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1.
Int J Biol Sci ; 18(12): 4756-4767, 2022.
Article in English | MEDLINE | ID: covidwho-1954687

ABSTRACT

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become an ongoing global health pandemic. Since 2019, the pandemic continues to cast a long shadow on all aspects of our lives, bringing huge health and economic burdens to all societies. With our in-depth understanding of COVID-19, from the initial respiratory tract to the later gastrointestinal tract and cardiovascular systems, the multiorgan involvement of this infectious disease has been discovered. Metabolic dysfunction-associated fatty liver disease (MAFLD), formerly named nonalcoholic fatty liver disease (NAFLD), is a major health issue closely related to metabolic dysfunctions, affecting a quarter of the world's adult population. The association of COVID-19 with MAFLD has received increasing attention, as MAFLD is a potential risk factor for SARS-CoV-2 infection and severe COVID-19 symptoms. In this review, we provide an update on the interactions between COVID-19 and MAFLD and its underlying mechanisms.


Subject(s)
COVID-19 , Non-alcoholic Fatty Liver Disease , Adult , Humans , Pandemics , Risk Factors , SARS-CoV-2
2.
Acta Gastroenterol Belg ; 85(2): 255-256, 2022.
Article in English | MEDLINE | ID: covidwho-1918386
3.
J Viral Hepat ; 29(9): 823-834, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1896011

ABSTRACT

Abnormal liver function tests (A-LFTs) during admission for coronavirus disease-19 (COVID-19) are frequent, but its evolution after COVID-19 resolution remains unexplored. We evaluated factors related to A-LFTs during COVID-19 and assessed the liver outcome after patients' discharge. This is a observational study including: (1) retrospective analysis of variables related to A-LFTs during COVID-19; and (2) follow-up evaluation with blood test, transient elastography and liver biopsy in those with persistent A-LFTs. A-LFTs were defined according to CTCAEv4.0. Among 595 patients, 366 (61.5%) showed A-LFTs. The ratio of partial pressure of oxygen and inspired oxygen fraction (P/F) below 200, ferritin ≥1000 ng/mL, male gender and antibiotic and immunomodulatory treatments were related to A-LFTs. Follow-up evaluation was performed in 153 individuals. Persistent A-LFTs at follow-up was similar in patients with/without A-LFTs during admission (14.1% vs. 4.9%, p = 0.104). Fifteen (93%) and 58 (39%) patients with/without A-LFTs at follow-up showed metabolic fatty liver disease criteria (p < 0.001), which were histologically confirmed. In conclusion, A-LFTs during COVID-19 were related to infection severity. Abnormalities remitted at follow-up in >80% of patients, and no correlation between A-LFTs at admission and at follow-up was found. Most patients with A-LFTs at follow-up had non-invasive and histologically proven fatty liver disease.

4.
Life (Basel) ; 12(6)2022 May 26.
Article in English | MEDLINE | ID: covidwho-1869691

ABSTRACT

Non-alcoholic fatty liver disease (NAFLD) is identified as a risk factor for developing severe COVID-19. While NAFLD is associated with chronic low-grade inflammation, mechanisms leading to immune system hyperactivation remain unclear. The aim of this prospective observational study is to analyze cytokine profiles in patients with severe COVID-19 and NAFLD. A total of 94 patients with severe COVID-19 were included. Upon admission, clinical and laboratory data were collected, a liver ultrasound was performed to determine the presence of steatosis, and subsequently, 51 were diagnosed with NAFLD according to the current guidelines. There were no differences in age, sex, comorbidities, and baseline disease severity between the groups. Serum cytokine concentrations were analyzed using a multiplex bead-based assay by flow cytometry. Upon admission, the NAFLD group had higher C-reactive protein, procalcitonin, alanine aminotransferase, lactate dehydrogenase, and fibrinogen. Interleukins-6, -8, and -10 and CXCL10 were significantly higher, while IFN-γ was lower in NAFLD patients. Patients with NAFLD who progressed to critical illness had higher concentrations of IL-6, -8, -10, and IFN-ß, and IL-8 and IL-10 appear to be effective prognostic biomarkers associated with time to recovery. In conclusion, NAFLD is associated with distinct cytokine profiles in COVID-19, possibly associated with disease severity and adverse outcomes.

5.
J Clin Exp Hepatol ; 2022 Apr 20.
Article in English | MEDLINE | ID: covidwho-1867325

ABSTRACT

Background: Fatty liver has been shown to be associated with severe COVID-19 disease without any impact on mortality. This is based on heterogenous criteria for defining both fatty liver as well as the severity parameters. Aim: To study the impact of fatty liver on the mortality and severity of disease in patients with COVID-19 pneumonia. Methods: In a case control study design, patients with COVID-19 pneumonia (COVID-19 CT severity index on HRCT chest of >1) with fatty liver (defined as liver to spleen attenuation index < 5 on non-contrast CT cuts of upper abdomen) were compared to those without fatty liver. The primary outcome measure was in-hospital mortality and secondary outcome measures were CTSI score need for ICU care, need for ventilatory support, duration of ICU stay and duration of Hospital stay. Results: 289 (64.7%) of 446 patients with COVID-19 pneumonia admitted to Max Hospital, Saket, India, between 1/1/2021 and 30/10/2021 had fatty liver. 59 of 446 patients died during the index admission. In-hospital mortality was not different between patients with fatty liver [38 1(3.24%)] or without fatty liver [21 (13.81%)]. COVID-19 CTSI score was found to be significantly higher among patients who had fatty liver [13.40 (5.16) vs 11.81 (5.50); p= 0.003]. There was no difference in the requirement of ICU [94 (32%) vs 62 (39.49%); p=0.752], requirement of ventilatory support [27 (9.34%) vs 14 (8.91%); p=0.385], duration of ICU stay [8.29 (6.87) vs 7.07 (5.71) days; p=0.208] and duration of hospital stay [10.10 (7.14) vs 10.69 (8.13) days; p=0.430] between the groups with fatty liver or no fatty liver. Similarly, no difference was found in primary or secondary outcomes measure between the group with severe fatty liver vs mild/moderate or no fatty liver. High Total leucocyte count and FIB-4 index were independently associated with mortality. Conclusions: Fatty liver may not be associated with increased mortality or clinical morbidity of patients who have COVID-19 pneumonia.

6.
International Journal of Molecular Sciences ; 23(9):4822, 2022.
Article in English | ProQuest Central | ID: covidwho-1842716

ABSTRACT

Obesity is one of the greatest health challenges affecting children of all ages and ethnicities. Almost 19% of children and adolescents worldwide are overweight or obese, with an upward trend in the last decades. These reports imply an increased risk of fat accumulation in hepatic cells leading to a series of histological hepatic damages gathered under the acronym NAFLD (Non-Alcoholic Fatty Liver Disease). Due to the complex dynamics underlying this condition, it has been recently renamed as ‘Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)’, supporting the hypothesis that hepatic steatosis is a key component of the large group of clinical and laboratory abnormalities of Metabolic Syndrome (MetS). This review aims to share the latest scientific knowledge on MAFLD in children in an attempt to offer novel insights into the complex dynamics underlying this condition, focusing on the novel molecular aspects. Although there is still no treatment with a proven efficacy for this condition, starting from the molecular basis of the disease, MAFLD’s therapeutic landscape is rapidly expanding, and different medications seem to act as modifiers of liver steatosis, inflammation, and fibrosis.

8.
Drugs Context ; 112022.
Article in English | MEDLINE | ID: covidwho-1687413

ABSTRACT

COVID-19 increases the risk of atrial fibrillation (AF) and thrombotic complications, particularly in severe cases, leading to higher mortality rates. Anticoagulation is the cornerstone to reduce thromboembolic risk in patients with AF. Considering the risk of hepatotoxicity in patients with severe COVID-19 as well as the risk of drug-drug interactions, drug-induced hepatotoxicity and bleeding, the ANIBAL protocol was developed to facilitate the anticoagulation approach at discharge after COVID-19 hospitalization. However, since the publication of the original algorithm, relevant changes have occurred. First, treatment of COVID-19 pneumonia has been modified with the use of dexamethasone or remdesivir during the first week in patients that require oxygen therapy, and of dexamethasone and/or tocilizumab or baricitinib during the second week in patients that necessitate supplementary oxygen or with a high inflammation state, respectively. On the other hand, metabolic syndrome is common in patients with AF as well as metabolic-associated fatty liver disease, and this could negatively impact the prognosis of patients with COVID-19, including high transaminase levels in patients treated with immunomodulators. The EHRA guidelines update also introduce some interesting changes in drug-drug interaction patterns with the reduction of the level of the interaction with dexamethasone, which is of paramount importance in this clinical context. Considering the new information, the protocol, named ANIBAL II, has been updated. In this new protocol, the anticoagulant of choice in patients with AF after COVID-19 hospitalization is provided according to three scenarios: with/without dexamethasone treatment at discharge and normal hepatic function, transaminases ≤2 times the upper limit of normal, or transaminases >2 times the upper limit of normal.

9.
Lipids Health Dis ; 20(1): 126, 2021 Oct 03.
Article in English | MEDLINE | ID: covidwho-1448237

ABSTRACT

The coronavirus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2). At present, the COVID-19 has been prevalent worldwide for more than a year and caused more than four million deaths. Liver injury was frequently observed in patients with COVID-19. Recently, a new definition of metabolic dysfunction associated fatty liver disease (MAFLD) was proposed by a panel of international experts, and the relationship between MAFLD and COVID-19 has been actively investigated. Several previous studies indicated that the patients with MAFLD had a higher prevalence of COVID-19 and a tendency to develop severe type of respiratory infection, and others indicated that liver injury would be exacerbated in the patients with MAFLD once infected with COVID-19. The mechanism underlying the relationship between MAFLD and COVID-19 infection has not been thoroughly investigated, and recent studies indicated that multifactorial mechanisms, such as altered host angiotensin converting enzyme 2 (ACE2) receptor expression, direct viral attack, disruption of cholangiocyte function, systemic inflammatory reaction, drug-induced liver injury, hepatic ischemic and hypoxic injury, and MAFLD-related glucose and lipid metabolic disorders, might jointly contribute to both of the adverse hepatic and respiratory outcomes. In this review, we discussed the relationship between MAFLD and COVID-19 based on current available literature, and summarized the recommendations for clinical management of MAFLD patients during the pandemic of COVID-19.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , COVID-19/complications , Chemical and Drug Induced Liver Injury/complications , Hypoxia/complications , Liver/metabolism , Non-alcoholic Fatty Liver Disease/complications , SARS-CoV-2/pathogenicity , Age Factors , Angiotensin-Converting Enzyme 2/genetics , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/drug therapy , COVID-19/pathology , COVID-19/virology , Chemical and Drug Induced Liver Injury/drug therapy , Chemical and Drug Induced Liver Injury/pathology , Chemical and Drug Induced Liver Injury/virology , Cytokines/genetics , Cytokines/metabolism , Dipeptides/therapeutic use , Gene Expression Regulation , Glucose/metabolism , Glycyrrhizic Acid/therapeutic use , Humans , Hypoxia/drug therapy , Hypoxia/pathology , Hypoxia/virology , Liver/drug effects , Liver/pathology , Liver/virology , Lung/drug effects , Lung/metabolism , Lung/pathology , Lung/virology , Non-alcoholic Fatty Liver Disease/drug therapy , Non-alcoholic Fatty Liver Disease/pathology , Non-alcoholic Fatty Liver Disease/virology , Receptors, Virus/genetics , Receptors, Virus/metabolism , Severity of Illness Index
10.
Liver Int ; 41(11): 2560-2577, 2021 11.
Article in English | MEDLINE | ID: covidwho-1434779

ABSTRACT

Metabolic diseases are associated with a higher risk of a severer coronavirus disease 2019 (COVID-19) course, since fatty liver is commonly associated with metabolic disorders, fatty liver itself is considered as a major contributor to low-grade inflammation in obesity and diabetes. Recently a comprehensive term, metabolic (dysfunction) associated fatty liver disease (MAFLD), has been proposed. The hepatic inflammatory status observed in MAFLD patients is amplified in presence of severe acute respiratory syndrome coronavirus 2 infection. Intestinal dysbiosis is a powerful activator of inflammatory mediator production of liver macrophages. The intestinal microbiome plays a key role in MAFLD progression, which results in non-alcoholic steatohepatitis and liver fibrosis. Therefore, patients with metabolic disorders and COVID-19 can have a worse outcome of COVID-19. This literature review attempts to disentangle the mechanistic link of MAFLD from COVID-19 complexity and to improve knowledge on its pathophysiology.


Subject(s)
COVID-19 , Metabolic Diseases , Non-alcoholic Fatty Liver Disease , Humans , Immunity , SARS-CoV-2
11.
Clin Res Hepatol Gastroenterol ; 46(3): 101807, 2022 03.
Article in English | MEDLINE | ID: covidwho-1415289

ABSTRACT

Obesity is a known risk factor for respiratory infection and many other chronic diseases, including metabolic dysfunction-associated fatty liver disease (MAFLD), previously known as nonalcoholic fatty liver disease (NAFLD). Recently, it has been considered an important and independent predictor for coronavirus disease 2019 (COVID-19) complications in adults, especially cardiopulmonary, presenting in a great number of individuals in critical care. In obesity, adipose tissue (AT) undergoes expansion via several processes: expansion of adipocytes and insufficient vascularization lead to hypoxia; adipocyte apoptosis/necrosis; irregular fatty acid flux; and enhanced secretion of inflammatory adipokines, cytokines, and chemokines. In individuals with obesity the liver can also become a target of COVID-19 infection, although major liver damage is uncommon. COVID-19 acute pandemic often develops in patients with major metabolic abnormalities, including fatty liver disease, which is part of a chronic pandemic together with body fat accumulation. During metabolic abnormalities, the expansion of metabolically active fat parallels chronic inflammatory changes, the development of Insulin Resistance (IR), and in the liver, the accumulation of fat, possibly, an underlying fibrosis. SARS-Cov-2 virus might affect the liver by direct or indirect mechanisms. The current epidemic of obesity and related metabolic diseases has extensively contributed to increase the number of severe cases and deaths from COVID-19, resulting in a health, political and economic crisis with long-lasting consequences. In this review, the authors explore the relationship between AT dysfunction and MAFLD in obesity on the scene of COVID-19.


Subject(s)
COVID-19 , Non-alcoholic Fatty Liver Disease , Adipose Tissue , Adult , COVID-19/complications , Humans , Non-alcoholic Fatty Liver Disease/complications , Obesity/complications , Obesity/epidemiology , SARS-CoV-2
12.
Nutrients ; 13(8)2021 Aug 18.
Article in English | MEDLINE | ID: covidwho-1360798

ABSTRACT

Throughout the 20th and 21st centuries, the incidence of non-communicable diseases (NCDs), also known as chronic diseases, has been increasing worldwide. Changes in dietary and physical activity patterns, along with genetic conditions, are the main factors that modulate the metabolism of individuals, leading to the development of NCDs. Obesity, diabetes, metabolic associated fatty liver disease (MAFLD), and cardiovascular diseases (CVDs) are classified in this group of chronic diseases. Therefore, understanding the underlying molecular mechanisms of these diseases leads us to develop more accurate and effective treatments to reduce or mitigate their prevalence in the population. Given the global relevance of NCDs and ongoing research progress, this article reviews the current understanding about NCDs and their related risk factors, with a focus on obesity, diabetes, MAFLD, and CVDs, summarizing the knowledge about their pathophysiology and highlighting the currently available and emerging therapeutic strategies, especially pharmacological interventions. All of these diseases play an important role in the contamination by the SARS-CoV-2 virus, as well as in the progression and severity of the symptoms of the coronavirus disease 2019 (COVID-19). Therefore, we briefly explore the relationship between NCDs and COVID-19.


Subject(s)
COVID-19/therapy , Metabolic Diseases/therapy , Animals , COVID-19/epidemiology , COVID-19/metabolism , COVID-19/physiopathology , Chronic Disease , Humans , Metabolic Diseases/epidemiology , Metabolic Diseases/physiopathology , Noncommunicable Diseases/epidemiology , Noncommunicable Diseases/therapy , Prevalence , Risk Factors , SARS-CoV-2/isolation & purification , Severity of Illness Index
13.
Arch Toxicol ; 95(7): 2235-2253, 2021 07.
Article in English | MEDLINE | ID: covidwho-1239455

ABSTRACT

Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease that affects about a quarter of the world population. MAFLD encompasses different disease stadia ranging from isolated liver steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis and hepatocellular carcinoma. Although MAFLD is considered as the hepatic manifestation of the metabolic syndrome, multiple concomitant disease-potentiating factors can accelerate disease progression. Among these risk factors are diet, lifestyle, genetic traits, intake of steatogenic drugs, male gender and particular infections. Although infections often outweigh the development of fatty liver disease, pre-existing MAFLD could be triggered to progress towards more severe disease stadia. These combined disease cases might be underreported because of the high prevalence of both MAFLD and infectious diseases that can promote or exacerbate fatty liver disease development. In this review, we portray the molecular and cellular mechanisms by which the most relevant viral, bacterial and parasitic infections influence the progression of fatty liver disease and steatohepatitis. We focus in particular on how infectious diseases, including coronavirus disease-19, hepatitis C, acquired immunodeficiency syndrome, peptic ulcer and periodontitis, exacerbate MAFLD. We specifically underscore the synergistic effects of these infections with other MAFLD-promoting factors.


Subject(s)
Bacterial Infections/complications , Non-alcoholic Fatty Liver Disease/complications , Parasitic Diseases/complications , Symptom Flare Up , Virus Diseases/complications , Acquired Immunodeficiency Syndrome/complications , Bacterial Infections/microbiology , COVID-19/complications , Hepatitis, Viral, Human/complications , Humans , Liver/physiopathology , Metabolic Syndrome , Non-alcoholic Fatty Liver Disease/microbiology , Non-alcoholic Fatty Liver Disease/parasitology , Non-alcoholic Fatty Liver Disease/virology , Parasitic Diseases/parasitology , Peptic Ulcer , Periodontitis , Risk Factors , Virus Diseases/virology
14.
Gastroenterol Hepatol ; 43(8): 472-480, 2020 Oct.
Article in English, Spanish | MEDLINE | ID: covidwho-1235898

ABSTRACT

The SARS-CoV-2 pandemic has proven to be a serious challenge for the Spanish healthcare system. The impact of the virus on the liver is not well known, but in patients with chronic liver disease, mostly in advanced stages, it can critically compromise survival and trigger decompensation. Treatment in this subpopulation is complex due to the potential hepatotoxicity of some of the medicinal products used. Moreover, the pandemic has also negatively impacted patients with liver disease who have not contracted COVID-19, since the reallocation of human and material resources to the care of patients with the virus has resulted in a decrease in the treatment, diagnosis and follow-up of patients with liver disease, which will surely have negative consequences in the near future. Efficient reorganization of hepatology units is a priority to minimise the impact of the pandemic on a population as vulnerable as liver disease patients.


Subject(s)
Betacoronavirus , Coronavirus Infections/epidemiology , Liver Diseases/epidemiology , Pandemics , Pneumonia, Viral/epidemiology , Adenosine Monophosphate/adverse effects , Adenosine Monophosphate/analogs & derivatives , Adenosine Monophosphate/therapeutic use , Age Factors , Alanine/adverse effects , Alanine/analogs & derivatives , Alanine/therapeutic use , Antiviral Agents/adverse effects , Antiviral Agents/therapeutic use , Bile Ducts/virology , COVID-19 , Chemical and Drug Induced Liver Injury/etiology , Chronic Disease , Comorbidity , Coronavirus Infections/drug therapy , Disease Susceptibility , Gastroenterology/organization & administration , Health Resources/supply & distribution , Hepatitis, Chronic/drug therapy , Hepatitis, Chronic/epidemiology , Humans , Immunosuppressive Agents/adverse effects , Liver/drug effects , Liver/pathology , Liver/virology , Liver Function Tests , Liver Transplantation , Obesity/epidemiology , Resource Allocation , Risk Factors , SARS-CoV-2
15.
Front Immunol ; 12: 651728, 2021.
Article in English | MEDLINE | ID: covidwho-1190315

ABSTRACT

The coronavirus infectious disease 2019 (COVID-19) pandemic has hit the world, affecting health, medical care, economies and our society as a whole. Furthermore, COVID-19 pandemic joins the increasing prevalence of metabolic syndrome in western countries. Patients suffering from obesity, type II diabetes mellitus, cardiac involvement and metabolic associated fatty liver disease (MAFLD) have enhanced risk of suffering severe COVID-19 and mortality. Importantly, up to 25% of the population in western countries is susceptible of suffering from both MAFLD and COVID-19, while none approved treatment is currently available for any of them. Moreover, it is well known that exacerbated innate immune responses are key in the development of the most severe stages of MAFLD and COVID-19. In this review, we focus on the role of the immune system in the establishment and progression of MAFLD and discuss its potential implication in the development of severe COVID-19 in MAFLD patients. As a result, we hope to clarify their common pathology, but also uncover new potential therapeutic targets and prognostic biomarkers for further research.


Subject(s)
Adaptive Immunity/immunology , COVID-19/immunology , COVID-19/pathology , Fatty Liver/immunology , Immunity, Innate/immunology , Angiotensin-Converting Enzyme 2/immunology , Angiotensin-Converting Enzyme 2/metabolism , CD4-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/immunology , Diabetes Mellitus, Type 2/pathology , Fatty Liver/pathology , Humans , Liver/immunology , Liver/pathology , Obesity/pathology , Risk Factors , SARS-CoV-2/immunology , Severity of Illness Index
16.
Front Endocrinol (Lausanne) ; 12: 604100, 2021.
Article in English | MEDLINE | ID: covidwho-1150686

ABSTRACT

Background and Aim: Circulating levels of interleukin (IL)-6, a well-known inflammatory cytokine, are often elevated in coronavirus disease-2019 (COVID-19). Elevated IL-6 levels are also observed in patients with metabolic dysfunction-associated fatty liver disease (MAFLD). Our study aimed to describe the association between circulating IL-6 levels and MAFLD at hospital admission with risk of severe COVID-19. Methods: A total of 167 patients with laboratory-confirmed COVID-19 from three Chinese hospitals were enrolled. Circulating levels of IL-2, IL-4, IL-6, IL-10, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ were measured at admission. All patients were screened for fatty liver by computed tomography. Forty-six patients were diagnosed as MAFLD. Results: Patients with MAFLD (n = 46) had higher serum IL-6 levels (median 7.1 [interquartile range, 4.3-20.0] vs. 4.8 [2.6-11.6] pg/mL, p = 0.030) compared to their counterparts without MAFLD (n = 121). After adjustment for age and sex, patients with MAFLD had a ~2.6-fold higher risk of having severe COVID-19 than those without MAFLD. After adjustment for age, sex and metabolic co-morbidities, increased serum IL-6 levels remained associated with higher risk of severe COVID-19, especially among infected patients with MAFLD (adjusted-odds ratio 1.14, 95% CI 1.05-1.23; p = 0.002). There was a significant interaction effect between serum IL-6 levels and MAFLD for risk of severe COVID-19 (p for interaction = 0.008). Conclusions: Patients with MAFLD and elevated serum IL-6 levels at admission are at higher risk for severe illness from COVID-19.


Subject(s)
COVID-19/complications , Fatty Liver/epidemiology , Interleukin-6/blood , Metabolic Diseases/physiopathology , SARS-CoV-2/isolation & purification , Severity of Illness Index , Adolescent , Adult , Aged , COVID-19/transmission , COVID-19/virology , China/epidemiology , Fatty Liver/blood , Fatty Liver/pathology , Fatty Liver/virology , Female , Humans , Male , Middle Aged , Retrospective Studies , Risk Factors , Young Adult
20.
J Clin Exp Hepatol ; 11(4): 484-493, 2021.
Article in English | MEDLINE | ID: covidwho-1002704

ABSTRACT

COVID-19 is characterized by predominant respiratory and gastrointestinal symptoms. Liver enzymes derangement is seen in 15-55% of the patients. Advanced age, hypertension, diabetes, obesity, malignancy, and cardiovascular disease predispose them to severe disease and the need for hospitalization. Data on pre-existing liver disease in patients with COVID-19 is limited, and most studies had only 3-8% of these patients. Patients with metabolic dysfunction-associated fatty liver (MAFLD) had shown a 4-6 fold increase in severity of COVID-19, and its severity and mortality increased in patients with higher fibrosis scores. Patients with chronic liver disease had shown that cirrhosis is an independent predictor of severity of COVID-19 with increased hospitalization and mortality. Increase in Child Turcotte Pugh (CTP) score and model for end-stage liver disease (MELD) score increases the mortality in these patients. Few case reports had shown SARS-CoV-2 as an acute event in the decompensation of underlying chronic liver disease. Immunosuppression should be reduced prophylactically in patients with autoimmune liver disease and post-transplantation with no COVID-19. Hydroxychloroquine and remdesivir is found to be safe in limited studies in a patient with cirrhosis and COVID-19. For hepatologists, cirrhosis with COVID-19 is a pertinent issue as the present pandemic will have severe disease in patients with chronic liver disease leading to more hospitalization and decompensation.

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