extracellular pathways of hepatic injury by coronavirus disease 2019 (COVID-19) are still being studied. Understanding them is important to treat this viral disease and other liver and biliary tract disorders. Thus, this paper aims to present three hypotheses about liver injury caused by COVID-19: (1) The interactions between severe acute respiratory syndrome coronavirus 2 spike protein and membrane receptors in the hepatocyte; (2) The dysbiosis and "gut-liver axis" disruption in patients with serious clinical presentations of COVID-19; and (3) The inflammatory response exacerbated through the production of interleukins such as interleukin-6. However, despite these new perspectives, the pathophysiological process of liver injury caused by COVID-19 is still complex and multifactorial. Thus, understanding all these variables is a challenge to science but also the key to propose individualized and effective patient therapies.


Subject(s)
COVID-19 , Liver Diseases , COVID-19/complications , Dysbiosis , Humans , Liver Diseases/etiology , Spike Glycoprotein, Coronavirus
4.
Medicine (Baltimore) ; 100(30): e26719, 2021 Jul 30.
Article in English | MEDLINE | ID: covidwho-1475908

ABSTRACT

ABSTRACT: Liver dysfunction in patients with COVID-19 (coronavirus disease 2019) has been described. However, it is not clear if the presence of abnormal liver function tests at presentation was related to underlying undiagnosed liver disease, or a result of the viral infection.We retrospectively examined the first 554 consecutive polymerase chain reaction positive SARS-CoV-2 patients admitted from February 2020 to April 2020 to our academic medical centre. We reviewed their clinical data, chest radiography and laboratory studies obtained within 24 hour of admission.Despite similar hemodynamic parameters, we found significant aspartate transaminase elevation (64 ±â€Š141 vs 35 ±â€Š23 U/L, P < .001) in those with pneumonia compared to those without. Elevated liver enzymes were seen in 102 patients (18.4%). They presented with higher temperatures (38.5 ±â€Š0.9 vs 37.5 ±â€Š0.8 degC, P = .011), higher total white cell counts (6.95 ±â€Š2.29 vs 6.39 ±â€Š2.19 x109/L, P = .021), serum ferritin (240 ±â€Š274 vs 165 ±â€Š198 ng/ml, P = .002) and lactate dehydrogenase (632 ±â€Š912 vs 389 ±â€Š107 U/L, P < .001). These patients were more likely to require intensive care (6.9% vs 2.7% P = .036) and mechanical ventilation (5.9% vs 2.2%, P = .046). Migrant workers from dormitories had a higher rate of baseline liver function test abnormalities (88/425 vs 14/129, P = .01), which were more likely to persist at the time of discharge.Despite relatively mild COVID-19 disease, there was a significant prevalence of liver dysfunction, particularly amongst migrant workers. Elevated liver enzymes were associated with more severe disease, despite similar haemodynamic characteristics. Future studies should explore whether pre-existing liver disease may predispose to more severe COVID-19 disease.


Subject(s)
Aspartate Aminotransferases/blood , COVID-19/complications , L-Lactate Dehydrogenase/blood , Liver Diseases/etiology , Adult , COVID-19/blood , Female , Ferritins/blood , Humans , Leukocyte Count , Liver Diseases/blood , Liver Function Tests , Male , Middle Aged , Retrospective Studies , Risk Factors , Singapore
5.
Eur J Gastroenterol Hepatol ; 33(1S Suppl 1): e1103, 2021 12 01.
Article in English | MEDLINE | ID: covidwho-1440676
6.
Medicine (Baltimore) ; 100(30): e26719, 2021 Jul 30.
Article in English | MEDLINE | ID: covidwho-1345775

ABSTRACT

ABSTRACT: Liver dysfunction in patients with COVID-19 (coronavirus disease 2019) has been described. However, it is not clear if the presence of abnormal liver function tests at presentation was related to underlying undiagnosed liver disease, or a result of the viral infection.We retrospectively examined the first 554 consecutive polymerase chain reaction positive SARS-CoV-2 patients admitted from February 2020 to April 2020 to our academic medical centre. We reviewed their clinical data, chest radiography and laboratory studies obtained within 24 hour of admission.Despite similar hemodynamic parameters, we found significant aspartate transaminase elevation (64 ±â€Š141 vs 35 ±â€Š23 U/L, P < .001) in those with pneumonia compared to those without. Elevated liver enzymes were seen in 102 patients (18.4%). They presented with higher temperatures (38.5 ±â€Š0.9 vs 37.5 ±â€Š0.8 degC, P = .011), higher total white cell counts (6.95 ±â€Š2.29 vs 6.39 ±â€Š2.19 x109/L, P = .021), serum ferritin (240 ±â€Š274 vs 165 ±â€Š198 ng/ml, P = .002) and lactate dehydrogenase (632 ±â€Š912 vs 389 ±â€Š107 U/L, P < .001). These patients were more likely to require intensive care (6.9% vs 2.7% P = .036) and mechanical ventilation (5.9% vs 2.2%, P = .046). Migrant workers from dormitories had a higher rate of baseline liver function test abnormalities (88/425 vs 14/129, P = .01), which were more likely to persist at the time of discharge.Despite relatively mild COVID-19 disease, there was a significant prevalence of liver dysfunction, particularly amongst migrant workers. Elevated liver enzymes were associated with more severe disease, despite similar haemodynamic characteristics. Future studies should explore whether pre-existing liver disease may predispose to more severe COVID-19 disease.


Subject(s)
Aspartate Aminotransferases/blood , COVID-19/complications , L-Lactate Dehydrogenase/blood , Liver Diseases/etiology , Adult , COVID-19/blood , Female , Ferritins/blood , Humans , Leukocyte Count , Liver Diseases/blood , Liver Function Tests , Male , Middle Aged , Retrospective Studies , Risk Factors , Singapore
7.
Int J Mol Sci ; 22(13)2021 Jun 24.
Article in English | MEDLINE | ID: covidwho-1304660

ABSTRACT

The liver is an organ with impressive regenerative potential and has been shown to heal sizable portions after their removal. However, certain diseases can overstimulate its potential to self-heal and cause excessive cellular matrix and collagen buildup. Decompensation of liver fibrosis leads to cirrhosis, a buildup of fibrotic ECM that impedes the liver's ability to efficiently exchange fluid. This review summarizes the complex immunological activities in different liver diseases, and how failure to maintain liver homeostasis leads to progressive fibrotic tissue development. We also discuss a variety of pathologies that lead to liver cirrhosis, such as alcoholic liver disease and chronic hepatitis B virus (HBV). Mesenchymal stem cells are widely studied for their potential in tissue replacement and engineering. Herein, we discuss the potential of MSCs to regulate immune response and alter the disease state. Substantial efforts have been performed in preclinical animal testing, showing promising results following inhibition of host immunity. Finally, we outline the current state of clinical trials with mesenchymal stem cells and other cellular and non-cellular therapies as they relate to the detection and treatment of liver cirrhosis.


Subject(s)
Disease Susceptibility , Liver Diseases/etiology , Liver Diseases/metabolism , Animals , Biomarkers , Combined Modality Therapy , Disease Management , Disease Progression , Disease Susceptibility/immunology , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , Humans , Liver Diseases/diagnosis , Liver Diseases/therapy
8.
Medicine (Baltimore) ; 100(19): e25913, 2021 May 14.
Article in English | MEDLINE | ID: covidwho-1262273

ABSTRACT

ABSTRACT: To evaluate the clinical characteristics and liver injury in coronavirus disease 2019 (COVID-19) patients, and analyze the differences between suspected and confirmed COVID-19 patients, this retrospective study was performed on 157 COVID-19 patients and 93 suspected patients who were ultimately excluded from COVID-19 (control patients). Differences in clinical characteristics and liver injury between suspected and confirmed COVID-19 patients were analyzed. Age, male sex, fever, chest tightness and dyspnea were related to the severity of COVID-19. C-reactive protein (CRP) and D-dimer may be predictors of the severity of COVID-19. Computed tomography (CT) played an important role in the screening of COVID-19 and the evaluation of disease severity. Multiple factors may cause liver injury in COVID-19 patients. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may be more likely to cause liver injury than common respiratory infectious diseases. Age, temperature (T), white blood cell (WBC), lymphocytes (LY), hematocrit (HCT), CRP, and finger pulse oxygen saturation (SpO2) may correlate with liver function impairment and may predict the occurrence and severity of liver function impairment. Some therapeutic drugs (like glucocorticoid) may be involved in the liver function impairment of COVID-19 patients. Most liver function indices improved significantly after active treatment. Although COVID-19 and other common respiratory infectious diseases share some clinical characteristics, COVID-19 has its own characteristics.


Subject(s)
COVID-19/complications , COVID-19/physiopathology , Liver Diseases/etiology , Liver Diseases/physiopathology , Adult , Age Factors , Aged , COVID-19/diagnostic imaging , China/epidemiology , Comorbidity , Female , Hematologic Tests , Humans , Liver Diseases/diagnostic imaging , Liver Function Tests , Male , Middle Aged , Oxygen/blood , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index , Sex Factors , Tomography, X-Ray Computed
9.
Virol J ; 18(1): 121, 2021 06 09.
Article in English | MEDLINE | ID: covidwho-1262511

ABSTRACT

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has spread to many countries around the world. In addition to lung disease, severe cases also displayed varying degrees of liver injury. This article will describe the latest developments regarding coronavirus and the pathogenesis of liver injury, the prone population and clinical characteristics of these patients, as well as providing some suggestions for clinical treatment.


Subject(s)
COVID-19/complications , Liver Diseases/etiology , SARS-CoV-2 , Antiviral Agents/adverse effects , Antiviral Agents/therapeutic use , Chemical and Drug Induced Liver Injury/pathology , Female , Humans , Incidence , Liver Diseases/diagnosis , Liver Diseases/therapy , Male , Medicine, Chinese Traditional/adverse effects
10.
J Hepatol ; 75(3): 647-658, 2021 09.
Article in English | MEDLINE | ID: covidwho-1228069

ABSTRACT

BACKGROUND AND AIMS: COVID-19 is associated with liver injury and elevated interleukin-6 (IL-6). We hypothesized that IL-6 trans-signaling in liver sinusoidal endothelial cells (LSECs) leads to endotheliopathy (a proinflammatory and procoagulant state) and liver injury in COVID-19. METHODS: Coagulopathy, endotheliopathy, and alanine aminotransferase (ALT) were retrospectively analyzed in a subset (n = 68), followed by a larger cohort (n = 3,780) of patients with COVID-19. Liver histology from 43 patients with COVID-19 was analyzed for endotheliopathy and its relationship to liver injury. Primary human LSECs were used to establish the IL-6 trans-signaling mechanism. RESULTS: Factor VIII, fibrinogen, D-dimer, von Willebrand factor (vWF) activity/antigen (biomarkers of coagulopathy/endotheliopathy) were significantly elevated in patients with COVID-19 and liver injury (elevated ALT). IL-6 positively correlated with vWF antigen (p = 0.02), factor VIII activity (p = 0.02), and D-dimer (p <0.0001). On liver histology, patients with COVID-19 and elevated ALT had significantly increased vWF and platelet staining, supporting a link between liver injury, coagulopathy, and endotheliopathy. Intralobular neutrophils positively correlated with platelet (p <0.0001) and vWF (p <0.01) staining, and IL-6 levels positively correlated with vWF staining (p <0.01). IL-6 trans-signaling leads to increased expression of procoagulant (factor VIII, vWF) and proinflammatory factors, increased cell surface vWF (p <0.01), and increased platelet attachment in LSECs. These effects were blocked by soluble glycoprotein 130 (IL-6 trans-signaling inhibitor), the JAK inhibitor ruxolitinib, and STAT1/3 small-interfering RNA knockdown. Hepatocyte fibrinogen expression was increased by the supernatant of LSECs subjected to IL-6 trans-signaling. CONCLUSION: IL-6 trans-signaling drives the coagulopathy and hepatic endotheliopathy associated with COVID-19 and could be a possible mechanism behind liver injury in these patients. LAY SUMMARY: Patients with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection often have liver injury, but why this occurs remains unknown. High levels of interleukin-6 (IL-6) and its circulating receptor, which form a complex to induce inflammatory signals, have been observed in patients with COVID-19. This paper demonstrates that the IL-6 signaling complex causes harmful changes to liver sinusoidal endothelial cells and may promote blood clotting and contribute to liver injury.


Subject(s)
COVID-19/complications , Endothelial Cells/pathology , Interleukin-6/physiology , Liver Diseases/etiology , SARS-CoV-2 , Adult , Blood Coagulation Disorders/etiology , Fibrinogen/analysis , Humans , Interleukin-6/blood , Janus Kinase 1/metabolism , Nitriles , Pyrazoles/pharmacology , Pyrimidines , Retrospective Studies , STAT3 Transcription Factor/metabolism , Signal Transduction/physiology , von Willebrand Factor/analysis
11.
Viral Immunol ; 34(6): 376-379, 2021.
Article in English | MEDLINE | ID: covidwho-1226517

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has a marked tropism for the biliary tract; it damages the bile ducts and hepatocytes and can lead to liver decompensation, cirrhosis, and sepsis. The pathogenesis of liver damage and its association with damage to the lung, heart, and brain and to the other protean manifestations of COVID-19 disease are not fully understood. In particular, tissue damage from thinning and leaky blood vessels appears to result from an inflammatory response to the virus rather than the virus itself. This article outlines a new hypothesis of the nature of the inflammatory factor responsible for tissue damage in COVID-19. Review of the literature reveals that COVID-19 disease closely resembles an endogenous form of hypervitaminosis A. We propose that SARS-CoV-2 virus-induced liver damage causes retinoic acid and stored retinyl esters to be released into the circulation in toxic concentrations, unbound to protein, with resulting damage to organs including the lungs, heart, blood vessels, and skin. Several lines of evidence support this model of disease causation. Subject to testing, strategies for the effective treatment and prevention of COVID-19 could include targeting the action and accumulation of retinoids.


Subject(s)
COVID-19/etiology , Liver Diseases/etiology , Retinoids/toxicity , SARS-CoV-2 , Adrenal Cortex Hormones/therapeutic use , Humans , Liver Cirrhosis/etiology , Non-alcoholic Fatty Liver Disease/etiology
12.
J Med Virol ; 93(1): 336-350, 2021 01.
Article in English | MEDLINE | ID: covidwho-1206801

ABSTRACT

Although not common, gastrointestinal and liver symptoms have reportedly been the initial presentation of coronavirus disease-2019 (COVID-19) in a large group of patients. Therefore, knowing the frequency and characteristics of these manifestations of COVID-19 is important for both clinicians and health policy makers. A systematic review and meta-analysis of the available data on the gastrointestinal and liver manifestations of patients with COVID-19 was performed. PubMed and Scopus databases and Google Scholar search engine were searched for published and unpublished preprint articles up to 10 April 2020. Original studies providing information on clinical digestive symptoms or biomarkers of liver function in patients with polymerase chain reaction confirmed diagnosis of COVID-19 were included. After quality appraisal, data were extracted. Prevalence data from individual studies were pooled using a random-effects model. Overall, 67 studies were included in this systematic review and meta-analysis, comprising a pooled population of 13 251 patients with confirmed COVID-19. The most common gastrointestinal symptoms were anorexia (10.2%, 95% confidence interval [CI] = 6.2%-16.4%), diarrhea (8.4%, 95% CI = 6.2%-11.2%), and nausea (5.7%, 95% CI = 3.7%-8.6%), respectively. Decreased albumin levels (39.8%, 95% CI = 15.3%-70.8%), increased aspartate aminotransferase (22.8%, 95% CI = 18.1%-28.4%), and alanine aminotransferase (20.6%, 95% CI = 16.7%-25.1%) were common hepatic findings. After adjusting for preexisting gastrointestinal (5.9%) and liver diseases (4.2%), the most common gastrointestinal findings were diarrhea (8.7%, 95% CI = 5.4%-13.9%), anorexia (8.0%, 95% CI = 3.0%-19.8%), and nausea (5.1%, 95% CI = 2.2%-14.3%). Gastrointestinal and liver manifestations are not rare in patients with COVID-19, but their prevalence might be affected by preexisting diseases. Diarrhea and mild liver abnormalities seem to be relatively common in COVID-19, regardless of comorbidities.


Subject(s)
COVID-19/complications , Gastrointestinal Diseases/etiology , Liver Diseases/etiology , SARS-CoV-2 , Humans
13.
Int Immunopharmacol ; 97: 107701, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1198830

ABSTRACT

SARS-CoV-2 or Coronavirus disease 2019 (COVID-19) outbreak which caused by the severe acute respiratory syndrome, has rapidly spread over the world. The exact mechanism how this virus will affect the liver remained elusive. The aim of this study was to evaluate the liver function in patients with severe acute respiratory syndrome coronavirus 2 and potential causes of hepatic enzymes disease in these patients. Clinical characteristics and laboratory findings were collected from patients with COVID-19 who were admitted to the corona center in Erbil city/Kurdistan region of Iraq, from March 10 to July 10, 2020. Serum was collected from patients with COVID-19 and liver enzyme tests were measured. Liver alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin (TBIL) were analyzed in these patients. Of the 74 patients, 25 (34.7%) had abnormal ALT activity, 28 (40%) had abnormal AST activity, 12 (20.3%) had abnormal ALP activity, and 39 (52.7%) had abnormal total bilirubin P-value < 0.05. The inflammatory biomarkers CRP and IL-6 in COVID-19 patients with abnormal liver function test (4.9 ± 1.0 mg/dl) and (231.2 ± 35.7 pg/ml) respectively. The levels of both biomarkers were statistically significantly higher than COVID-19 patients with normal liver function test (2.1 ± 0.5 mg/dl) and (2.1 ± 0.5 mg/dl) respectively, P-value < 0.05. However, CRP and IL-6 were not statistically significant different between male and female COVID-19 patients P-value < 0.05. In conclusion, we found that most of the patients with SARS-CoV-2 have abnormal hepatic enzyme activities and that is might related to virus replication in the liver.


Subject(s)
COVID-19/enzymology , COVID-19/virology , Liver/enzymology , Liver/virology , Adolescent , Adult , Aged , Alanine Transaminase/blood , Alkaline Phosphatase/blood , Aspartate Aminotransferases/blood , Bilirubin/blood , Biomarkers/blood , COVID-19/blood , COVID-19/complications , Carrier State/blood , Child , Female , Humans , Interleukin-6/blood , Liver Diseases/blood , Liver Diseases/enzymology , Liver Diseases/etiology , Liver Diseases/virology , Liver Function Tests , Male , Middle Aged , Receptors, Immunologic/blood , Young Adult
15.
Indian J Med Microbiol ; 39(2): 262-264, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1157422

ABSTRACT

As the world fights with the Coronavirus, most of the hospitals are gearing up for the care of these patients. As most of the attention these days is being given on Coronavirus, the patients suffering from other clinical infections are being neglected. SARS-CoV-2 is being kept as the top differential in patients presenting with fever and respiratory distress. We hereby present a case of patient returning from Indonesia during the pandemic presenting with a history of hepatic, renal dysfunction with fever and cough. Due to the pandemic, the patient's fever and cough outweighed the hepatic and renal dysfunction, and the patient had to undergo dialysis before the final diagnosis of leptospirosis could be made.


Subject(s)
COVID-19/diagnosis , Leptospirosis/diagnosis , SARS-CoV-2 , Aged , Humans , Kidney Diseases/etiology , Liver Diseases/etiology , Male
16.
Toxicology ; 455: 152765, 2021 05 15.
Article in English | MEDLINE | ID: covidwho-1152677

ABSTRACT

Liver damage is observed in up to half of hospitalized COVID-19 patients and can result either from actions of SARS-CoV-2 as such or from pharmacological treatment. The present paper introduces an adverse outcome pathway construct that mechanistically describes the pathways induced by SARS-CoV-2 leading to liver injury. This can be caused by direct binding of the virus and local actions in cholangiocytes, but may also indirectly result from the general state of hypoxia and systemic inflammation in COVID-19 patients. Further research is urgently needed to fill remaining knowledge gaps. This will be anticipated to create a solid basis for future and more targeted development of vaccines and, in particular, therapies.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/metabolism , Liver Diseases/metabolism , SARS-CoV-2/metabolism , Angiotensin-Converting Enzyme 2/antagonists & inhibitors , Animals , Antiviral Agents/adverse effects , Antiviral Agents/therapeutic use , COVID-19/complications , COVID-19/drug therapy , Humans , Inflammation/chemically induced , Inflammation/etiology , Inflammation/metabolism , Liver/drug effects , Liver/metabolism , Liver Diseases/etiology , SARS-CoV-2/drug effects
17.
J Hepatol ; 75(3): 739-740, 2021 09.
Article in English | MEDLINE | ID: covidwho-1141980
18.
IUBMB Life ; 73(5): 739-760, 2021 05.
Article in English | MEDLINE | ID: covidwho-1135107

ABSTRACT

Gastrointestinal symptoms and liver injury are common in patients with coronavirus disease 2019 (COVID-19). However, profiles of different pharmaceutical interventions used are relatively underexplored. Chinese herbal medicine (CHM) has been increasingly used for patients with COVID-19, but the efficacy of CHM used in COVID-19 on gastrointestinal symptoms and liver functions has not been well studied with definitive results based on the updated studies. The present study aimed at testing the efficacy of CHM on digestive symptoms and liver function (primary outcomes), the aggravation of COVID-19, and the time to viral assay conversion (secondary outcomes), among patients with COVID-19, compared with standard pharmacotherapy. The literature search was undertaken in 11 electronic databases from December 1, 2019 up to November 8, 2020. Appraisal of the evidence was conducted with Cochrane risk of bias tool or Newcastle Ottawa Scale. A random-effects model or subgroup analysis was conducted when significant heterogeneity was identified in the meta-analysis. The certainty of the evidence was assessed with the grading of recommendations assessment, development, and evaluation approach. Forty-eight included trials involving 4,704 participants were included. Meta-analyses favored CHM plus standard pharmacotherapy for COVID-19 on reducing the aggravation of COVID-19 and the time to viral assay conversion compared with standard pharmacotherapy. However, the present CHM as a complementary therapy for treating COVID-19 may not be beneficial for improving most gastrointestinal symptoms and liver function based on the current evidence. More well-conducted trials are warranted to confirm the potential efficacy of CHM furtherly.


Subject(s)
COVID-19/drug therapy , Drugs, Chinese Herbal/therapeutic use , Gastrointestinal Diseases/drug therapy , Liver Diseases/drug therapy , Adolescent , Adult , Aged , Anorexia/virology , COVID-19/etiology , Diarrhea/drug therapy , Diarrhea/virology , Drugs, Chinese Herbal/pharmacology , Female , Gastrointestinal Diseases/virology , Humans , Liver Diseases/etiology , Liver Diseases/virology , Liver Function Tests , Male , Middle Aged , Nausea/drug therapy , Nausea/virology , Young Adult
19.
PLoS One ; 16(2): e0244781, 2021.
Article in English | MEDLINE | ID: covidwho-1090568

ABSTRACT

PURPOSE: This study was conducted to evaluate the role of liver sonography in patients with coronavirus disease 2019 (COVID-19) and elevated liver enzymes. MATERIALS AND METHODS: In this retrospective study, patients tested positive for SARS-CoV-2 in our emergency ward between January 01 and April 24, 2020 and elevated liver enzymes were included (Cohort 1). Additionally, the local radiology information system was screened for sonographies in COVID-19 patients at the intensive care unit in the same period (Cohort 2). Liver sonographies and histologic specimen were reviewed and suspicious findings recorded. Medical records were reviewed for clinical data. Ultrasound findings and clinical data were correlated with severity of liver enzyme elevation. RESULTS: Cohort 1: 126 patients were evaluated, of which 47 (37.3%) had elevated liver enzymes. Severity of liver enzyme elevation was associated with death (p<0.001). 8 patients (6.3%) had suspicious ultrasound findings, including signs of acute hepatitis (n = 5, e.g. thickening of gall bladder wall, hepatomegaly, decreased echogenicity of liver parenchyma) and vascular complications (n = 4). Cohort 2: 39 patients were evaluated, of which 14 are also included in Cohort 1. 19 patients (48.7%) had suspicious ultrasound findings, of which 13 patients had signs of acute hepatitis and 6 had vascular complications. Pathology was performed in 6 patients. Predominant findings were severe cholestasis and macrophage activation. CONCLUSION: For most hospitalized COVID-19 patients, elevated liver enzymes cause little concern as they are only mild to moderate. However, in severely ill patients bedside sonography is a powerful tool to reveal different patterns of vascular, cholestatic or inflammatory complications in the liver, which are associated with high mortality. In addition, macrophage activation as histopathologic correlate for a hyperinflammatory syndrome seems to be a frequent complication in COVID-19.


Subject(s)
COVID-19 , Liver Diseases , Liver/diagnostic imaging , SARS-CoV-2 , Adult , Aged , Aged, 80 and over , COVID-19/complications , COVID-19/diagnostic imaging , Female , Humans , Liver Diseases/diagnostic imaging , Liver Diseases/etiology , Male , Middle Aged , Retrospective Studies , Ultrasonography
20.
Neurogastroenterol Motil ; 33(3): e14104, 2021 03.
Article in English | MEDLINE | ID: covidwho-1085279

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is associated with gastrointestinal and hepatic manifestation in up to one fifth of patients. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of COVID-19, infects gastrointestinal epithelial cells expressing angiotensin-converting enzyme 2 (ACE2) receptors triggering a cascade of events leading to mucosal and systemic inflammation. Symptomatic patients display changes in gut microbiota composition and function which may contribute to intestinal barrier dysfunction and immune activation. Evidence suggests that SARS-CoV-2 infection and related mucosal inflammation impact on the function of the enteric nervous system and the activation of sensory fibers conveying information to the central nervous system, which, may at least in part, contribute symptom generation such as vomiting and diarrhea described in COVID-19. Liver and pancreas dysfunctions have also been described as non-respiratory complications of COVID-19 and add further emphasis to the common view of SARS-CoV-2 infection as a systemic disease with multiorgan involvement. PURPOSE: The aim of this review was to highlight the current knowledge on the pathophysiology of gastrointestinal SARS-CoV-2 infection, including the crosstalk with the gut microbiota, the fecal-oral route of virus transmission, and the potential interaction of the virus with the enteric nervous system. We also review the current available data on gastrointestinal and liver manifestations, management, and outcomes of patients with COVID-19.


Subject(s)
COVID-19/complications , COVID-19/physiopathology , Gastrointestinal Diseases/etiology , Gastrointestinal Diseases/physiopathology , Gastrointestinal Microbiome/physiology , Gastrointestinal Tract/physiopathology , Animals , Diarrhea/etiology , Diarrhea/physiopathology , Diarrhea/virology , Dysbiosis/etiology , Dysbiosis/physiopathology , Dysbiosis/virology , Enteric Nervous System/physiopathology , Enteric Nervous System/virology , Gastrointestinal Diseases/virology , Gastrointestinal Tract/virology , Humans , Liver Diseases/etiology , Liver Diseases/physiopathology , Liver Diseases/virology , Pancreatic Diseases/etiology , Pancreatic Diseases/physiopathology , Pancreatic Diseases/virology
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