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1.
Cells ; 11(7)2022 Mar 24.
Article in English | MEDLINE | ID: covidwho-1785535

ABSTRACT

Sarcopenia is a common complication affecting liver disease patients, yet the underlying mechanisms remain unclear. We aimed to elucidate the cellular mechanisms that drive sarcopenia progression using an in vitro model of liver disease. C2C12 myotubes were serum and amino acid starved for 1-h and subsequently conditioned with fasted ex vivo serum from four non-cirrhotic non-alcoholic fatty liver disease patients (NAFLD), four decompensated end-stage liver disease patients (ESLD) and four age-matched healthy controls (CON) for 4- or 24-h. After 4-h C2C12 myotubes were treated with an anabolic stimulus (5 mM leucine) for 30-min. Myotube diameter was reduced following treatment with serum from ESLD compared with CON (-45%) and NAFLD (-35%; p < 0.001 for both). A reduction in maximal mitochondrial respiration (24% and 29%, respectively), coupling efficiency (~12%) and mitophagy (~13%) was identified in myotubes conditioned with NAFLD and ESLD serum compared with CON (p < 0.05 for both). Myostatin (43%, p = 0.04) and MuRF-1 (41%, p = 0.03) protein content was elevated in myotubes treated with ESLD serum compared with CON. Here we highlight a novel, experimental platform to further probe changes in circulating markers associated with liver disease that may drive sarcopenia and develop targeted therapeutic interventions.


Subject(s)
End Stage Liver Disease , Non-alcoholic Fatty Liver Disease , Sarcopenia , Humans , Muscle Fibers, Skeletal , Non-alcoholic Fatty Liver Disease/complications , Protein Biosynthesis , Sarcopenia/complications
2.
Can J Gastroenterol Hepatol ; 2022: 7235860, 2022.
Article in English | MEDLINE | ID: covidwho-1770044

ABSTRACT

Methods: We identified relevant cohort studies that assessed the relationship between liver fibrosis scores (e.g., FIB-4, NAFLD fibrosis score (NFS), and aspartate aminotransferase to platelet ratio index (APRI)) and associated prognosis outcomes by searching the PubMed, EMBASE, and medRxiv databases. The potential dose-response effect was performed using a stage robust error meta-regression. Results: Sixteen studies with 8,736 hospitalized patients with COVID-19 were included. One-point score in FIB-4 increase was significantly associated with increased mechanical ventilation (RR: 2.23, 95% CI: 1.37-3.65, P=0.001), severe COVID-19 (RR: 1.82, 95% CI: 1.53-2.16, P < 0.001), and death (RR: 1.47, 95% CI: 1.31-1.65, P < 0.001), rather than hospitalization (RR: 1.35, 95% CI: 0.72-2.56, P=0.35). Furthermore, there is a significant positive linear relationship between FIB-4 and severe COVID-19 (P nonlinearity=0.12) and mortality (P nonlinearity=0.18). Regarding other liver scores, one unit elevation in APRI increased the risk of death by 178% (RR: 2.78, 95% CI: 1.10-6.99, P=0.03). Higher NFS (≥-1.5) and Forns index were associated with increased risk of severe COVID-19 and COVID-19-associated death. Conclusion: Our dose-response meta-analysis suggests high liver fibrosis scores are associated with worse prognosis in patients with COVID-19. For patients with COVID-19 at admission, especially for those with coexisting chronic liver diseases, assessment of liver fibrosis scores might be useful for identifying high risk of developing severe COVID-19 cases and worse outcomes.


Subject(s)
COVID-19 , Non-alcoholic Fatty Liver Disease , COVID-19/epidemiology , Hospitalization , Humans , Liver Cirrhosis/complications , Non-alcoholic Fatty Liver Disease/complications , Respiration, Artificial/adverse effects
3.
Lancet Diabetes Endocrinol ; 10(4): 284-296, 2022 04.
Article in English | MEDLINE | ID: covidwho-1692744

ABSTRACT

Non-alcoholic fatty liver disease (NAFLD) has become an epidemic, much like other non-communicable diseases (NCDs), such as cancer, obesity, diabetes, and cardiovascular disease. The pathophysiology of NAFLD, particularly involving insulin resistance and subclinical inflammation, is not only closely linked to that of those NCDs but also to a severe course of the communicable disease COVID-19. Genetics alone cannot explain the large increase in the prevalence of NAFLD during the past 2 decades and the increase that is projected for the next decades. Impairment of glucose and lipid metabolic pathways, which has been propelled by the worldwide increase in the prevalence of obesity and type 2 diabetes, is most likely behind the increase in people with NAFLD. As the prevalence of NAFLD varies among subgroups of patients with diabetes and prediabetes identified by cluster analyses, stratification of people with diabetes and prediabetes by major pathological mechanistic pathways might improve the diagnosis of NAFLD and prediction of its progression. In this Review, we aim to understand how diabetes can affect the development of hepatic steatosis and its progression to advanced liver damage. First, we emphasise the extent to which NAFLD and diabetes jointly occur worldwide. Second, we address the major mechanisms that are involved in the pathogenesis of NAFLD and type 2 diabetes, and we discuss whether these mechanisms place NAFLD in an important position to better understand the pathogenesis of NCDs and communicable diseases, such as COVID-19. Third, we address whether this knowledge can be used for personalised treatment of NAFLD in the future. Finally, we discuss the current treatment strategies for people with type 2 diabetes and their effectiveness in treating the spectrum of hepatic diseases from simple steatosis to non-alcoholic steatohepatitis and hepatic fibrosis.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Insulin Resistance , Non-alcoholic Fatty Liver Disease , Prediabetic State , COVID-19/complications , COVID-19/epidemiology , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/epidemiology , Humans , Liver/metabolism , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/epidemiology , Prediabetic State/metabolism
4.
Nutrients ; 14(3)2022 Jan 27.
Article in English | MEDLINE | ID: covidwho-1667256

ABSTRACT

The coronavirus disease 2019 (COVID-19) lockdown dramatically changed people's lifestyles. Diet, physical activity, and the PNPLA3 gene are known risk factors for non-alcoholic fatty liver disease (NAFLD). Aim: To evaluate changes in metabolic and hepatic disease in NAFLD patients after the COVID-19 lockdown. Three hundred and fifty seven NAFLD patients were enrolled, all previously instructed to follow a Mediterranean diet (MD). Anthropometric, metabolic, and laboratory data were collected before the COVID-19 lockdown in Italy and 6 months apart, along with ultrasound (US) steatosis grading and information about adherence to MD and physical activity (PA). In 188 patients, PNPLA3 genotyping was performed. After the lockdown, 48% of patients gained weight, while 16% had a worsened steatosis grade. Weight gain was associated with poor adherence to MD (p = 0.005), reduced PA (p = 0.03), and increased prevalence of PNPLA3 GG (p = 0.04). At multivariate analysis (corrected for age, sex, MD, PA, and PNPLA3 GG), only PNPLA3 remained independently associated with weight gain (p = 0.04), which was also associated with worsened glycemia (p = 0.002) and transaminases (p = 0.02). During lockdown, due to a dramatic change in lifestyles, half of our cohort of NAFLD patients gained weight, with a worsening of metabolic and hepatologic features. Interestingly, the PNPLA3 GG genotype nullified the effect of lifestyle and emerged as an independent risk factor for weight gain, opening new perspectives in NAFLD patient care.


Subject(s)
COVID-19 , Non-alcoholic Fatty Liver Disease , Communicable Disease Control , Genotype , Humans , Life Style , Lipase/genetics , Membrane Proteins/genetics , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/epidemiology , Non-alcoholic Fatty Liver Disease/genetics , SARS-CoV-2/genetics
5.
Skelet Muscle ; 11(1): 27, 2021 12 11.
Article in English | MEDLINE | ID: covidwho-1571932

ABSTRACT

BACKGROUND: Several chronic inflammatory diseases co-exist with and accelerate sarcopenia (reduction in muscle strength, function and mass) and negatively impact on both morbidity and mortality. There is currently limited research on the extent of sarcopenia in such conditions, how to accurately assess it and whether there are generic or disease-specific mechanisms driving sarcopenia. Therefore, this study aims to identify potential mechanisms driving sarcopenia within chronic inflammatory disease via a multi-modal approach; in an attempt to help define potential interventions for future use. METHODS: This prospective cohort study will consist of a multi-modal assessment of sarcopenia and its underlying mechanisms. Recruitment will target three chronic inflammatory diseases: chronic liver disease (CLD) (n=50), with a subset of NAFLD (n=20), inflammatory bowel disease (IBD) (n=50) and rheumatoid arthritis (RA) (n=50) both before and after therapeutic intervention. In addition, 20 age and sex matched healthy individuals will be recruited for comparison. Participants will undergo 4 assessment visits at weeks 0, 2, 12 and 24. Visits will consist of the following assessments: blood tests, anthropometrics, functional assessment, quadriceps muscle imaging, actigraphy, quality of life questionnaires, food diary collection and muscle biopsy of the vastus lateralis (at weeks 2 and 24 only). In addition, stool and urine samples will be collected for future microbiome and metabolomics analysis. DISCUSSION: This is the first study to use a multi-modal assessment model to phenotype sarcopenia in these chronic inflammatory diseases. We hope to identify generic as well as disease-specific mechanisms driving sarcopenia. We appreciate that these cohorts do require separate standards of care treatments which limit comparison between groups. ETHICS AND DISSEMINATION: The study is approved by the Health Research Authority - West Midlands Solihull Research Ethics Service Committee Authority (REC reference: 18/WM/0167). Recruitment commenced in January 2019 and will continue until July 2021. The study was halted in March 2020 and again in January 2021 with the COVID-19 pandemic. The findings will be disseminated through peer-reviewed publications and conference presentations. All data will be stored on a secure server. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04734496.


Subject(s)
End Stage Liver Disease/complications , Sarcopenia/etiology , Adult , Arthritis, Rheumatoid/complications , Case-Control Studies , Female , Humans , Inflammatory Bowel Diseases/complications , Male , Non-alcoholic Fatty Liver Disease/complications , Prospective Studies
6.
J Korean Med Sci ; 36(41): e291, 2021 Oct 25.
Article in English | MEDLINE | ID: covidwho-1485031

ABSTRACT

BACKGROUND: Evidence for the association between underlying non-alcoholic fatty liver disease (NAFLD), the risk of testing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive, and the clinical consequences of coronavirus disease 2019 (COVID-19) is controversial and scarce. We aimed to investigate the association between the presence of NAFLD and the risk of SARS-CoV-2 infectivity and COVID-19-related outcomes. METHODS: We used the population-based, nationwide cohort in South Korea linked with the general health examination records between January 1, 2018 and July 30, 2020. Data for 212,768 adults older than 20 years who underwent SARS-CoV-2 testing from January 1 to May 30, 2020, were obtained. The presence of NAFLDs was defined using three definitions, namely hepatic steatosis index (HSI), fatty liver index (FLI), and claims-based definition. The outcomes were SARS-CoV-2 test positive, COVID-19 severe illness, and related death. RESULTS: Among 74,244 adults who completed the general health examination, there were 2,251 (3.0%) who were SARS-CoV-2 positive, 438 (0.6%) with severe COVID-19 illness, and 45 (0.06%) COVID-19-related deaths. After exposure-driven propensity score matching, patients with pre-existing HSI-NAFLD, FLI-NAFLD, or claims-based NAFLD had an 11-23% increased risk of SARS-CoV-2 infection (HSI-NAFLD 95% confidence interval [CI], 1-28%; FLI-NAFLD 95% CI, 2-27%; and claims-based NAFLD 95% CI, 2-31%) and a 35-41% increased risk of severe COVID-19 illness (HSI-NAFLD 95% CI, 8-83%; FLI-NAFLD 95% CI, 5-71%; and claims-based NAFLD 95% CI, 1-92%). These associations are more evident as liver fibrosis advanced (based on the BARD scoring system). Similar patterns were observed in several sensitivity analyses including the full-unmatched cohort. CONCLUSION: Patients with pre-existing NAFLDs have a higher likelihood of testing SARS-CoV-2 positive and severe COVID-19 illness; this association was more evident in patients with NAFLD with advanced fibrosis. Our results suggest that extra attention should be given to the management of patients with NAFLD during the COVID-19 pandemic.


Subject(s)
COVID-19/etiology , Non-alcoholic Fatty Liver Disease/complications , SARS-CoV-2 , Adult , Aged , Cohort Studies , Disease Susceptibility , Female , Humans , Male , Middle Aged , Severity of Illness Index
7.
Viruses ; 13(7)2021 07 01.
Article in English | MEDLINE | ID: covidwho-1448932

ABSTRACT

Infection has recently started receiving greater attention as an unusual causative/inducing factor of obesity. Indeed, the biological plausibility of infectobesity includes direct roles of some viruses to reprogram host metabolism toward a more lipogenic and adipogenic status. Furthermore, the probability that humans may exchange microbiota components (virome/virobiota) points out that the altered response of IFN and other cytokines, which surfaces as a central mechanism for adipogenesis and obesity-associated immune suppression, is due to the fact that gut microbiota uphold intrinsic IFN signaling. Last but not least, the adaptation of both host immune and metabolic system under persistent viral infections play a central role in these phenomena. We hereby discuss the possible link between adenovirus and obesity-related nonalcoholic fatty liver disease (NAFLD). The mechanisms of adenovirus-36 (Ad-36) involvement in hepatic steatosis/NAFLD consist in reducing leptin gene expression and insulin sensitivity, augmenting glucose uptake, activating the lipogenic and pro-inflammatory pathways in adipose tissue, and increasing the level of macrophage chemoattractant protein-1, all of these ultimately leading to chronic inflammation and altered lipid metabolism. Moreover, by reducing leptin expression and secretion Ad-36 may have in turn an obesogenic effect through increased food intake or decreased energy expenditure via altered fat metabolism. Finally, Ad-36 is involved in upregulation of cAMP, phosphatidylinositol 3-kinase, and p38 signaling pathways, downregulation of Wnt10b expression, increased expression of CCAAT/enhancer binding protein-beta, and peroxisome proliferator-activated receptor gamma 2 with consequential lipid accumulation.


Subject(s)
Inflammation , Lipid Metabolism , Non-alcoholic Fatty Liver Disease/complications , Obesity/etiology , Obesity/virology , Adenoviridae/immunology , Adenoviridae Infections/complications , Adenoviridae Infections/immunology , Animals , Diet, High-Fat , Glucose/metabolism , Humans , Lipogenesis , Mice , Mice, Inbred C57BL , Non-alcoholic Fatty Liver Disease/virology , Obesity/complications , Obesity/immunology , Signal Transduction
8.
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
9.
Medicina (Kaunas) ; 57(10)2021 Oct 03.
Article in English | MEDLINE | ID: covidwho-1444271

ABSTRACT

The COVID-19 pandemic was and still is a global burden with more than 178,000,000 cases reported so far. Although it mainly affects respiratory organs, COVID-19 has many extrapulmonary manifestations, including, among other things, liver injury. Many hypotheses have been proposed to explain direct and indirect impacts of the SARS-CoV-2 virus on the liver. Studies have shown that around 15-30% of patients with COVID-19 have underlying liver disease, and 20-35% of patients with COVID-19 had altered liver enzymes at admission. One of the hypotheses is reactivation of an underlying liver disease, such as non-alcoholic fatty liver disease (NAFLD). Some studies have shown that NAFLD is associated with severe COVID-19 and poor outcome; nevertheless, other studies showed no significant difference between groups in comparing complications and clinical outcomes. Patients with NAFLD may suffer severe COVID-19 due to other comorbidities, especially cardiovascular diseases. The link between NAFLD and COVID-19 is not clear yet, and further studies and research are needed.


Subject(s)
COVID-19 , Non-alcoholic Fatty Liver Disease , Humans , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/epidemiology , Pandemics , SARS-CoV-2
10.
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
11.
J Formos Med Assoc ; 121(2): 454-466, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1330958

ABSTRACT

This review evaluates the ability of the fibrosis index based on four factors (FIB-4) identifying fibrosis stages, long-time prognosis in chronic liver disease, and short-time outcomes in acute liver injury. FIB-4 was accurate in predicting the absence or presence of advanced fibrosis with cut-offs of 1.0 and 2.65 for viral hepatitis B, 1.45 and 3.25 for viral hepatitis C, 1.30 (<65 years), 2.0 (≥65 years), and 2.67 for non-alcoholic fatty liver disease (NAFLD), respectively, but had a low-to-moderate accuracy in alcoholic liver disease (ALD) and autoimmune hepatitis. It performed better in excluding fibrosis, so we built an algorithm for identifying advanced fibrosis by combined methods and giving work-up and follow-up suggestions. High FIB-4 in viral hepatitis, NAFLD, and ALD was associated with significantly high hepatocellular carcinoma incidence and mortality. Additionally, FIB-4 showed the ability to predict high-risk varices with cut-offs of 2.87 and 3.91 in cirrhosis patients and predict long-term survival in hepatocellular carcinoma patients after hepatectomy. In acute liver injury caused by COVID-19, FIB-4 had a predictive value for mechanical ventilation and 30-day mortality. Finally, FIB-4 may act as a screening tool in the secondary prevention of NAFLD in the high-risk population.


Subject(s)
COVID-19 , Liver Neoplasms , Non-alcoholic Fatty Liver Disease , Fibrosis , Humans , Liver/pathology , Liver Cirrhosis/pathology , Liver Neoplasms/pathology , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/diagnosis , Non-alcoholic Fatty Liver Disease/pathology , SARS-CoV-2 , Severity of Illness Index
12.
Biochimie ; 179: 266-274, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-1326918

ABSTRACT

Obese patients who often present metabolic dysfunction-associated fatty liver disease (MAFLD) are at risk of severe presentation of coronavirus disease 2019 (COVID-19). These patients are more likely to be hospitalized and receive antiviral agents and other drugs required to treat acute respiratory distress syndrome and systemic inflammation, combat bacterial and fungal superinfections and reverse multi-organ failure. Among these pharmaceuticals, antiretrovirals such as lopinavir/ritonavir and remdesivir, antibiotics and antifungal agents can induce drug-induced liver injury (DILI), whose mechanisms are not always understood. In the present article, we hypothesize that obese COVID-19 patients with MAFLD might be at higher risk for DILI than non-infected healthy individuals or MAFLD patients. These patients present several concomitant factors, which individually can favour DILI: polypharmacy, systemic inflammation at risk of cytokine storm, fatty liver and sometimes nonalcoholic steatohepatitis (NASH) as well as insulin resistance and other diseases linked to obesity. Hence, in obese COVID-19 patients, some drugs might cause more severe (and/or more frequent) DILI, while others might trigger the transition of fatty liver to NASH, or worsen pre-existing steatosis, necroinflammation and fibrosis. We also present the main mechanisms whereby drugs can be more hepatotoxic in MAFLD including impaired activity of xenobiotic-metabolizing enzymes, mitochondrial dysfunction, altered lipid homeostasis and oxidative stress. Although comprehensive investigations are needed to confirm our hypothesis, we believe that the current epidemic of obesity and related metabolic diseases has extensively contributed to increase the number of cases of DILI in COVID-19 patients, which may have participated in presentation severity and death.


Subject(s)
COVID-19/complications , COVID-19/drug therapy , Chemical and Drug Induced Liver Injury , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/metabolism , Chemical and Drug Induced Liver Injury/physiopathology , Humans , Liver/drug effects , Liver/physiopathology
13.
J Clin Lab Anal ; 35(8): e23880, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1293190

ABSTRACT

BACKGROUND: There is still little knowledge about the association of liver fibrosis with the clinical outcomes of COVID-19 patients with non-alcoholic fatty liver disease (NAFLD). The aim of the study was to determine the association of NAFLD fibrosis score (NFS)-determined liver fibrosis with clinical outcomes of COVID-19 patients with NAFLD. METHODS: The NAFLD was diagnosed by the Hepatic Steatosis Index (HSI) in the absence of other causes of chronic liver diseases. NFS was used to evaluate the severity of liver fibrosis. RESULTS: A total of 86 COVID-19 patients with NAFLD were included. The median age was 43.5 years, and 58.1% of patients were male. Thirty-eight (44.2%) patients had advanced liver fibrosis according to the NFS. Multivariate analysis indicated that concurrent diabetes (odds ratio [OR] 8.264, 95% confidence interval [CI] 1.202-56.830, p = 0.032) and advanced liver fibrosis (OR 11.057, 95% CI 1.193-102.439, p = 0.034) were independent risk factors of severe illness in COVID-19 patients with NAFLD. CONCLUSION: NAFLD patients with NFS-determined advanced liver fibrosis are at higher risk of severe COVID-19.


Subject(s)
COVID-19/etiology , Liver Cirrhosis/pathology , Non-alcoholic Fatty Liver Disease/complications , Adult , Female , Hospitalization , Humans , Liver Cirrhosis/virology , Logistic Models , Male , Middle Aged , Non-alcoholic Fatty Liver Disease/pathology , Non-alcoholic Fatty Liver Disease/virology , Retrospective Studies , Risk Factors , Severity of Illness Index
14.
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
15.
Can J Gastroenterol Hepatol ; 2021: 5556354, 2021.
Article in English | MEDLINE | ID: covidwho-1211615

ABSTRACT

The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased significantly over the last few decades mirroring the increase in obesity and type II diabetes mellitus. NAFLD has become one of the most common indications for liver transplantation. The deleterious effects of NAFLD are not isolated to the liver only, for it has been recognized as a systemic disease affecting multiple organs through protracted low-grade inflammation mediated by the metabolic activity of excessive fat tissue. Extrahepatic manifestations of NAFLD such as cardiovascular disease, polycystic ovarian syndrome, chronic kidney disease, and hypothyroidism have been well described in the literature. In recent years, it has become evident that patients suffering from NAFLD might be at higher risk of developing various infections. The proposed mechanism for this association includes links through hyperglycemia, insulin resistance, alterations in innate immunity, obesity, and vitamin D deficiency. Additionally, a risk independent of these factors mediated by alterations in gut microbiota might contribute to a higher burden of infections in these individuals. In this narrative review, we synthetize current knowledge on several infections including urinary tract infection, pneumonia, Helicobacter pylori, coronavirus disease 2019, and Clostridioides difficile as they relate to NAFLD. Additionally, we explore NAFLD's association with hidradenitis suppurativa.


Subject(s)
COVID-19/epidemiology , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/microbiology , Clostridioides difficile , Clostridium Infections/epidemiology , Helicobacter Infections/epidemiology , Helicobacter pylori , Humans , Pneumonia/epidemiology , Urinary Tract Infections/epidemiology
16.
Clin Nutr ESPEN ; 43: 329-334, 2021 06.
Article in English | MEDLINE | ID: covidwho-1193265

ABSTRACT

BACKGROUND & AIMS: Given reports of changes in dietary habits during covid-19 lockdown, our aim was to assess weight changes, over a 3-month Covid-19 national lockdown in a cohort of NAFLD-HIV patients on a dietary intervention trial. METHODS: After NAFLD screening in an outpatient Infectious Diseases Clinic, NAFLD patients were randomly allocated to general dietary recommendations (SC group) or to a structured dietary intervention based on the Mediterranean diet (intervention group). During lockdown, follow-up consultations in the intervention group were done by video and/or phone. After 3 months of lockdown, all patients (intervention and SC group) consented to a telephone interview which aimed to characterize eating habits and lifestyle changes and evaluate stress and depression. Biochemical data when available, was compared between the peri-period of confinement. RESULTS: One hundred and twelve patients were screened. From the 55 NAFDL identified, 27 were allocated to dietary intervention and 28 to SC and were followed before lockdown for a mean period of 5.0 ± 1.5 months in which SC group gained a median of 0.65 kg vs. a median loss of 1.5 kg in the intervention group (p < 0.001). During lockdown, 93.3% of patients in the SC group referred that "diet got worse" vs. 6.7% in the intervention group p < 0.01), and 35.3% vs. 15.7% (p = 0.014) reported increase in appetite, respectively. Both groups gained weight, SC group vs. 0.7 ± 1.7 kg in the intervention group, p < 0.001). Higher weight gain was associated with changes in the dietary pattern (3.8 ± 2.1 kg vs. 2.0 ± 1.3 kg in "no change in dietary pattern"; p = 0.002). Glucose blood levels increased after lockdown in the SC group, with a mean increase of 15 mg/dl (p = 0.023). The remaining metabolic parameters remained unchanged. CONCLUSION: The maintenance of dietary intervention, using telemedicine, can mitigate the adverse change in dietary habits and physical activity pattern, preventing a substantial increase in body weight.


Subject(s)
Body Weight , COVID-19 , Diet, Mediterranean , HIV Infections/diet therapy , Non-alcoholic Fatty Liver Disease/diet therapy , Physical Distancing , Telemedicine , Adult , Appetite , Blood Glucose/metabolism , COVID-19/complications , COVID-19/prevention & control , COVID-19/psychology , Communicable Disease Control , Depression , Feeding Behavior/psychology , Female , HIV Infections/complications , HIV Infections/metabolism , Humans , Life Style , Male , Middle Aged , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/metabolism , Pandemics , SARS-CoV-2 , Social Isolation/psychology , Stress, Psychological , Weight Gain , Weight Loss
17.
Diabetes Metab Syndr ; 15(3): 813-822, 2021.
Article in English | MEDLINE | ID: covidwho-1163662

ABSTRACT

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) patients represent a vulnerable population that may be susceptible to more severe COVID-19. Moreover, not only the underlying NAFLD may influence the progression of COVID-19, but the COVID-19 may affect the clinical course of NAFLD as well. However, comprehensive evidence on clinical outcomes in patients with NAFLD is not well characterized. OBJECTIVES: To systematically review and meta-analysis the evidence on clinical outcomes in NAFLD patients with COVID-19. METHODS: MEDLINE, EMBASE, and Cochrane Central were searched from inception through November 2020. Epidemiological studies assessing the clinical outcomes in COVID-19 patients with NAFLD were included. Newcastle-Ottawa Scale (NOS) was used to assess study quality. Generic inverse variance method using RevMan was used to determine the pooled estimates using the random-effects model. RESULTS: Fourteen studies consisting of 1851 NAFLD patients, were included. Significant heterogeneity was observed among the studies, and studies were of moderate to high quality [mean, (range):8 (6, 8)]. For NAFLD patients, the adjusted odds ratio (aOR) for the severe COVID-19 was 2.60 (95%CI:2.24-3.02; p < 0.001) (studies,n:8), aOR for admission to ICU due to COVID-19 was 1.66 (95%CI:1.26-2.20; p < 0.001) (studies,n:2), and aOR for mortality for was 1.01 (95%CI:0.65-1.58; p = 0.96) (studies,n:2). CONCLUSIONS: An increased risk of severe COVID-19 infection and admission to ICU due to COVID-19 with no difference in mortality was observed between NAFLD and non-NAFLD patients. Future studies should include the mortality outcome to conclusively elucidate the impact of NAFLD in patients with COVID-19.


Subject(s)
COVID-19/diagnosis , Non-alcoholic Fatty Liver Disease/diagnosis , Adolescent , Adult , Aged , COVID-19/complications , COVID-19/epidemiology , COVID-19/pathology , Female , Hospitalization/statistics & numerical data , Humans , Male , Middle Aged , Mortality , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/epidemiology , Prognosis , Risk Factors , Severity of Illness Index , Young Adult
18.
Sci Rep ; 11(1): 5494, 2021 03 09.
Article in English | MEDLINE | ID: covidwho-1125236

ABSTRACT

It is important to pay attention to the indirect effects of the social distancing implemented to prevent the spread of coronavirus disease 2019 (COVID-19) pandemic on children and adolescent health. The aim of the present study was to explore impacts of a reduction in physical activity caused by COVID-19 outbreak in pediatric patients diagnosed with obesity. This study conducted between pre-school closing and school closing period and 90 patients aged between 6- and 18-year-old were included. Comparing the variables between pre-school closing period and school closing period in patients suffering from obesity revealed significant differences in variables related to metabolism such as body weight z-score, body mass index z-score, liver enzymes and lipid profile. We further evaluated the metabolic factors related to obesity. When comparing patients with or without nonalcoholic fatty liver disease (NAFLD), only hemoglobin A1c (HbA1c) was the only difference between the two time points (p < 0.05). We found that reduced physical activity due to school closing during COVID-19 pandemic exacerbated obesity among children and adolescents and negatively affects the HbA1C increase in NAFLD patients compared to non-NAFLD patients.


Subject(s)
COVID-19/pathology , Glucose Intolerance/diagnosis , Pediatric Obesity/diagnosis , Adolescent , Alanine Transaminase/analysis , Aspartate Aminotransferases/analysis , Body Mass Index , Body Weight , COVID-19/virology , Child , Exercise , Female , Glucose Intolerance/complications , Glycated Hemoglobin A/analysis , Humans , Lipids/analysis , Liver/enzymology , Male , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/diagnosis , Pediatric Obesity/complications , Quarantine , SARS-CoV-2/isolation & purification
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