# pos

id: cord-018318-vzzrsqsn
pos: NNPS
token:
  www.uptodate.com/contents/hepatotoxicity-due-to-herbal-medications-anddietary-supplements?source=search_result&search=hepatotoxicity+due+to+herbal+medications

lemma:
  www.uptodate.com/contents/hepatotoxicity-due-to-herbal-medications-anddietary-supplements?source=search_result&search=hepatotoxicity+due+to+herbal+medications


# ent

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type: PROTEIN
entity:
  zwischen dem hyperakuten 7 Tage dem akuten 7 28 Tage und dem subakuten 28 Tage 6 Monate Leberversagen 9


id: cord-005949-8po9xe5g
type: PROTEIN
entity:
  VIII XIII von Willebrandfaktor bei Hypofibrinogenämie 100 mg dl verwendet Zur Prävention der statistisch häufigen


id: cord-005949-8po9xe5g
type: PROTEIN
entity:
  Transplantationsbedingungen Patienten mit paracetamolinduziertem ALV sind hierbei am meisten beeinträchtigt Ebenso zeigen Patienten über 50 Jahre eine 2


id: cord-005949-8po9xe5g
type: CHEMICAL
entity:
  sich das nebenwirkungsarme NAC Schema generell auch bei allen anderen Entitäten des ALV Eine spezifische Behandlung sollte bei der akuten Hepatitis B Infektion eingeleitet


id: cord-005949-8po9xe5g
type: CHEMICAL
entity:
  Patienten rekrutiert werden können Da der Verlauf des ALV in seiner Geschwindigkeit kaum vorhersagbar ist empfiehlt sich


id: cord-016130-5q9ufu28
type: CELL_TYPE
entity:
  human T lymphocyte proliferation 145 146 and vitamin D analogs have been shown to be effective in the prevention and treatment of some models of autoimmune disease in rodents particularly autoimmune diabetes in mice 144 147 148 In 1997 Muhe and colleagues 110 149


id: cord-016130-5q9ufu28
type: ORG
entity:
  Medicaid The Special Supplemental Nutrition Program for Women Infants and Children or the Food Stamp Program


id: cord-016130-5q9ufu28
type: ORG
entity:
  the United States Department of Agriculture USDA Special Supplemental Nutrition Program for Women Infants and Children WIC


id: cord-016130-5q9ufu28
type: ORG
entity:
  Free Radical Scavenging Enzyme Activity Profiles in Risk Assessment of Idiosyncratic Drug Reactions Free


id: cord-016130-5q9ufu28
type: ORG
entity:
  American Medical Association International Classification of Diseases 9th Revision Clinical Modification Compliance


id: cord-016130-5q9ufu28
type: ORG
entity:
  The Norwegian National Council on Nutrition and Physical Activity Feeding Recommendations for Infants for Health Care Workers


id: cord-014770-cgtzlra1
type: ORG
entity:
  Gastrointestinal Defenses against Injury and Inflammation and Immunology of the Gastrointestinal Tract


id: cord-016880-q44623s8
type: GGP
entity:
  vandaar dat levertransplantatie zo mogelijk voor dat moment moet plaatsvinden Seropositiviteit voor HIV


id: cord-016880-q44623s8
type: DISEASE
entity:
  redelijk stabiel De tienjaarsoverleving bij kinderen na levertransplantatie bedraagt 75 tot 80 procent


id: cord-032131-ghgciqfk
type: PROTEIN
entity:
  Interleukin 2 Rezeptors aktivierter T Zellen blockiert Dieser Antikörper wird als Induktionstherapie


id: cord-032131-ghgciqfk
type: PROTEIN
entity:
  dem Zusammenhang mit dem Auftreten maligner Lymphome posttransplant lymphoproliferative disease PTLD Abb 19 3 Das PTLD Risiko scheint nicht nur


id: cord-032131-ghgciqfk
type: PROTEIN
entity:
  einem geeigneten Transplantationszentrum und unter Ausnutzung sämtlicher möglicher Transplantationstechniken


id: cord-032131-ghgciqfk
type: PROTEIN
entity:
  nicht mit dem Blutspiegel oder der eingenommenen Dosis des jeweiligen Toxins O Grady et al 1989 Für das ALV bei Paracetamolintoxikation konnte


id: cord-032131-ghgciqfk
type: PROTEIN
entity:
  nicht zu extrahepatischen Komplikationen vor allem HE kommt selbst bei extremen Gerinnungsstörungen relativ gut Allerdings scheint auch beim M Wilson z B eine ausgeprägte Hyperbilirubinämie 300 µmol l bzw 17 5 mg dl evtl auch eine Hyperphosphatämie Zeichen für eine schlechte Prognose zu sein z Therapie und klinisches Management Die Therapie des pädiatrischen ALV beruht auf 3 Säulen Supportivtherapie spezifische Therapie der zugrunde liegenden Erkrankung und Leberersatztherapie Eine


id: cord-032131-ghgciqfk
type: CHEMICAL
entity:
  Lebenswochen mit einem Ikterus prolongatus mit einer Hyperbilirubinämie durch direktes Bilirubin sowie acholischen


id: cord-032131-ghgciqfk
type: CHEMICAL
entity:
  Je nach Ausprägungsgrad der Gallengangatresie sind laborchemisch im Serum erhöhte Cholestaseparameter alkalische


id: cord-032131-ghgciqfk
type: CHEMICAL
entity:
  beobachtet wird Interessanterweise wird eine aplastische Anämie bei dieser Ätiologie auch nach erfolgreicher


id: cord-032131-ghgciqfk
type: CHEMICAL
entity:
  Patienten rechtzeitig erwogen werden Hierbei ist auch zu bedenken dass nach den derzeit geltenden Regeln von Euro Transplant eine höchst dringliche high urgency Meldung


id: cord-001567-3bw7jbzq
type: PROTEIN
entity:
  high density lipoprotein particle proteasome accessory complex peroxisome extracellular vesicular exosome


id: cord-001567-3bw7jbzq
type: PROTEIN
entity:
  EGF Epidermal growth factor EGFR Epidermal growth factor receptor EPS15 Epidermal growth factor receptor substrate


id: cord-001567-3bw7jbzq
type: PROTEIN
entity:
  glycation endproduct S100A1 S100 calcium binding protein A1 SAM S adenosylmethionine Short hairpin RNA


id: cord-001567-3bw7jbzq
type: GGP
entity:
  ASS Argininosuccinate synthetase 1 ATP Adenosine triphosphate CK Creatine kinase CK2Α Casein kinase II subunit alpha


id: cord-001567-3bw7jbzq
type: GGP
entity:
  EGF Epidermal growth factor EGFR Epidermal growth factor receptor EPS15 Epidermal growth factor receptor substrate 15 EPS15R Epidermal growth factor receptor substrate


id: cord-001567-3bw7jbzq
type: GGP
entity:
  mouse MEK Mitogen activated protein kinase kinase NAD Nicotinamide adenine dinucleotide NAD P H Nicotinamide adenine dinucleotide phosphate NADP Nicotinamide adenine dinucleotide phosphate NO Nitric oxide OGP n


id: cord-006391-esnsa4u5
type: CELL_LINE
entity:
  Cirrhotic Rat S Jenkins P Devitt and R Shields Department of Surgery University of Liverpool Liverpool U K


id: cord-006391-esnsa4u5
type: PROTEIN
entity:
  NACH2 tetrazolium reductase 21 33 glucose 6 phosphatase 48 33 alphanaphthylacetat esterase 31 33 ATP ase 71 0 5 nucleotidase 38 67 PAS reaction 56 0 MGP staining 30 67 Aspartate


id: cord-006391-esnsa4u5
type: GGP
entity:
  vasopressin 5 58 0 7 to 4 35 0 68 ml 5 min Acute blood loss sufficient to lower the central venous pressure by 5 cm of water


id: cord-006391-esnsa4u5
type: GGP
entity:
  norreals 0 18 0 09p 0 01 indicating a failure of metabolic compensation for reduced bloodflow and oxygen


id: cord-005892-3yuznrdv
type: PROTEIN
entity:
  Infektionen mit septischem Schock 60 100 15 16 17 erscheint eine aggressive antiinfektive Präventions


id: cord-023033-tgt69ir6
type: PROTEIN
entity:
  Hepatocyte growth factor HGF epidermal growth factor EGF fibroblast growth factor FGF vascular endothelial growth factor VEGF platelet


id: cord-023033-tgt69ir6
type: ORG
entity:
  Massachusetts General Hospital Harvard Medical School Boston MA Gregory Beck University of Massachusetts Boston


id: cord-016757-3d320c0a
type: DISEASE
entity:
  fulminant and subfulminant hepatic failure Fulminante Hepatitis bei Listeriensepsis Fulminant herpes hepatitis


id: cord-022300-9w0lehal
type: DNA
entity:
  celiac and common hepatic artenes Congenital Hepatoportal Microvascular p lasia Hepatoportal microvascular dyspla Sl IS char ct


id: cord-022300-9w0lehal
type: CELL_LINE
entity:
  cat Congenital feline portosystemic shunts EA The accessory gall bladder An embryological and comparative study of aberrant biliary vesicles


id: cord-022300-9w0lehal
type: DNA
entity:
  human mucopolysaccharidosis VII Mucopolysaccharidosis VI Maroteaux Lamy syndrome arylsulfatase B deficient mucopolysaccharidosis


id: cord-022300-9w0lehal
type: DISEASE
entity:
  abnormal vascular connections between the portal and systemic venous circulations Boothe et ai 1996 Bostwick


id: cord-292501-2jv7xkfn
type: ORG
entity:
  the Ethics Committee of the First Affiliated Hospital College of Medicine Zhejiang University Reference Number


id: cord-292501-2jv7xkfn
type: ORG
entity:
  State Administration of Traditional Chinese Medicine Diagnosis and Treatment Protocol for Novel Coronavirus Pneumonia Trial Version 6 2020


id: cord-025168-be7zube4
type: PROTEIN
entity:
  growth factor 1 IGF 1 basic fibroblast growth factor bFGF nerve growth factor NGF Transforming growth factor beta 1 TGF b1 placental growth factor PGF stromal cell derived factor 1 SDF 1 CXCL12 monocyte chemoattractant protein 1 MCP 1 CCL2 hepatocyte growth factor HGF interleukin 6 IL 6 IL 8 IL 10 IL 13 G CSF


id: cord-025168-be7zube4
type: PROTEIN
entity:
  growth factor 1 bFGF Basic fibroblast growth factor NGF Nerve growth factor TGF b1 Transforming growth beta 1 IFN


id: cord-025168-be7zube4
type: PROTEIN
entity:
  IL 1α Interleukin 1 alpha IL 1β Interleukin 1 beta PGF Placental growth factor SDF 1 CXCL12 Stromal cell derived factor 1 MCP 1 CCL2 Monocyte chemoattractant protein 1


id: cord-025168-be7zube4
type: GGP
entity:
  growth factor 1 IGF 1 basic fibroblast growth factor bFGF nerve growth factor NGF Transforming growth factor beta 1 TGF b1 placental growth factor PGF stromal cell derived factor 1 SDF 1 CXCL12 monocyte chemoattractant protein 1 MCP 1 CCL2 hepatocyte growth factor HGF interleukin 6 IL 6 IL 8 IL 10 IL 13 G CSF and GM CSF 72 73 74 75 There are various tissue specific factors


id: cord-025168-be7zube4
type: GGP
entity:
  growth factor 1 bFGF Basic fibroblast growth factor NGF Nerve growth factor TGF b1 Transforming growth beta 1 IFN γ Interferon γ TNF α Tumor necrosis factor α IL 1α Interleukin 1 alpha IL 1β Interleukin 1 beta PGF Placental growth factor SDF 1 CXCL12 Stromal cell derived factor 1 MCP 1 CCL2 Monocyte chemoattractant protein 1 HGF Hepatocyte growth factor G CSF Granulocyte


id: cord-309795-2kozsv4z
type: ORG
entity:
  the American Association for the Study of Liver Diseases EASL EASD EASO Clinical Practice Guidelines


id: cord-309795-2kozsv4z
type: WORK_OF_ART
entity:
  Fatty Liver Disease Evidence against Pathway Selective Hepatic Insulin Resistance in Mice Mechanisms of Disease


id: cord-309795-2kozsv4z
type: WORK_OF_ART
entity:
  The Opportunities and Challenges of Peroxisome Proliferator Activated Receptors Ligands in Clinical Drug Discovery and Development Elafibranor an Agonist of the Peroxisome Proliferator Activated Receptor


id: cord-309795-2kozsv4z
type: ORG
entity:
  the Phase 2b CENTAUR Study Statin Use and Risk of Cirrhosis and Related Complications in Patients With Chronic Liver Diseases


id: cord-305956-l02xdq87
type: ORG
entity:
  Boehringer Ingelheim Galmed Genfit Gilead Sciences Intercept Pharmaceuticals Novartis Roche Siemens Healthineers


id: cord-271635-tydlyc1q
type: GGP
entity:
  malondialdehyde AFP α fetoprotein IL 6 interleukin 6 ROS reactive oxygen species NO nitric oxide GSH glutathione t


id: cord-318755-fip8wj6y
type: GPE
entity:
  the United States Hepatopulmonary Syndrome and Portopulmonary Hypertension Implications for Liver Transplantation Portopulmonary Hypertension and Liver Transplant Recent Review of the Literature Portopulmonary hypertension


id: cord-022555-a7ie82fs
type: PROTEIN
entity:
  Cat DOI 10 1016 b978 1 4377 0660 4 00023 5 sha 43302f8eebca5d76d6388fe2286ead361a68209a doc_id 22555 cord_uid a7ie82fs nan


id: cord-022555-a7ie82fs
type: CELL_TYPE
entity:
  intestinal mast cell tumors adenomatous polyps eosinophilic sclerosing fibroplasia gastrointestinal stromal tumors leiomyosarcoma and hemangiosarcoma Mast cell tumors MCT


id: cord-022555-a7ie82fs
type: DNA
entity:
  dog and the other causes of portal hypertension Budd Chiari syndrome heartworm caval syndrome pulmonary hypertension


id: cord-022555-a7ie82fs
type: DNA
entity:
  dog and cat Pharmacokinetics and suggested oral dosing regimen of cisapride a study in healthy cats Intussusception


id: cord-022555-a7ie82fs
type: CELL_LINE
entity:
  cat Feline exocrine pancreatic insufficiency 16 cases Pancreatitis associated with a feline herpesvirus infection Pancreatic pseudocysts


id: cord-022555-a7ie82fs
type: GGP
entity:
  Clostridium piliforme Tyzzer s disease 71 and Anaerobiospirillum sp 36 Specific diagnosis of these and other


id: cord-284693-mgpxnnk0
type: CELL_LINE
entity:
  Hematopoietic Stem Cell or Solid Organ Transplantation Transplant Infections Infections after liver transplantation Infections in solid organ transplant recipients Oral acyclovir therapy for mucocutaneous herpes simplex virus infections in immunocompromised marrow transplant recipients Absolute bioavailability and metabolic disposition of valaciclovir the L valyl ester of acyclovir following oral administration to humans Herpes simplex virus in solid organ transplantation Incidence and risk factors


id: cord-290412-m6fesoyb
type: PROTEIN
entity:
  growth factors 1 IGF 1 phosphatidylinositol 3 kinase PI3K extracellular signal regulated kinase ERK p38 mitogen activated protein kinase p38


id: cord-290412-m6fesoyb
type: DISEASE
entity:
  viral hepatitis nonalcoholic fatty liver alcoholic liver disease autoimmune liver disease schistosomiasis liver disease


id: cord-030369-4dn02a35
type: GGP
entity:
  Hepatitis B DOI 10 1007 978 94 024 1603 9_1 sha 7e36a1fdf8bdb67e47d744f4a8dabc982e5bac5e doc_id 30369 cord_uid 4dn02a35


id: cord-324529-xbrdtxnz
type: PROTEIN
entity:
  ESR procalcitonin PCT ferritin cytokines interleukin 1β IL 1β interleukin 2 receptor IL 2R interleukin 6 IL 6 interleukin 8 IL 8 interleukin 10 IL 10 tumor necrosis factor


id: cord-324529-xbrdtxnz
type: GGP
entity:
  troponin I cTnI N terminal pro brain type natriuretic peptide NT proBNP hypersensitive C reactive protein hsCRP erythrocyte


id: cord-324529-xbrdtxnz
type: GGP
entity:
  ESR procalcitonin PCT ferritin cytokines interleukin 1β IL 1β interleukin 2 receptor IL 2R interleukin 6 IL 6 interleukin 8 IL 8 interleukin 10 IL 10 tumor necrosis factor α


id: cord-340576-dabcs3w5
type: ORG
entity:
  Efficacy of Branched Chain Amino Acid Supplementation and Walking Exercise for Preventing Sarcopenia in Patients with Liver Cirrhosis Supplementation


id: cord-340576-dabcs3w5
type: WORK_OF_ART
entity:
  The Liver Frailty Index Improves Mortality Prediction of the Subjective Clinician Assessment in Patients with Cirrhosis Looking


id: cord-340576-dabcs3w5
type: ORG
entity:
  Portal Hypertension Endotoxemia and Systemic Inflammation in Patients With Cirrhosis Effect of Lactulose on Ammonia Production


id: cord-340576-dabcs3w5
type: ORG
entity:
  Management of Acute Episode of Hepatic Encephalopathy An Open Labeled Randomized Clinical Trial Arab Primary Prophylaxis to Prevent the Development of Hepatic Encephalopathy


id: cord-340576-dabcs3w5
type: WORK_OF_ART
entity:
  a Randomized Trial of Patients With Minimal Hepatic Encephalopathy Randomised Clinical Trial Rifaximin


id: cord-340576-dabcs3w5
type: FAC
entity:
  Microbiome Metabolome and Endotoxemia in Patients With Cirrhosis Effects of the Adjunctive Probiotic VSL 3


id: cord-340576-dabcs3w5
type: WORK_OF_ART
entity:
  Treatment of Minimal Hepatic Encephalopathy A Randomized Double Blind Placebo Controlled Trial of Probiotics in Minimal Hepatic Encephalopathy Bifidobacterium


id: cord-288721-3bv3aak6
type: PROTEIN
entity:
  Cytochrome C oxidase COX IV Cytochrome C Cyt C Glyceraldehyde 3 phosphate dehydrogenase GAPDH Glucose regulated protein 78 GRP78 Histon 2B H2B


id: cord-288721-3bv3aak6
type: GGP
entity:
  Cytochrome C oxidase COX IV Cytochrome C Cyt C Glyceraldehyde 3 phosphate dehydrogenase GAPDH Glucose


id: cord-283120-hyzk59qv
type: GGP
entity:
  ALT 1 85 1 49 2 29 p 0 00001 were significantly associated with higher odds of poor outcomes CONCLUSION Our meta


id: cord-009987-biop7gyd
type: PROTEIN
entity:
  serum aspartate aminotransaminase 35 and 31 alanine aminotransaminase 50 and 42 gamma glutamyl transpeptidase 56 and 49 alkaline phosphatase 46 and 37 total bilirubin 61 and 48 and liver MDA


id: cord-009987-biop7gyd
type: CHEBI
entity:
  carbon tetrachloride GSH glutathione SOD superoxide dismutase GR glutathione reductase CYP Cytochrome


id: cord-009987-biop7gyd
type: CHEMICAL
entity:
  Salvia miltiorrhiza Bunge Astragalus membranaceus Fisch Bunge Capparis spinosa L Cichorium intybus L Solanum nigrum L Sapindus mukorossi Gaertn Ginkgo biloba L Woodfordia fruticosa L Kurz Vitex trifolia L Schisandra chinensis Turcz Baill Cuscuta chinensis Lam Lycium barbarum Angelica sinensis Oliv Diels and Litsea coreana H Lev The probable modes of


id: cord-009987-biop7gyd
type: CHEMICAL
entity:
  Nelumbo nucifera Gaertn Leaves Catechin glycoside myricitrin 3 O glucoside hyperin isoquercitrin quercetin 3 O rhamnoside astragalin Lotus leaf extract


id: cord-022754-ehq9qnoo
type: DNA
entity:
  cord 022754 ehq9qnoo authors nan title Liver date 2012 07 25 journal Canine and Feline Gastroenterology DOI 10 1016 b978 1 4160 3661 6 00061 4 sha 938a53e7f870ea74d6347fe145f7ec1d9c657aaf doc_id 22754 cord_uid ehq9qnoo nan


id: cord-022754-ehq9qnoo
type: PROTEIN
entity:
  N O and S dealkylation aromatic aliphatic or N hydroxylation N oxidation sulfoxidation deamination and dehalogenation Phase II


id: cord-022754-ehq9qnoo
type: DNA
entity:
  dog and cat WSAVA Standards for Clinical and Histological Diagnosis of Canine and Feline Liver Diseases History clinical signs and physical findings


id: cord-022754-ehq9qnoo
type: CELL_LINE
entity:
  Dog and Cat Infectious canine hepatitis and canine acidophil cell hepatitis Experimental viral hepatitis in the dog production of persistent disease in partially immune animals Canine adenoviruses and herpesvirus A


id: cord-022754-ehq9qnoo
type: GGP
entity:
  skatoles 4 34 39 Hyperammonemia also leads to impaired glial function through increased intracellular glutamine


id: cord-022754-ehq9qnoo
type: GGP
entity:
  triiodothyronine 22 23 Hyperthyroxinemia increases hepatic metabolism without proportionate increases in hepatic blood flow with the overall consequence of reduced oxygen


id: cord-022754-ehq9qnoo
type: LAW
entity:
  Pathophysiology The Biological Principles of Disease Skills for Communicating with Patients Teaching and Learning Communication Skills in Medicine Liver


id: cord-022754-ehq9qnoo
type: DISEASE
entity:
  dysfunction of other organs One example is hepatic encephalopathy metabolic dysfunctions of the liver


id: cord-022754-ehq9qnoo
type: DISEASE
entity:
  congestion of splanchnic organs Intestinal vasculature congestion reduces intestinal water resorption


id: cord-022754-ehq9qnoo
type: DISEASE
entity:
  intestinal mucosa kidney cortex bone marrow pancreas testicle brain lung kidney medulla lymph node liver skin spleen skeletal muscle and cardiac muscle


id: cord-022754-ehq9qnoo
type: DISEASE
entity:
  granulomatous hepatitis fungal infections intrahepatic cholestasis bacterial cholangitis leptospirosis


id: cord-022754-ehq9qnoo
type: DISEASE
entity:
  cystic hyperplasia dysmotility of gallbladder smooth muscle and biliary mucocele 1 Familial hypercholesterolemia


id: cord-023017-k6edtg58
type: PROTEIN
entity:
  neural stem cell marker alpha fetoprotein cytokeratinl9 connexin43 negative albumin transferrin tyrosine aminotransferase gamma glutamyl transpeptidase


id: cord-023017-k6edtg58
type: PROTEIN
entity:
  PEG2b 1 5 and 3 0 mcglkglwk 25 vs 24 overall and 13 vs 14 for adverse events The frequencies of subjective adverse events


id: cord-023017-k6edtg58
type: PROTEIN
entity:
  fibroblast markers fibroblast specific protein 1 FSPl alpha smooth muscle actin alpha SMA and type I collagen


id: cord-023017-k6edtg58
type: PROTEIN
entity:
  pools core B ElA NS3 protease 2 NS3 helicase 3 NS3 helicase 4 NS3 helicase 5 NS3 helicase 6 NS4B 2 NS5A 2 NS5A 3 NS5B 2


id: cord-355395-rckzi8vz
type: ORG
entity:
  the Chinese Center for Disease Control and Prevention Clinical Characteristics of Coronavirus Disease 2019


id: cord-348024-n8wn4och
type: ORG
entity:
  the American College of Cardiology American Heart Association Task Force on Clinical Practice Guidelines


id: cord-348024-n8wn4och
type: DISEASE
entity:
  chronic obstructive pulmonary disease COPD type 2 diabetes mellitus T2DM hypertension coronary heart disease cerebrovascular disease chronic liver disease


id: cord-353633-a4pu6rlu
type: RNA
entity:
  392 several small RNA molecules ribosomal small nuclear and nucleolar between healthy NASH and cirrhotic patients 102


id: cord-353633-a4pu6rlu
type: GGP
entity:
  carbohydrate J o u r n a l P r e p r o o f 26 metabolism reflect NAFLD severity and are implicated in hepatocellular carcinomas 102 Expression levels of lesser non coding molecules


id: cord-353633-a4pu6rlu
type: WORK_OF_ART
entity:
  A Pathophysiologic Approach Combining Genetics and Insulin Resistance to Predict the Severity of Nonalcoholic Fatty Liver Disease A Protein Truncating HSD17B13 Variant and Protection


id: cord-353633-a4pu6rlu
type: ORG
entity:
  Noninvasive Detection of Nonalcoholic Steatohepatitis Using Clinical Markers and Circulating Levels of Lipids and Metabolites Development and Validation of a Scoring System


id: cord-340325-0oh40b6r
type: ORG
entity:
  Lipid Nanoparticles for Systemic Delivery of RNAi Therapeutics Synthesis and Characterization of Degradable Multivalent


id: cord-340325-0oh40b6r
type: WORK_OF_ART
entity:
  Inotersen Treatment for Patients with Hereditary Transthyretin Amyloidosis Phase 1 Trial of an RNA Interference Therapy for Acute Intermittent Porphyria GS 14 ENVISION


id: cord-032181-gmcugd8h
type: PROTEIN
entity:
  liver excepting factor III tissue factor factor IV factor VI activated factor V factor VIII and factor VIIIa 69 Massive hepatic necrosis


id: cord-032181-gmcugd8h
type: GGP
entity:
  Hepatitis B DOI 10 1007 978 94 024 1603 9_2 sha 9ea691cc78ff15dbc59a8fd39ea9aa27a2e60223 doc_id 32181 cord_uid gmcugd8h


id: cord-032181-gmcugd8h
type: GGP
entity:
  PCO 2 5 89 kPa PaO 2 FiO 2 26 7 200 mmHg P Aa DO 2 FiO 2 1 0 26 7 kPa 200 mmHg X ray of chest shows alveolar consolidation 1 2


id: cord-032181-gmcugd8h
type: ORG
entity:
  International Liver Transplant Society Practice Guidelines Diagnosis and Management of Hepatopulmonary Syndrome


id: cord-000083-3p81yr4n
type: PROTEIN
entity:
  alpha 1 B glycoprotein leucine rich alpha 2 glycoprotein 1 SP40 40 A1BG protein vitamin D binding protein group


id: cord-000083-3p81yr4n
type: DNA
entity:
  1q23 1q25 1q31 1q32 41 1q32 2 1q41 1q43 5q15 5q21 8p22 8p23 9p24 10q11 2 10q11 2 10q2 1 10q11 2 10q21 1 and 20q13 3


id: cord-000083-3p81yr4n
type: PROTEIN
entity:
  HBsAg J D Jia 1 L Wei 2 X X Zhang 3 Y L Mao 4 L L Wang 5 Z L Gao 6 J L Hou 7 J Zhang 8 W Melchior 9 W Van der Helm 9 10 1 Beijing Friendship Hospital Beijing China 2 Beijing People Hospital Beijing China 3 Ruijin Hospital Shanghai China 4 Beijing 302


id: cord-000083-3p81yr4n
type: PROTEIN
entity:
  nucleocapsid B Tang 1 J Xia 1 Y M Wang 2 H F Wang 1 1 Liver Failure Treatment and Research Center 302rd Military Hospital 2 The Dept Aims


id: cord-000083-3p81yr4n
type: PROTEIN
entity:
  glucose regulated protein 78kD GRP78 Bip heterogeneous nuclear ribonucleoprotein hnRNP Far upstream element binding protein


id: cord-000083-3p81yr4n
type: PROTEIN
entity:
  alpha smooth muscle actin SMA vimentin CD31 CD34 CD68 CEA CD10 cellular retinol binding protein1 CRBP 1 and synemin


id: cord-000083-3p81yr4n
type: DNA
entity:
  KCTD9 gene promoter B Pi 1 J S Wang 1 M F Han 1 Y Y Zhou 1 X J Liu 1 X P Luo 2 Q Ning 1 1 Department of Infectious Disease Tongji Hospital Tongji Medical College Huazhong University of Science and Technology 2 Department


id: cord-000083-3p81yr4n
type: CELL_TYPE
entity:
  Hepatocellular Carcinoma Cells R Tsunedomi 1 2 S Harada 1 N Iizuka 1 M Oka 1 1 Dept of Digestive Surgery


id: cord-000083-3p81yr4n
type: PROTEIN
entity:
  proteinases collagen 1 P 0 01 SMA p 0 01 MMP 9 P 0 05 and TIMP 1 P 0 05 Conclusion Chronic administration of ethanol to rats


id: cord-000083-3p81yr4n
type: CELL_LINE
entity:
  CMILI Mouse Model I Nassar 1 T Pasupati 1 I Segarra 1 J P Judson 1 1 International Medical University Kuala Lumpur Malaysia Background Imatinib


id: cord-000083-3p81yr4n
type: PROTEIN
entity:
  Membranous TNFRII T N Lin 1 C H Chao 1 I S Sheen 1 Y P Ho 1 W T Chen 1 C J Lin 1 C T Yeh 1 C Y Lin 1 1 Liver Research Unit Linkou Medical Center Chang Gung Memorial Hospital Chang Gung University Taoyuan Taiwan Background Aim


id: cord-000083-3p81yr4n
type: GGP
entity:
  alpha 1 B glycoprotein leucine rich alpha 2 glycoprotein 1 SP40 40 A1BG protein vitamin D binding protein


id: cord-000083-3p81yr4n
type: GGP
entity:
  E Goto 1 S Shiina 1 R Tateishi 1 R Masuzaki 1 K Enooku 1 T Sato 1 J Imamura 1 T Goto 1 Y Sugioka 2 H Ikeda 1 2 H Yoshida 1 M Omata 1 1


id: cord-000083-3p81yr4n
type: GGP
entity:
  Hepatitis B Virus Infection Y Zhang 1 J Q Lian 1 C X Huang 1 X Wei 1 J P Wang 1 P Z Wang 1 X F Bai 1 1


id: cord-000083-3p81yr4n
type: GGP
entity:
  K Hirano 1 T Kodani 1 S Sato 1 Y Narita 1 T Kikuchi 1 T Genda 1 K Iijima 1 K Ogawa 1 T Ichida 1 1 Background Aim


id: cord-000083-3p81yr4n
type: GGP
entity:
  proteinases collagen 1 P 0 01 SMA p 0 01 MMP 9 P 0 05 and TIMP 1 P 0 05 Conclusion Chronic administration of ethanol


id: cord-000083-3p81yr4n
type: GGP
entity:
  MHE n 37 grade 1 n 17 grade 2 n 41 grade 3 n 44 and grade 4 n 10 were 6 2 0 4 9 5 0 6 15 0 7 26 3 1 7


id: cord-000083-3p81yr4n
type: GGP
entity:
  E Kakazu 1 Y Ueno 1 Y Kondo 1 K Fukushima 1 M Shina 1 J Inoue 1 K Tamai 1 M Ninomiya 1 T Shimosegawa 1 1


id: cord-000083-3p81yr4n
type: WORK_OF_ART
entity:
  The Results of Entevavir Treatment in Patients with Chronic Hepatitis B S Kose 1 G Akkoclu 1 M Turkeri 1


id: cord-000083-3p81yr4n
type: PRODUCT
entity:
  1 S Sumie 1 M Nakano 1 1 Division of Gastroenterology Department of Medicine Kurume University School of Medicine Background


id: cord-000083-3p81yr4n
type: ORG
entity:
  Organ Transplantation Service 2 Department of Gastroenterology University of Tokyo 3 Department of Surgery University of Tokyo


id: cord-000083-3p81yr4n
type: ORG
entity:
  Department of Public Health 2 Department of Gastroenterology Yamagata University Faculty of Medicine Background Aims


id: cord-000083-3p81yr4n
type: ORG
entity:
  Department of Infectious Disease Tongji Hospital Tongji Medical College Huazhong University of Science and Technology 2 Department of Pediatrics Tongji Hospital Tongji Medical College Huazhong University of Science and Technology


id: cord-000083-3p81yr4n
type: WORK_OF_ART
entity:
  The Study on the Apoptosis of Hepatoma Cells Synergeticly Induced By Plasmid Mediated Anti Angiogenesis and Immunopotentiation Therapy


id: cord-000083-3p81yr4n
type: ORG
entity:
  Table 2 Department of Internal Medicine Seoul National University Hospital Gangnam Healthcare Center


id: cord-000083-3p81yr4n
type: WORK_OF_ART
entity:
  An Imbalance in Plasma Amino Acids of Advaced Cirrhotic Patients Impairs the Maturation Of Dendritic Cells


id: cord-000083-3p81yr4n
type: CHEMICAL
entity:
  Mahtab 1 S Rahman 1 F Akbar 2 F Karim 1 A Shrestha 1 M Khan 1 M Kamal 1 1 Bangabandhu Sheikh Mujib Medical University 2 Toshiba


id: cord-000083-3p81yr4n
type: DISEASE
entity:
  chronically infected with HCV Furthermore serum PRL levels were compared in 27 male patients before and after interferon


id: cord-000083-3p81yr4n
type: DISEASE
entity:
  HBV Related Liver Cirrhosis X Q Wang 1 Y Zhang 1 X F Bai 1 J Q Lian 1 1 Background To detect circulating CD4 CD25 regulatory T


id: cord-000083-3p81yr4n
type: CHEMICAL
entity:
  amikacin cefoperazone levofloxacin piperacillin tazobactam trimethoprimsulfamethoxazole aztreonam cefotaxime piperacillin


id: cord-000083-3p81yr4n
type: DISEASE
entity:
  abnormal liver tests Background As the common indexes ALT AST and PLT play an important role in disease


# bib

id: cord-000083-3p81yr4n
title: Poster Exhibition
author: nan
date: 2009-01-31
txt: ./txt/cord-000083-3p81yr4n.txt
cache: ./cache/cord-000083-3p81yr4n.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712310/
doi: 10.1007/s12072-009-9123-4
abstract: nan
summary:
  R. China Background: The objective of this study was to evaluate the early virologic response for prediction of achievement of HBeAg seroconversion and hepatitis B virus (HBV) DNA negativity after two years of lamivudine treatment in chronic hepatitis B (CHB) patients. Methods: A total of 620 patients who tested positive for hepatitis B surface antigen and were referred to Chiba University Hospital between February 1985 and March 2008 were included in the study, and their following characteristics were analyzed: age, gender, the status of HBeAg, ALT, HBV-DNA level, and PLT. Methods: A total of 60 patients with chronic hepatitis B, 32 (53.3%) were HBeAg positive (group A) while 28(46.7%) were HBeAg negative (group B) were included in this study after meeting the following criteria: age 18 to 60 years, HBsAg positive for more than 6 months, serum HBV-DNA was >5 log(10) copies/mL and ALT more than two times the upper normal limit.


id: cord-001567-3bw7jbzq
author: Borlak, Jürgen
date: 2015-02-25
txt: ./txt/cord-001567-3bw7jbzq.txt
cache: ./cache/cord-001567-3bw7jbzq.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4357185/
doi: 10.1186/s12864-015-1312-z
summary:
  title: Proteome mapping of epidermal growth factor induced hepatocellular carcinomas identifies novel cell metabolism targets and mitogen activated protein kinase signalling events Importantly, 11 out of 54 mouse tumour specific proteins were likewise uniquely expressed in human HCC and 49 disease regulated proteins identified in EGF induced liver cancer were similarly regulated in human HCC, as determined by immunhistochemistry using different antibodies and the information given in the publically available Human Protein Atlas depository. Likewise, the genes coding for igals3, i.e. a beta-galactoside-binding protein frequently overexpressed in cancers and pcbp1 that is involved in transcription and functions as an inhibitor of invasion [65] were up-regulated in transgenic nontumour livers (ur-Tr-nT) whereas transcript expression of aars, a member of tRNA synthases and anaxa6, a calcium-dependent, phospholipid-binding protein with important roles in the tumour microenvironment and metastasis were repressed (dr-Tr-nT).

title:
  Proteome mapping of epidermal growth factor induced hepatocellular carcinomas identifies novel cell metabolism targets and mitogen activated protein kinase signalling events

abstract:
  BACKGROUND: Hepatocellular carcinoma (HCC) is on the rise and the sixth most common cancer worldwide. To combat HCC effectively research is directed towards its early detection and the development of targeted therapies. Given the fact that epidermal growth factor (EGF) is an important mitogen for hepatocytes we searched for disease regulated proteins to improve an understanding of the molecular pathogenesis of EGF induced HCC. Disease regulated proteins were studied by 2DE MALDI-TOF/TOF and a transcriptomic approach, by immunohistochemistry and advanced bioinformatics. RESULTS: Mapping of EGF induced liver cancer in a transgenic mouse model identified n = 96 (p < 0.05) significantly regulated proteins of which n = 54 were tumour-specific. To unravel molecular circuits linked to aberrant EGFR signalling diverse computational approaches were employed and this defined n = 7 key nodes using n = 82 disease regulated proteins for network construction. STRING analysis revealed protein-protein interactions of > 70% disease regulated proteins with individual proteins being validated by immunohistochemistry. The disease regulated network proteins were mapped to distinct pathways and bioinformatics provided novel insight into molecular circuits associated with significant changes in either glycolysis and gluconeogenesis, argine and proline metabolism, protein processing in endoplasmic reticulum, Hif- and MAPK signalling, lipoprotein metabolism, platelet activation and hemostatic control as a result of aberrant EGF signalling. The biological significance of the findings was corroborated with gene expression data derived from tumour tissues to evntually define a rationale by which tumours embark on intriguing changes in metabolism that is of utility for an understanding of tumour growth. Moreover, among the EGF tumour specific proteins n = 11 were likewise uniquely expressed in human HCC and for n = 49 proteins regulation in human HCC was confirmed using the publically available Human Protein Atlas depository, therefore demonstrating clinical significance. CONCLUSION: Novel insight into the molecular pathogenesis of EGF induced liver cancer was obtained and among the 37 newly identified proteins several are likely candidates for the development of molecularly targeted therapies and include the nucleoside diphosphate kinase A, bifunctional ATP-dependent dihydroyacetone kinase and phosphatidylethanolamine-binding protein1, the latter being an inhibitor of the Raf-1 kinase. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12864-015-1312-z) contains supplementary material, which is available to authorized users.


id: cord-002272-c7f1l13s
author: Sauter, Kristin A.
date: 2016-07-21
txt: ./txt/cord-002272-c7f1l13s.txt
cache: ./cache/cord-002272-c7f1l13s.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5076001/
doi: 10.1152/ajpgi.00116.2016
summary:
  title: Macrophage colony-stimulating factor (CSF1) controls monocyte production and maturation and the steady-state size of the liver in pigs Combined with earlier data from the mouse, this study supports the existence of a CSF1-dependent feedback loop, linking macrophages of the liver with bone marrow and blood monocytes, to mediate homeostatic control of the size of the liver. The expected increase in half-life was confirmed, and CSF1-Fc administration to mice produced substantial increases in circulating monocyte and tissue macrophage numbers, at much lower doses than the native protein. Cluster 2 (Fig. 9B) , the set of genes reduced in the CSF1-Fc-treated pigs, most likely reflects the functional zonation of the liver between periportal and perivenous regions of liver lobules (8, 19, 48) and the selective proliferation of cells derived from portal progenitors that has been observed in regenerating liver (15, 34, 36) .

title:
  Macrophage colony-stimulating factor (CSF1) controls monocyte production and maturation and the steady-state size of the liver in pigs

abstract:
  Macrophage colony-stimulating factor (CSF1) is an essential growth and differentiation factor for cells of the macrophage lineage. To explore the role of CSF1 in steady-state control of monocyte production and differentiation and tissue repair, we previously developed a bioactive protein with a longer half-life in circulation by fusing pig CSF1 with the Fc region of pig IgG1a. CSF1-Fc administration to pigs expanded progenitor pools in the marrow and selectively increased monocyte numbers and their expression of the maturation marker CD163. There was a rapid increase in the size of the liver, and extensive proliferation of hepatocytes associated with increased macrophage infiltration. Despite the large influx of macrophages, there was no evidence of liver injury and no increase in circulating liver enzymes. Microarray expression profiling of livers identified increased expression of macrophage markers, i.e., cytokines such as TNF, IL1, and IL6 known to influence hepatocyte proliferation, alongside cell cycle genes. The analysis also revealed selective enrichment of genes associated with portal, as opposed to centrilobular regions, as seen in hepatic regeneration. Combined with earlier data from the mouse, this study supports the existence of a CSF1-dependent feedback loop, linking macrophages of the liver with bone marrow and blood monocytes, to mediate homeostatic control of the size of the liver. The results also provide evidence of safety and efficacy for possible clinical applications of CSF1-Fc.


id: cord-003921-8r8z0otz
title: The Evolving Role of Neutrophils in Liver Transplant Ischemia-Reperfusion Injury
author: Nakamura, Kojiro
date: 2019-01-29
txt: ./txt/cord-003921-8r8z0otz.txt
cache: ./cache/cord-003921-8r8z0otz.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6786799/
doi: 10.1007/s40472-019-0230-4
summary:
  PURPOSE OF REVIEW: Hepatic ischemia-reperfusion injury (IRI), an inevitable event during liver transplantation, represents a major risk factor for the primary graft dysfunction as well as the development of acute and chronic rejection. In IRI-LT pathophysiology, both Kupffer cells (donor-origin) and liver-infiltrating bone marrow-derived macrophages (recipient-origin) play dominant roles in priming innate immune responses [9] [10] [11] , with the majority of studies focusing on macrophage regulation [12, 13] . Indeed, hepatocyte-specific HMGB1 deficient mice showed decreased hepatic necrosis and neutrophil accumulation, whereas the number of their macrophages remained unchanged in acetaminophen-induced liver injury model [28] . In addition, CXCL1 blocking antibody alleviated hepatic infiltration in necrotic cellinduced neutrophil mobilization model [31] , whereas in a carbon tetrachloride (CCl4)-induced acute liver injury, defective CXCL2 expression in TLR2-knockout or S100A9-knockout mice was accompanied by suppressed hepatic neutrophil recruitment [32] . CD4 T cells promote tissue inflammation via CD40 signaling without de novo activation in a murine model of liver ischemia/reperfusion injury

abstract:
  PURPOSE OF REVIEW: Hepatic ischemia-reperfusion injury (IRI), an inevitable event during liver transplantation, represents a major risk factor for the primary graft dysfunction as well as the development of acute and chronic rejection. Neutrophils, along macrophages, are pivotal in the innate immune-driven liver IRI, whereas the effective neutrophil-targeting therapies remain to be established. In this review, we summarize progress in our appreciation of the neutrophil biology and discuss neutrophil-based therapeutic perspectives. RECENT FINDINGS: New technological advances enable to accurately track neutrophil movements and help to understand molecular mechanisms in neutrophil function, such as selective recruitment to IR-stressed tissue, formation of neutrophil extracellular traps, or reverse migration into circulation. In addition to pro-inflammatory and tissue-destructive functions, immune regulatory and tissue-repairing phenotype associated with distinct neutrophil subsets have been identified. SUMMARY: Newly recognized and therapeutically attractive neutrophil characteristics warrant comprehensive preclinical and clinical attention to target IRI in transplant recipients.


id: cord-005892-3yuznrdv
author: Hübener, P.
date: 2017-02-16
txt: ./txt/cord-005892-3yuznrdv.txt
cache: ./cache/cord-005892-3yuznrdv.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7095908/
doi: 10.1007/s00063-017-0263-3
summary:
  Acute-on-chronic liver failure (ACLF) is an emerging clinical syndrome in patients with underlying liver disease that is usually triggered by one or multiple insults and characterized by progressive hepatic and nonhepatic organ failure, a significant risk of infections, and high short-term mortality rates. Im Rahmen dieses ärztlichen Entscheidungsprozesses müssen neben der unmittelbaren Schwere der Erkrankung beispielsweise auch der mutmaßliche Patientenwunsch, jeweilige lokale und nationale Überlebensraten, eine potenzielle Reversibilität der Or-Das akut-auf-chronische Leberversagen als diagnostische und therapeutische Herausforderung der Intensivmedizin Zusammenfassung Das akut-auf-chronische Leberversagen ("acute-on-chronic liver failure", ACLF) ist ein emergentes Krankheitssyndrom, das durch einen oder mehrere akute Trigger bei vorgeschädigter Leber ausgelöst wird und vom progressiven hepatalen und nichthepatalen Organversagen, einem gravierenden Risiko infektiöser Komplikationen sowie hoher kurzfristiger Letalität gekennzeichnet ist. Leberversagen · Zirrhose · Infektion · Organversagen · Transplantation Acute-on-chronic liver failure: a diagnostic and therapeutic challenge for intensive care Abstract Acute-on-chronic liver failure (ACLF) is an emerging clinical syndrome in patients with underlying liver disease that is usually triggered by one or multiple insults and characterized by progressive hepatic and nonhepatic organ failure, a significant risk of infections, and high short-term mortality rates.

title:
  Das akut-auf-chronische Leberversagen als diagnostische und therapeutische Herausforderung der Intensivmedizin

abstract:
  Acute-on-chronic liver failure (ACLF) is an emerging clinical syndrome in patients with underlying liver disease that is usually triggered by one or multiple insults and characterized by progressive hepatic and nonhepatic organ failure, a significant risk of infections, and high short-term mortality rates. Despite our incomplete understanding of the underlying pathophysiology, ACLF requires timely diagnostic and therapeutic measures aiming at the identification and elimination of causative factors as well as the prevention of complications to improve the prognosis of affected patients.


id: cord-005949-8po9xe5g
title: Akutes Leberversagen: Übersicht zur aktuellen Diagnostik und Therapie
author: Streetz, K.L.
date: 2013-11-06
txt: ./txt/cord-005949-8po9xe5g.txt
cache: ./cache/cord-005949-8po9xe5g.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7096005/
doi: 10.1007/s00063-013-0285-4
summary:
  Die amerikanische "acute liver failure study group" unterscheidet in Bezug auf die Zeit zwischen dem Auftreten von Koagulopathie und beginnender hepatischer Enzephalopathie weiterhin zwischen dem hyperakuten (<7 Tage), dem akuten (7-28 Tage) und dem subakuten (28 Tage -6 Monate) Leberversagen [9] . Die etablierte Therapie des häufigen paracetamolinduzierten ALV besteht in der intravenösen Gabe von N-Acetylcystein (NAC) in Form eines 72-stündigen Reduktionsschemas (NAC: 150 mg/kg/h für 1 h, dann 12,5 mg/kg/h für 4 h und 6,25 mg/kg/h für 67 h). Interessanterweise wurde in einer prospektiven multizentrischen Studie gezeigt, dass es beim nicht durch Paracetamol bedingtem ALV unter Gabe von NAC zumindest bei Patienten mit niedriggradiger hepatischer Enzephalopathie (°I-II) ebenfalls zu einer Verbesserung des transplantatfreien Überlebens kommt [10] . Hier wurde gezeigt, dass 84% der Patienten mit ALV nach Erhalt einer frühen Transplantation überlebten, während die Überlebensrate ohne Lebertransplantation bei nur 34% lag.

abstract:
  Although acute liver failure is a rare disease with a prevalence of 5 per 1 million people, it has a considerablely high mortality rate of 34 %. The main causes in western civilizations are drug overdose (acetaminophen) and viral hepatitis. Patients are affected by the loss of liver synthesis function and are at risk of developing hepatic encephalopathy and possible multiorgan failure. Specific therapies consisting of the administration of N-acetylcysteine (acetaminophen) or of nucleotide/nucleoside analogs (hepatitis B) are possible, but are often not adequate. Orthotopic liver transplantation is, therefore, frequently the only remaining effective therapy for severe acute liver failure. Due to organ shortage, new prognostic tools, e.g., the Acute Liver Failure Study Group (ALFSG) score, have been developed to improve patient selection using sufficiently stringent selection criteria.


id: cord-006391-esnsa4u5
title: Abstracts 5(th) Tripartite Meeting Salzburg/Austria, September 9–11,1982
author: nan
date: 1982
txt: ./txt/cord-006391-esnsa4u5.txt
cache: ./cache/cord-006391-esnsa4u5.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101735/
doi: 10.1007/bf01279099
abstract: nan
summary:
  In our parallel tests using an excision-sample technique [2] which is considerably more sensitive than the DGHM procedure, we have observed the following mean reductions in the counts of accessible bacteria: iodine in ethanol, 96%; povidone-iodine, 89%; chlorhexidine in ethanol, 88%; iso-propanol, The purpose of this study was to compare radiation injury in Guinea Pig small bowel (1) devoid of contents (2) containing bile (3) containing pancreatic juice. Studies in vitro employing isolated perfused rat pancreas and stomach revealed following results: Mean basal pancreatic somatostatin release in normal, diabetic and transplanted rats were 12___3, 24-t-7, and 17__+4 pg/ml, respectively. As these changes appear closely correlated to the blood glucose levels which show a 30 % decrease at 4 h and progressive restoration towards normal values up to 24 h, attempts have been made to alter the insulin/glucagon ratio by glucose infusion after PH and study its relation to liver regeneration.


id: cord-009987-biop7gyd
author: Ali, Muhammad
date: 2017-10-19
txt: ./txt/cord-009987-biop7gyd.txt
cache: ./cache/cord-009987-biop7gyd.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167792/
doi: 10.1002/ptr.5957
summary:
  & Thonn., Salvia miltiorrhiza Bunge., Astragalus membranaceus (Fisch.) Bunge, Capparis spinosa (L.), Cichorium intybus (L.), Solanum nigrum (L.), Sapindus mukorossi Gaertn., Ginkgo biloba (L.), Woodfordia fruticosa (L.) Kurz, Vitex trifolia (L.), Schisandra chinensis (Turcz.) Baill., Cuscuta chinensis (Lam.), Lycium barbarum, Angelica sinensis (Oliv.) Diels, and Litsea coreana (H. Herbal medicines are claimed to both treat and prevent diseases, which adds to a deep belief that these Abbreviations: ALT, alanine aminotransaminase; ASP, Angelica sinensis polysaccharides; AST, aspartate transaminase; EGF, epidermal growth factor; HBV, Hepatitis B virus; LBPs, Lycium barbarum polysaccharides; WF4, Woodfordia fruticosa flower extract.

title:
  Selected hepatoprotective herbal medicines: Evidence from ethnomedicinal applications, animal models, and possible mechanism of actions

abstract:
  Insight into the hepatoprotective effects of medicinally important plants is important, both for physicians and researchers. Main reasons for the use of herbal medicine include their lesser cost compared with conventional drugs, lesser undesirable drug reactions and thus high safety, and reduced side effects. The present review focuses on the composition, pharmacology, and results of experimental trials of selected medicinal plants: Silybum marianum (L.) Gaertn., Glycyrrhiza glabra, Phyllanthus amarus Schumach. & Thonn., Salvia miltiorrhiza Bunge., Astragalus membranaceus (Fisch.) Bunge, Capparis spinosa (L.), Cichorium intybus (L.), Solanum nigrum (L.), Sapindus mukorossi Gaertn., Ginkgo biloba (L.), Woodfordia fruticosa (L.) Kurz, Vitex trifolia (L.), Schisandra chinensis (Turcz.) Baill., Cuscuta chinensis (Lam.), Lycium barbarum, Angelica sinensis (Oliv.) Diels, and Litsea coreana (H. Lev.). The probable modes of action of these plants include immunomodulation, stimulation of hepatic DNA synthesis, simulation of superoxide dismutase and glutathione reductase to inhibit oxidation in hepatocytes, reduction of intracellular reactive oxygen species by enhancing levels of antioxidants, suppression of ethanol‐induced lipid accumulation, inhibition of nucleic acid polymerases to downregulate viral mRNA transcription and translation, free radical scavenging and reduction of hepatic fibrosis by decreasing the levels of transforming growth factor beta‐1, and collagen synthesis in hepatic cells. However, further research is needed to identify, characterize, and standardize the active ingredients, useful compounds, and their preparations for the treatment of liver diseases.


id: cord-014770-cgtzlra1
title: Book reviews
author: Brandt, Lawrence J.
date: 1995
txt: ./txt/cord-014770-cgtzlra1.txt
cache: ./cache/cord-014770-cgtzlra1.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7087769/
doi: 10.1007/bf02065002
abstract: nan
summary:
  The volume combines some basic reviews, such as chapters on the pathophysiology of viral diarrhea and gastrointestinal tract immunology, with detailed exploration of more focused topics, such as rotavirus proteins. While interesting and one of the more clinically applicable sections of the book, the inclusion of a chapter on bacterial diarrhea in a volume dedicated to viral gastroenteritis is somewhat puzzling. While this book has certain outstanding features, there are some shortcomings which warrant mention, most notably a paucity of references beyond 1990 in some chapters and the failure to recognize viral pathogens which, through gastrointestinal tract infection, cause significant disease other than diarrhea. The final chapter in the book is devoted to the therapeutic aspects of gastrointestinal motility, including biofeedback training for fecal incontinence. Once again, adequate references are provided for those who desire more in-depth study, The next several chapters begin at the oropharynx and proceed through the gastrointestinal tract, presenting a discussion of the motility of each area.


id: cord-016130-5q9ufu28
author: Linday, Linda A.
date: 2010-12-17
txt: ./txt/cord-016130-5q9ufu28.txt
cache: ./cache/cord-016130-5q9ufu28.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7120316/
doi: 10.1007/978-1-59259-880-9_21
summary:
  Our clinical research demonstrates that daily supplementation with a flavored cod liver oil (which meets European purity standards) and a children''s multivitamin-mineral with trace metals, including Se, can decrease morbidity from upper respiratory tract illnesses, otitis media, and sinusitis in young children living in the United States. This chapter discusses the role of essential fatty acids, vitamins, and trace metals in the pathophysiology of inflammation; reviews our clinical research on the use of a lemon-flavored cod liver oil (which meets European purity standards) and a children''s chewable multivitamin-mineral with Se for the prevention and adjunctive treatment of these disorders; reviews the history of cod liver oil, including its importance in the discovery of vitamin D and the anti-infective properties of vitamin A; and discusses the current clinical use of these supplements.

title:
  Nutritional Supplements and Upper Respiratory Tract Illnesses in Young Children in the United States

abstract:
  KEY POINTS: In the United States, children have lower blood levels than adults of eicosapentaenoic acid (EPA), an important ω-3 fatty acid that helps decrease inflammation; vitamin A, the “anti-infective” vitamin; and selenium (Se), a trace metal that is an intrinsic part of glutathione peroxidase, an important free-radical scavenging enzyme. EPA, vitamin A, and Se are important in controlling inflammation and can be supplied by oral nutritional supplements. Cod liver oil contains EPA (and other important ω-3 fatty acids), and vitamin A as well as vitamin D. Fish oil contains ω-3 fatty acids (including EPA) but no vitamins. Our clinical research demonstrates that daily supplementation with a flavored cod liver oil (which meets European purity standards) and a children’s multivitamin-mineral with trace metals, including Se, can decrease morbidity from upper respiratory tract illnesses, otitis media, and sinusitis in young children living in the United States. These supplements can be used by practitioners on an individual basis, when clinically indicated; the supplements can be purchased in the United States without a prescription. Socioeconomically disadvantaged children are at risk for micronutrient deficiencies. However, their families may not be able to afford to purchase these supplements, which are not available through Medicaid, The Special Supplemental Nutrition Program for Women, Infants and Children, or the Food Stamp Program. If our results are confirmed in larger studies, a system change will be needed to provide these supplements to nutritionally vulnerable, socioeconomically disadvantaged children living in the United States.


id: cord-016757-3d320c0a
title: Acute and chronic liver insufficiency
author: nan
date: 2008
txt: ./txt/cord-016757-3d320c0a.txt
cache: ./cache/cord-016757-3d320c0a.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121136/
doi: 10.1007/978-3-540-76839-5_20
summary:
  Hepatic coma can be subdivided according to its aetiology as follows: (1.) hepatocyte disintegration coma (ϭ endogenous coma due to the loss of parenchyma), (2 ( ( .) liver cell failure coma (ϭ exogenous coma due to metabolic disorders, almost always in the presence of cirrhosis), (3.) electrolyte coma (ϭ so-called "false" coma due to dyselectrolytaemia, almost always iatrogenic), and (4.) mixed forms of coma. Acute liver failure (ALF) is defined as an acute clinical picture with jaundice due to a most severe disorder in the liver function and/or massive liver cell necrosis which, without any pre-existing liver disease, culminates in hepatic coma (ϭ endogenous coma) within 8 weeks. 11) Consequently, severe damage to liver cells and widespread necrosis are usually the result of a network of altered cellular and humoral reactions, which for their part are often the initial cause of acute liver failure due to their synergistic and interactive effects (H. Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation

abstract:
  The term “liver insufficiency” denotes a break down in the functions of the liver. The syndrome of functional liver failure covers a wide spectrum of clinical, biochemical and neurophysiological changes. In principle, liver insufficiency can occur without previous liver damage as well as with already existing liver disease. It is characterized by a deterioration in the synthesizing, regulatory and detoxifying function of the liver. This final stage of liver disease terminates in hepatic coma.


id: cord-016880-q44623s8
title: 22 Levertransplantatie
author: van Hoek, B.
date: 2015-01-02
txt: ./txt/cord-016880-q44623s8.txt
cache: ./cache/cord-016880-q44623s8.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121307/
doi: 10.1007/978-90-313-7437-3_22
summary:
  Uit analyse van patiënten die getransplanteerd zijn terwijl ze buiten de Milaan-criteria vielen, blijkt dat met name micro-angio-invasie een slechte prognostische marker is en dat de overleving bij grotere of meer dan drie tumoren nog goed kan zijn als er geen micro-angio-invasie is. [29] Bij een hemodynamisch instabiele patiënt kan OLT -of auxiliaire levertransplantatie met een grote resectie van de natieve lever [30] -beter zijn omdat resectie van de necrotische lever het toxic liver-syndroom -door cytokines -kan tegengaan. [48] Het Epstein-Barr-virus (EBV) kan (bij 1% van de levertransplantaties) leiden tot posttransplantatielymfomen (PTLD); die zijn tegenwoordig vaak curatief te behandelen en voor een deel mogelijk te voorkomen door EBV-DNA-metingen in het eerste jaar, met zonodig aanpassen van de immuunsuppressie. Bij de levende donor wordt een resectie verricht van de linkslaterale segmenten van de lever, die vervolgens gebruikt worden voor transplantatie bij het kind.

abstract:
  In 1963 verrichtte Thomas Starzl in Denver de eerste levertransplantatie bij de mens. In 1966 werden in Nederland de eerste twee (auxiliaire, zie par. 22.3.6) levertransplantaties verricht in Leiden en Arnhem, in 1968 startte Cambridge. Helaas resulteerden de eerste levertransplantaties niet in langetermijnoverleving als gevolg van niet-optimale operatietechniek, matige immuunsuppressie en onbekendheid met complicaties.


id: cord-017603-wq4cgqs2
title: Acute Liver Failure in Children
author: Shanmugam, Naresh
date: 2018-10-16
txt: ./txt/cord-017603-wq4cgqs2.txt
cache: ./cache/cord-017603-wq4cgqs2.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122201/
doi: 10.1007/978-3-319-96400-3_8
summary:
  Trying to address this issue, Bhaduri and Vergani defined ALF in children as "a rare multisystem disorder in which severe impairment of liver function, with or without encephalopathy, occurs in association with hepatocellular necrosis in a patient with no recognized underlying chronic liver disease" [2] . They used the following criteria to define acute liver failure (ALF) in children: (1) hepatic-based coagulopathy defined as a prothrombin time (PT) ≥ 15 s or international normalized ratio (INR) ≥ 1.5 not corrected by vitamin K in the presence of clinical hepatic encephalopathy (HE) or a PT ≥ 20 s or INR ≥ 2.0 regardless of the presence or absence of clinical hepatic encephalopathy (HE), (2) biochemical evidence of acute liver injury and (3) no known evidence of chronic liver disease [3] . A similar study in children failed to show any benefit, and Paediatric Acute Liver Failure study group does not recommend routine use of in non-acetaminophen-induced ALF in children [33] .

abstract:
  “Acute liver failure” (ALF) and “fulminant liver failure” are terms used interchangeably to describe severe and sudden onset of liver cell dysfunction leading on to synthetic and detoxification failure across all age groups. Considerable variations exist between ALF in children and adults, in terms of aetiology and prognosis. Encephalopathy is not essential to make a diagnosis of ALF in children but when present has a bad prognosis. Early recognition of ALF and initiation of supportive management improve the outcome. Liver transplantation remains the only definitive treatment when supportive medical management fails.


id: cord-018225-dozmy3lb
title: The liver in critical illness
author: Hawker, Felicity H.
date: 2008
txt: ./txt/cord-018225-dozmy3lb.txt
cache: ./cache/cord-018225-dozmy3lb.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123050/
doi: 10.1007/978-1-84800-145-9_7
summary:
  The paper by Harrison and co-workers, again from the King''s Liver Unit, investigates the effects of n-acetylcysteine in patients with acute liver failure, and the findings of this study have resulted in widespread use of this agent in this setting. The incidence of hypoxic hepatitis was prospectively studied for 1 year in a group of high-risk patients suffering from low cardiac output in a coronary care unit. In intensive care patients, a rapid decrease in MEGX test values is associated with increased risk of developing multiple organ failure, and a poor outcome, and consequently may have a role in investigation of the role of the liver in the multiple organ failure syndrome. We studied the effect of acetylcysteine on systemic hemodynamics and oxygen transport in 12 patients with acetaminophen-induced fulminant hepatic failure, and 8 patients with acute liver failure from other causes. The increase in oxygen delivery and consumption in response to acetylcysteine may account for its beneficial effect on survival in patients with fulminant hepatic failure induced by acetaminophen.

abstract:
  The liver is in some ways the forgotten organ in intensive care practice. Very many more laboratory and clinical studies have investigated the role, function, and support of the lung, heart, brain, and kidney in critical illness than have studied the liver. Nevertheless, in the time of the Greek scholars, there was already acknowledgement of the role of the liver in non-hepatic diseases such as systemic sepsis, and an understanding that such involvement confers a poorer prognosis – hence the inclusion of the wisdom of Hippocrates in this compilation of classic papers. In the review article by Matuschak and Rinaldo, the reasons why liver dysfunction is associated with a poorer outcome in critical illness are explored, and the concept of the liver being a ‘driving force’ in multiple organ dysfunction is developed. In addition, jaundice without significant liver dysfunction is associated with left ventricular dysfunction, at least in the dog model developed by Professor Otto Better and his colleagues in Israel. This observation is relevant to the progressive resistance to inotropic and vasopressor agents in jaundiced critically ill patients.


id: cord-018318-vzzrsqsn
title: Postoperative Liver Failure
author: Naidu, C. Sudeep
date: 2017-02-08
txt: ./txt/cord-018318-vzzrsqsn.txt
cache: ./cache/cord-018318-vzzrsqsn.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123164/
doi: 10.1007/978-981-10-2678-2_3
summary:
  They focussed on serum bilirubin (SB) and prothrombin time (PT) as important prognostic markers of postoperative liver functional status and proposed the ''50-50'' criteria for the defi nition of PLF, i.e. the combination of PT >50 % of baseline normal and SB >50 μmol/L on postoperative day (POD) 5 (the ''50-50'' criteria) was found to be strongly predictive of mortality. In a study, mortality was signifi cantly higher in patients who had resection of hepatocellular carcinoma (HCC) in cirrhosis associated with active hepatitis (8.7 versus 1.5 %; p < 0.05) [ 13 ] . PLF and postoperative renal dysfunction are independent predictors of 90-day mortality following liver resection but the predictive value for mortality is significantly higher when both systems fail simultaneously. The patient''s liver status, hepatic reserve potential and functional aspect need to be investigated along with the metabolic and haematological derangements, which may lead to PLF.

abstract:
  Technical innovations in surgical techniques, anaesthesia, critical care and a spatial understanding of the intra-hepatic anatomy of the liver, have led to an increasing number of liver resections being performed all over the world. However, the number of complications directly attributed to the procedure and leading to inadequate or poor hepatic functional status in the postoperative period remains a matter of concern. There has always been a problem of arriving at a consensus in the definition of the term: postoperative liver failure (PLF). The burgeoning rate of living donor liver transplants, with lives of perfectly healthy donors involved, has mandated a consensual definition, uniform diagnosis and protocol for management of PLF. The absence of a uniform definition has led to poor comparison among various trials. PLF remains a dreaded complication in resection of the liver, with a reported incidence of up to 8 % [1], and mortality rates of up to 30–70 % have been quoted [2]. Several studies have quoted a lower incidence of PLF in eastern countries, but when it occurs the mortality is as high as in the West [3].


id: cord-018414-6ffhm895
title: Anesthesia Management of Liver Transplantation
author: Kang, Yoogoo
date: 2016-07-22
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123279/
doi: 10.1007/978-3-319-07209-8_9
abstract:
  Anesthesia for liver transplantation pertains to a continuum of critical care of patients with end-stage liver disease. Hence, anesthesiologists, armed with a comprehensive understanding of pathophysiology and physiologic effects of liver transplantation on recipients, are expected to maintain homeostasis of all organ function. Specifically, patients with fulminant hepatic failure develop significant changes in cerebral function, and cerebral perfusion is maintained by monitoring cerebral blood flow and cerebral metabolic rate of oxygen, and intracranial pressure. Hyperdynamic circulation is challenged by the postreperfusion syndrome, which may lead to cardiovascular collapse. The goal of circulatory support is to maintain tissue perfusion via optimal preload, contractility, and heart rate using the guidance of right-heart catheterization and transesophageal echocardiography. Portopulmonary hypertension and hepatopulmonary syndrome have high morbidity and mortality, and they should be properly evaluated preoperatively. Major bleeding is a common occurrence, and euvolemia is maintained using a rapid infusion device. Pre-existing coagulopathy is compounded by dilution, fibrinolysis, heparin effect, and excessive activation. It is treated using selective component or pharmacologic therapy based on the viscoelastic properties of whole blood. Hypocalcemia and hyperkalemia from massive transfusion, lack of hepatic function, and the postreperfusion syndrome should be aggressively treated. Close communication between all parties involved in liver transplantation is also equally valuable in achieving a successful outcome.


id: cord-018620-3kqx8arn
title: Hepatic Failure
author: Rueda, Mario
date: 2016-10-09
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123541/
doi: 10.1007/978-3-319-33341-0_18
abstract:
  The progression of liver disease can cause several physiologic derangements that may precipitate hepatic failure and require admission to an intensive care unit. The underlying pathology may be acute, acute-on chronic, or chronic in nature. Liver failure may manifest with a variety of clinical signs and symptoms that need prompt attention. The compromised synthetic and metabolic activity of the failing liver affects all organ systems, from neurologic to integumentary. Supportive care and specific therapies should be instituted in order to improve outcome and minimize time of recovery. In this chapter we will discuss the definition, clinical manifestations, workup, and management of acute and chronic liver failure and the general principles of treatment of these patients. Management of liver failure secondary to certain common etiologies will also be presented. Finally, liver transplantation and alternative therapies will also be discussed.


id: cord-018801-amet0wx4
title: Care of the Patient with Liver Failure Requiring Transplantation
author: Park, Caroline
date: 2018-05-04
txt: ./txt/cord-018801-amet0wx4.txt
cache: ./cache/cord-018801-amet0wx4.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123773/
doi: 10.1007/978-3-319-71712-8_55
summary:
  Depending on acuity, patients with decompensated chronic or acute fulminant liver failure generally require preoperative intensive care unit admission to manage organ dysfunction. Depending on acuity, patients with decompensated chronic or acute fulminant liver failure generally require preoperative intensive care unit (ICU) admission to manage organ dysfunction. In patients that develop AKI post-liver transplantation, treatment includes the prevention of hypotension and decreased use of unnecessary blood products. Early postoperative infections in liver transplant patients are typically bacterial and related to the donor''s status (previous infections from advanced cirrhosis), the surgical procedure itself, prolonged use of invasive catheters, and duration of mechanical ventilation. The resulting lack of blood flow and developing ischemia and necrosis from hepatic artery thrombosis present with signs and symptoms similar to fulminant liver failure patients with elevated liver serum tests, coagulopathy, and severe metabolic acidosis.

abstract:
  Patients undergo liver transplantation to address chronic liver failure, acute fulminant liver failure, or primary liver cancer. Depending on acuity, patients with decompensated chronic or acute fulminant liver failure generally require preoperative intensive care unit admission to manage organ dysfunction. Those with chronic liver failure are allocated an organ based on waiting list position determined by their local organ procurement organization (OPO). This position is dependent upon blood type and Model for End- Stage Liver Disease (MELD) score. These patients thus are critically ill and require preoperative ICU monitoring and care. Patients with hepatocellular carcinoma (HCC) who require liver transplantation are given a MELD exception and rarely require preoperative ICU care. The patient’s ability to undergo liver transplant in the setting of HCC is determined by the Milan criteria or the University of California, San Francisco (UCSF) criteria.


id: cord-022300-9w0lehal
title: The Liver and Pancreas
author: Hoskins, Johnny D.
date: 2009-05-15
txt: ./txt/cord-022300-9w0lehal.txt
cache: ./cache/cord-022300-9w0lehal.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7155544/
doi: 10.1016/b978-0-7216-7665-4.50015-2
abstract: nan
summary:
  Several different types of congenital PSS occur in young dogs and cats, including but not limited to (1) persistent patent fetal ductus venosus, (2) direct portal vein to caudal vena cava, (3) direct portal vein to azygos vein, (4) combination of portal vein with caudal vena cava into the azygos vein, (5) left gastric vein to vena caval shunt, (6) portal vein hypoplasia or atresia with secondary anomalous vessel, and (7) anomalous malformation of the caudal vena cava (Center et aI, 1995) . Ultrasonographic findings in puppies with congenital PSS include small liver, reduced visibility of intrahepatic portal vasculature, and an anomalous blood vessel draining into the caudal vena cava or sometimes into the azygos vein (Lamb, 1996) . A chronic active liver disease associated with an age-related accumulation of hepatic copper occurs in Bedlington terrier dogs (Hultgren et al, 1986 ).


id: cord-022483-hdmwv540
title: Gastrointestinal Disease
author: nan
date: 2009-06-05
txt: ./txt/cord-022483-hdmwv540.txt
cache: ./cache/cord-022483-hdmwv540.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156017/
doi: 10.1016/b978-1-4160-2353-1.50016-8
abstract: nan
summary:
  In the neonatal period, commonly reported causes of abdominal pain are meconium impaction, small-intestinal volvulus, enteritis or colitis, uroperitoneum, intussusception, gastric ulcers, and ileus secondary to prematurity, septicemia, or neonatal encephalopathy. Lower-intestinal contrast studies (i.e., barium enema) have been reported to have 100% sensitivity and 100% specificity for identifying mechanical obstruction (meconium impaction, atresia coli) of the transverse colon or small colon in foals less than 30 days of age ( Figure 11-14) . The only published study on 20 foals less than two weeks of age with acute abdominal pain reported that an exploratory celiotomy revealed functional ileus (45%), meconium impaction (25%), large-colon displacement (15%), small intestine displaced around the base of the cecum (10%), ruptured gastric ulcer, and small colon obstructed by the ovarian ligament. 8 These reports underscore the difficulty in definitively identifying the cause of abdominal pain prior to exploratory celiotomy in neonatal foals, as clearly some of these cases, such as enteritis and functional ileus, would not be considered to be predominantly surgical diseases.


id: cord-022555-a7ie82fs
title: Digestive System, Liver, and Abdominal Cavity
author: nan
date: 2011-12-05
txt: ./txt/cord-022555-a7ie82fs.txt
cache: ./cache/cord-022555-a7ie82fs.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7158306/
doi: 10.1016/b978-1-4377-0660-4.00023-5
abstract: nan
summary:
  One study found that, of cats investigated for gastrointestinal disease, 9 of 33 cats (27%) had no pathology recognized proximal to the jejunum (i.e., the effective length of diagnostic endoscopes would have precluded diagnosis), and other organs were affected in 9 of 10 cats with inflammatory bowel diseases and 7 of 8 cats with intestinal small cell lymphoma. 60, 64 Quantification of serum cobalamin levels is recommended in cats with clinical signs of small bowel diarrhea, ones suspected to have an infiltrative disease of the small intestine (inflammatory bowel disease or gastrointestinal lymphoma), or ones with pancreatic dysfunction. Survey radiographs may be normal in cats with esophagitis and strictures, but are useful to rule out other causes for the clinical signs, such as a foreign body, or to detect related problems, such as aspiration pneumonia. 8, 29 Other non-neoplastic causes reported for gastric or gastroduodenal ulceration in cats include parasites (e.g., Ollulanus tricuspis, Toxocara cati, Aonchotheca putorii, Gnathostoma spp.), bacterial infections, toxins, inflammatory bowel disease, and foreign bodies.


id: cord-022754-ehq9qnoo
title: Liver
author: nan
date: 2012-07-25
txt: ./txt/cord-022754-ehq9qnoo.txt
cache: ./cache/cord-022754-ehq9qnoo.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161409/
doi: 10.1016/b978-1-4160-3661-6.00061-4
abstract: nan
summary:
  Conversely, in cases of chronic end-stage liver disease, such as cirrhosis, serum hepatic enzyme activities may not be markedly increased, or may even be within the reference interval as a result of the replacement of hepatocytes with fibrous tissue. World Small Animal Veterinary Association (WSAVA) Standards for the Clinical and Histological Diagnosis of Canine and Feline Liver Disease suggest that the cytologic evaluation of bile forms part of the minimum diagnostic requirement for cats with extrahepatic cholestasis and for dogs guidance. 32 Hyperglobulinemia can be seen in dogs with cirrhosis, but it remains to be determined whether this corresponds with increased autoantibodies as occurs in humans with autoimmune hepatitis, or whether it reflects nonspecific systemic antibody production in response to antigens from the portal blood which bypass the liver through acquired PSSs. 83 Mild nonregenerative anemia may be a reflection of chronic disease.


id: cord-023017-k6edtg58
title: AASLD Abstracts (pp. 282A–382A)
author: nan
date: 2006-02-10
txt: ./txt/cord-023017-k6edtg58.txt
cache: ./cache/cord-023017-k6edtg58.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7165819/
doi: 10.1002/hep.1840380505
abstract: nan
summary:
  14/55 (25%) patients in AC who did not discontinue by week 24 received ribavirin dose reduction in comparison to 31/108 ( The clinical outcome in response to combination therapy for treatment of chronic hepatitis C virus (HCV) infection appears to be different for Caucasian versus African American patients. Over the period of combination therapy, most patients in which serum virus titers were reduced to non detectable levels had significant increases in T cell responses to HCV proteins. CHRONIC Background: Recent large prospective trials demonstrated that the combination therapy of interferon (1FN)-alphalribavirin significantly increased the ratio of a sustained virological response in patients with chronic hepatitis C in comparison with IFN monotherapy, especially in patients with high HCV-RNA titer and genotype lb. Results: Patients with chronic HCV infection showed higher MxA gene expression levels than healthy controls, indicating that hepatitis C virus induces IFN production.


id: cord-023033-tgt69ir6
title: Poster Session (pp. 78A–178A)
author: nan
date: 2006-02-10
txt: ./txt/cord-023033-tgt69ir6.txt
cache: ./cache/cord-023033-tgt69ir6.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7165951/
doi: 10.1002/hep.1840380503
abstract: nan
summary:
  Methods: We performed a retrospective analysis comparing outcomes, and the incidence, timing, and severity of histologic recurrence of HCV following transplantation in patients who underwent living donor liver transplant compared to recipients of cadaveric organs. Local liver immune responses are thought to play a major role in chronic autoimmune diseases directed at biliary epithelium.Using the apical sodium dependent bile acid transporter (ASBT) promoter to drive biliary epithelial cell -specific expression of a membrane form of ovalbumin (OVA), we have previously developed OVA-BIL transgenic mice. Thus, our AIM was to ascertain whether Kupffer cells express death ligands and contribute to hepatocyte apoptosis and liver fibrosis in the bile duct ligated mouse, an animal model of cholestasis. Control experiments confirmed that Y2 protein inhibited IFNa-induced ISRE-mediated signaling in Huh-T7 cells; relative luciferase activity was reduced from 653 (pH771 IFNP nAb increased HCV core Ag replication by 42% and 23% compared to no treatment (p=O.O1).


id: cord-025168-be7zube4
title: Perspective of placenta derived mesenchymal stem cells in acute liver failure
author: Saleh, Mahshid
date: 2020-05-24
txt: ./txt/cord-025168-be7zube4.txt
cache: ./cache/cord-025168-be7zube4.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7245988/
doi: 10.1186/s13578-020-00433-z
summary:
  Adipose tissue-derived mesenchymal stem cells (AD-MSCs) are isolated from adipose tissue by liposuction, are capable of differentiation to hepatocytelike cells in the presence of HGF, FGF-1, and FGF-4 factors and participate in the regeneration of hepatocytes and vasculogenesis [61] . Several studies have shown that MSCs secrete tropic factors and can be effective in reducing inflammation, fibrosis and apoptosis of liver cells as well as repairing damaged tissue by stimulating angiogenesis [74] . It can be argued that the beneficial effects of MSCs in liver diseases (including ALF) are not limited to hepatocyte repair, but rather the tropical factors released by Fig. 1 Mesenchymal stem cells and its effects on acute liver failure them modulate the deleterious effects of the immune response [142] . Bone marrow-derived mesenchymal stem cells inhibits hepatocyte apoptosis after acute liver injury In vivo hepatic differentiation potential of human umbilical cord-derived mesenchymal stem cells: therapeutic effect on liver fibrosis/cirrhosis

abstract:
  Acute Liver failure (ALF) is a life-threatening disease and is determined by coagulopathy (with INR ≥ 1.5) and hepatic encephalopathy as a result of severe liver injury in patients without preexisting liver disease. Since there are problems with liver transplantation including lack of donors, use of immunosuppressive drugs, and high costs of this process, new therapeutic approaches alongside current treatments are needed. The placenta is a tissue that is normally discarded after childbirth. On the other hand, human placenta is a rich source of mesenchymal stem cells (MSCs), which is easily available, without moral problems, and its derived cells are less affected by age and environmental factors. Therefore, placenta-derived mesenchymal stem cells (PD-MSCs) can be considered as an allogeneic source for liver disease. Considering the studies on MSCs and their effects on various diseases, it can be stated that MSCs are among the most important agents to be used for novel future therapies of liver diseases. In this paper, we will investigate the effects of mesenchymal stem cells through migration and immigration to the site of injury, cell-to-cell contact, immunomodulatory effects, and secretory factors in ALF.


id: cord-029138-avfvpqs5
title: The Changing Landscapes in DCD Liver Transplantation
author: Croome, Kristopher P.
date: 2020-07-13
txt: ./txt/cord-029138-avfvpqs5.txt
cache: ./cache/cord-029138-avfvpqs5.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7357263/
doi: 10.1007/s40472-020-00283-1
summary:
  Initial reports examining the use of liver grafts from DCD described inferior longterm outcomes when compared with donation after brain death donors (DBD). More recent single center publications from high volume DCD programs have demonstrated equivalent outcomes between DCD and DBD liver transplantation (LT), with appropriate donor and recipient selection [5] [6] [7] . A previous publication demonstrated that after the implementation of the Share 35 policy, more HCC patients have received livers from DCD donors [22] , potentially as the result of the highest quality organs being preferentially utilized by higher MELD recipients with broader sharing. As the collective experience with DCD LT increased, a concept of functional donor warm ischemic time (fDWIT) arose from the notion that individual events during DCD procurement, such as variations in hemodynamics, mandatory wait period, time from incision to cannulation of the aorta and cross-clamp, all of which are included in total DWIT, may have different impacts on the outcome of the liver graft [25, 26] .

abstract:
  PURPOSE OF REVIEW: The transplant community continues to look for ways to help address the discordance between donor liver graft availability and patients on the liver transplant waiting list. Donation after circulatory death (DCD) donor livers represents one potential means to help address this discordance. The present review describes the changing landscape of DCD liver transplantation (LT). RECENT FINDINGS: The number of DCD LTs performed annually within the USA has continued to grow on an annual basis. Importantly, national data has demonstrated that outcomes with DCD LT have been improving. This improvement has been driven by better understanding of how to successfully utilize these organs through better donor and recipient matching and careful evaluation of both hemodynamics during withdrawal of life support and the refinement of the procurement operation. SUMMARY: Despite these improvements in outcome, ischemic cholangiopathy (IC) continues to be the Achilles heel of DCD LT. Emerging technologies such as various forms of machine perfusion may allow for reduction of complications and better prognostication of the risk associated with DCD liver grafts.


id: cord-030369-4dn02a35
title: Clinical Manifestations and Laboratory Tests of AECHB and Severe Hepatitis (Liver Failure)
author: Peng, Liang
date: 2019-05-21
txt: ./txt/cord-030369-4dn02a35.txt
cache: ./cache/cord-030369-4dn02a35.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7418529/
doi: 10.1007/978-94-024-1603-9_1
summary:
  Once pulmonary infection is present, the disease condition will likely deteriorate, directly causing death; (3) a majority of infections are nosocomial infection, and pathogens are usually resistant to common antibiotics, making therapy challenging; (4) the pathogens causing infection are diverse but mainly Gram-negative bacteria, although the incidence of Gram-positive and fungal infections is increasing; (5) infection is closely related to the prognosis for liver failure patients. Although their clinical manifestation differ significantly, the "coexistence of acute and chronic failures" is shared by failures of all those organs; (2) CLF classification has been generally recognized at home and abroad, and the necessity of classification are further proved by the difference between CLF and the other three types; (3) CLF cases are relatively large in proportion (nearly 30%), which is still increasing (since the proportion of ALF/SALF are lowering); (4) Complications of CLF are common and are found in various forms, with bad prognosis; (5) In CLF patients with correlation to HBV, virus replication are commonly found, which is closely related to decompensation.

abstract:
  This chapter describes the clinical symptoms and signs of AECHB and HBV ACLF, classification, grading of HBV ACLF and their features, diagnostic principles and standards in liver pathology, biochemistry, and virology of HBV ACLF. 1. Liver failure is defined as serious damage to the liver cause by a variety of etiologies, leading to liver function disorder or even decompensation, and clinical syndromes with coagulopathy, jaundice, hepatic encephalopathy, and ascites. 2. Severe hepatitis B can be indicated pathologically by apparent hepatocellular necrosis, including extensive multifocal, confluent, bridging, sub-massive or massive necrosis. 3. Laboratory tests during the course of severe exacerbation of chronic hepatitis B can reflect pathological changes and liver function in a timely manner, providing objective and informative reference data for evaluation of disease severity and treatment efficacy. Among the most important laboratory tests are those for prothrombin activity, international normalized ratio, and increases in total bilirubin concentration. 4. Severe hepatitis B is associated with interactions between the virus and host factors. Detection of HBV DNA, HBV genotype, quasispecies and HBV mutation can provide important theoretical bases for the prevention, control or mitigation of the progress of severe hepatitis B. 5. Noninvasive imaging modalities can be used to visualize the entire liver and parts of it. Measuring liver volume to evaluate liver size and liver reserve capacity is regarded as important in diagnosis, surgical approach and prognostic evaluation of patients with severe exacerbation of chronic hepatitis B and liver failure. 6. Model for End-Stage Liver Disease (MELD) is the first quantitative method developed to assess whether a patient with liver failure requires a liver transplant. The predictive value of the MELD model has been improved by the MELD-Na, iMELD, and MESO models. Several other valuable prognostic models have been developed. For example, for patients with HBV-ACLF, the established TPPM scoring system was found to be more predictive than MELD score.


id: cord-032131-ghgciqfk
title: Lebertransplantation und Leberversagen
author: Ganschow, Rainer
date: 2013
txt: ./txt/cord-032131-ghgciqfk.txt
cache: ./cache/cord-032131-ghgciqfk.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7498809/
doi: 10.1007/978-3-642-24710-1_19
summary:
  16.2) handelt es sich um eine Erkrankung des frühen Säuglingsalters, bei der insbesondere die großen Gallengänge außerhalb der Leber (extrahepatische Gallengangatresie) zerstört werden, es können aber auch die intrahepatischen Gallenwege mit betroffen sein. Bislang wurden keine verlässlichen immunologischen Parameter identifiziert, die ein komplettes Absetzen der Immunsuppression nach einigen Therapiejahren bei selektiven Patienten rechtfertigen würden, so dass derzeit von einer lebenslangen immunsuppressiven Therapie ausgegangen werden muss. Durch eine frühzeitige Vorstellung von Kindern mit akutem oder chronischem Leberversagen in einem geeigneten Transplantationszentrum und unter Ausnutzung sämtlicher möglicher Transplantationstechniken sollte es möglich sein, die Mortalität auf der Lebertransplantationswarteliste für Kinder auf Null zu senken. So ist eine Autoimmunhepatitis, vor allem bei jüngeren Kindern, mit einer schlechten Prognose (selbst nach Lebertransplantation) assoziiert, wenn diese nicht kurzfristig auf eine immunsuppressive Therapie (Steroid, Azathioprin) anspricht (Vogel et al.

abstract:
  Es kann geschätzt werden, dass etwa 2 von 10.000 Neugeborenen oder 1–2 Neugeborene pro 1 Mio. Einwohner jährlich auf eine Lebertransplantation angewiesen sein werden.


id: cord-032181-gmcugd8h
title: Main Complications of AECHB and Severe Hepatitis B (Liver Failure)
author: Song, Jian-Xin
date: 2019-05-21
txt: ./txt/cord-032181-gmcugd8h.txt
cache: ./cache/cord-032181-gmcugd8h.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7498917/
doi: 10.1007/978-94-024-1603-9_2
summary:
  3. Hepatorenal syndrome, which is characterized by renal failure, hemodynamic changes in arterial circulation and abnormalities in the endogenous vascular system, is a common clinical complication of end-stage liver disease, and one of the important indicators for the prognosis of patients with severe hepatitis. The latest report indicated that basic laboratory examinations for coagulation function testing in common use at present, such as PT, APTT, international normalized ratio (INR) etc., have little correlation with occurrence of gastrointestinal bleeding in these patients, thereby revealing the importance to search and pay close attention to those complicating disease upregulating bleeding risk, such as bacterial infection, renal failure, hemodynamic change after portal hypertension, dysfunction of endotheliocyte as well as macrophagocyte and so on [107] .

abstract:
  This chapter describes the clinical features, and diagnosis of complications in AECHB including secondary bacterial infections, coagulation disorder, water electrolyte disorder, hepatorenal syndrome, hepatic encephalopathy, hepatopulmonary syndrome and endotoxemia: 1. Patients with severe hepatitis have impaired immunity and are therefore vulnerable to all kinds of infections. After infection, these patients may experience shock, DIC and multiple organ failure, all of which seriously affect their prognosis and are major causes of death. Concurrent infections consist primarily of infections of the lungs, intestines, biliary tract, and urinary tract, as well as spontaneous bacterial peritonitis and sepsis. 2. Severe hepatitis may reduce the synthesis of coagulation factors and enhance their dysfunction and increase anticoagulants and platelet abnormalities, leading to coagulopathy. Infection, hepatorenal syndrome and complications can further aggravate coagulopathy, resulting in DIC and seriously affecting patient prognosis. 3. Hepatorenal syndrome, which is characterized by renal failure, hemodynamic changes in arterial circulation and abnormalities in the endogenous vascular system, is a common clinical complication of end-stage liver disease, and one of the important indicators for the prognosis of patients with severe hepatitis. 4. Water electrolyte disorder (water retention, hyponatremia, hypokalemia, hyperkalaemia) and acid-base imbalance are common in patients with severe hepatitis. These internal environment disorders can lead to exacerbation and complication of the illness. 5. Hepatic encephalopathy is a neurological and psychiatric anomaly syndrome based on metabolic disorder, and an important prognostic indicator for patients with severe hepatitis. 6. The hepatopulmonary syndrome is an important vascular complication in lungs due to systemic hypoxemia in patients with cirrhosis and portal hypertension. The majority of patients with HPS are asymptomatic. Long-term oxygen therapy remains the most frequently recommended therapy for symptoms in patients with severe hypoxemia. 7. Endotoxemia, an important complication of severe hepatitis, is not only a second hit to the liver, but also leads to other complications including SIRS and MODS.


id: cord-033821-i14dmmps
title: Antihepatic Fibrosis Drugs in Clinical Trials
author: Guo, Yue-Cheng
date: 2020-08-24
txt: ./txt/cord-033821-i14dmmps.txt
cache: ./cache/cord-033821-i14dmmps.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7562798/
doi: 10.14218/jcth.2020.00023
summary:
  11 Treatment based on the etiology may not completely attenuate all fibrosis patients, as there are currently no effective managements for eliminating the cause of certain liver diseases, such as autoimmune hepatitis. In a multicenter, randomized, placebo-controlled trial, 19 patients with NASH exhibited improvements of liver histological features after treatment with OCA (25 mg, 72 weeks). Currently, two active phase II clinical trials (NCT03486912, NCT03486899) are investigating the efficacy and safety of pegbelfermin in patients with NASH-related fibrosis as determined by liver biopsy. A phase II clinical trial 51 showed that pirfenidone (1200 mg daily, 24 months) improved inflammation, fibrosis, and steatosis in patients with hepatitis C virusrelated cirrhosis. 52 A phase II clinical trial (NCT02499562) has explored the effective dose and safety of hydronidone capsules in patients with liver fibrosis induced by hepatitis B virus infection in Shanghai General Hospital, Shanghai, China.

abstract:
  Liver fibrosis is not an independent disease. It refers to the abnormal proliferation of connective tissues in the liver caused by various pathogenic factors. Thus far, liver fibrosis has been considered to be associated with a set of factors, such as viral infection, alcohol abuse, non-alcoholic fatty liver disease, and autoimmune hepatitis, as well as genetic diseases. To date, clinical therapeutics for liver fibrosis still face challenges, as elimination of potential causes and conventional antifibrotic drugs cannot alleviate fibrosis in most patients. Recently, potential therapeutic targets of liver fibrosis, such as metabolism, inflammation, cell death and the extracellular matrix, have been explored through basic and clinical research. Therefore, it is extremely urgent to review the antihepatic fibrosis therapeutics for treatment of liver fibrosis in current clinical trials.


id: cord-033914-a9e3rncp
author: Kauffman-Ortega, E.
date: 2020-10-17
txt: ./txt/cord-033914-a9e3rncp.txt
cache: ./cache/cord-033914-a9e3rncp.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568669/
doi: 10.1016/j.rgmxen.2020.10.006
abstract: nan
summary:
  His paternal grandmother, Josepha, and his father, Johann van Beethoven, suffered from alcohol use disorder, which led to his father''s death when Ludwig was 21 years old. 1 Numerous pathologies in the differential diagnosis have been proposed for Beethoven''s sensorineural hearing loss, and the most sustainable are: 1) lead poisoning, based on the presence of residuals of lead 100 times higher than normal in his hair and bones, according to an analysis performed in the United States in the mid 1990s, 4 2) Cogan''s syndrome, characterized by bilateral sensorineural hearing loss and interstitial keratitis secondary to vasculitis, albeit there is no evidence of vestibular dysfunction in Beethoven''s texts; that syndrome can be associated with idiopathic inflammatory bowel disease and reactive arthritis, 5 and 3) Paget''s disease is supported by the frontal bone prominence, tinnitus, and headache. Alcohol consumption appears to be the most probable cause of Beethoven''s cirrhosis of the liver, despite the macronodular appearance described in the autopsy.

title:
  In memoriam Ludwig van Beethoven. Clinical history and possible diagnoses of the genius of musical composition in silence()


id: cord-261608-4sjlg0p0
title: COVID-19-INDUCED LIVER INJURY: A CLINICAL DISTRACTION?
author: Trejo-Paredes, Camila
date: 2020-10-31
txt: ./txt/cord-261608-4sjlg0p0.txt
cache: ./cache/cord-261608-4sjlg0p0.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/S0012369220330877
doi: 10.1016/j.chest.2020.08.901
abstract: nan
summary:
  title: COVID-19-INDUCED LIVER INJURY: A CLINICAL DISTRACTION? His hospital course was also complicated by acute renal failure requiring renal replacement therapy, coagulopathy, and encephalopathy which coincided with liver injury trailing behind the peak of inflammatory markers. Emerging data support the hypothesis that liver injury in COVID-19 is often the result of SARS-CoV-2 directly binding to ACE2+ cholangiocytes, leading to cholangiohepatitis. In addition, cytokine storm may further exacerbate the hepatic injury in COVID-19 (2). Hepatic congestion in ventilated patients, shock liver and particularly, drug-induced liver injury (DILI) remains an important consideration in COVID-19 patients. CONCLUSIONS: COVID-19 induced viral hepatitis is now being increasingly identified as a self-resolving complication and the physician should be mindful of it and in the right setting, it may only be a clinical distraction. We should be cognizant of other potential causes of liver injury in COVID-19 patients like concurrent infection, sepsis-induced and DILI. Liver injury in COVID-19: The current evidence COVID-19 and the liver: little cause for concern.


id: cord-262152-gdnc51m5
author: Chaibi, Sayma
date: 2020-10-19
txt: ./txt/cord-262152-gdnc51m5.txt
cache: ./cache/cord-262152-gdnc51m5.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/S2210740120302977?v=s5
doi: 10.1016/j.clinre.2020.10.002
summary:
  title: Liver Function Test Abnormalities Are Associated With A Poorer Prognosis In Covid-19 Patients: Results Of A French Cohort AIM: To assess the impact of liver function test (LFT) abnormalities on the prognosis of patients with coronavirus disease 2019 (COVID-19) in a French cohort of hospitalized patients. Similar results were obtained for patients with cholestatic liver injury (Table Table 5 shows the association of factors with the composite severity endpoint (admission to ICU, respiratory failure requiring mechanical ventilation, CT scan injury >50% and global mortality). Severe infection is known to be more frequent among those patients, but they had mostly imbalanced diabetes or hypertension, which was not the case in our study Global mortality was also similar (16.0%), yet the number of admissions to ICU (15.3%) was higher than previously reported 1 .

title:
  Liver Function Test Abnormalities Are Associated With A Poorer Prognosis In Covid-19 Patients: Results Of A French Cohort

abstract:
  AIM: To assess the impact of liver function test (LFT) abnormalities on the prognosis of patients with coronavirus disease 2019 (COVID-19) in a French cohort of hospitalized patients. PATIENTS AND METHOD: From March 13 to April 22, 2020, we collected on a computerized and anonymized database, medical records, laboratory data and clinical outcomes of patients hospitalized for confirmed cases of COVID-19 infection (RT–PCR and/or CT-scan). Patients were followed up until April 22 2020 or until death or discharge. We have considered for statistical analysis, LFT abnormalities with levels greater than two times the upper limit of normal. Composite endpoint included admission to ICU, mechanical ventilation, severe radiologic injury and death to define disease severity. RESULTS: Among 281 patients (median age 60 years) with COVID-19, 102 (36.3%) had abnormal LFT. Hypertension (45.6%) and diabetes (29.5%) were the main comorbidities. 20.2% were taken liver-toxic drugs at the admission and 27.4% were given drugs known to induce hepatic cytolysis during hospitalization. Patients with elevated levels of ALT or AST were significantly more severe with a higher rate of admission to ICU (40.0% vs 6.0%, p < 0.0001), and global mortality (26.7% vs 12.1%, p = 0.03). In multivariate analysis, obesity and cytolytic profil were associated with the composite endpoint (respectively 2.37 [1.21; 4.64], p = 0.01 and OR 6.20, 95% confidence interval [1.84, 20.95], p-value 0.003) CONCLUSION: Most of liver injuries are mild and transient during COVID-19. LFT abnormalities are associated with a poorer prognosis and could be a relevant biomarker for early detection of severe infection.


id: cord-271635-tydlyc1q
author: Abdel-Hamid, Nabil M.
date: 2018-11-30
txt: ./txt/cord-271635-tydlyc1q.txt
cache: ./cache/cord-271635-tydlyc1q.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/S075333221834280X
doi: 10.1016/j.biopha.2018.08.104
summary:
  They can inhibit the liver cancer development and progression in several ways as protecting against liver carcinogens, enhancing effects of chemotherapeutic drugs, inhibiting tumor cell growth and metastasis, and suppression of oxidative stress and chronic inflammation. The co-treatment with LPP, orally, in NAFLD in rats, showed a significant improvement in the hepatic histology, reduction in the fibrosis, oxidative stress, inflammation, accumulation of fats and apoptosis, through modulating the transcriptional factors NF-κB and activator protein-1 (AP-1). The major polyphenol of green tea, epigallocatechin-3-gallate (EGCG), was used in CCl 4 -treated mice and showed a significant therapeutic potential in hepatic damage, inflammation and oxidative stress induced by CCl 4 in a dose-dependent manner at both biochemical and histological levels [34] . It was also reported that co-treatment of the whole green tea extract with alcohol administration showed an effective reduction of the hepatic oxidative stress and reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase systems in experimental alcohol-induced liver injury [35] .

title:
  Herbal management of hepatocellular carcinoma through cutting the pathways of the common risk factors

abstract:
  Abstract Hepatocellular carcinoma (HCC) is considered the most frequent tumor that associated with high mortality rate. Several risk factors contribute to the pathogenesis of HCC, such as chronic persistent infection with hepatitis C virus or hepatitis B virus, chronic untreated inflammation of liver with different etiology, oxidative stress and fatty liver disease. Several treatment protocols are used in the treatment of HCC but they also associated with diverse side effects. Many natural products are helpful in the co-treatment and prevention of HCC. Several mechanisms are involved in the action of these herbal products and their bioactive compounds in the prevention and co-treatment of HCC. They can inhibit the liver cancer development and progression in several ways as protecting against liver carcinogens, enhancing effects of chemotherapeutic drugs, inhibiting tumor cell growth and metastasis, and suppression of oxidative stress and chronic inflammation. In this review, we will discuss the utility of diverse natural products in the prevention and co-treatment of HCC, through its capturing of the common risk factors known to lead to HCC and shed the light on their possible mechanisms of action. Our theory assumes that shutting down the risk factor to cancer development pathways is a critical strategy in cancer prevention and management. We recommend the use of these plants side by side to recent chemical medications and after stopping these chemicals, as a maintenance therapy to avoid HCC progression and decrease its global incidence.


id: cord-275637-ea6w2kqv
author: Roca-Fernandez, A.
date: 2020-06-05
txt: ./txt/cord-275637-ea6w2kqv.txt
cache: ./cache/cord-275637-ea6w2kqv.txt
extension: .txt
mime: text/plain
url: http://medrxiv.org/cgi/content/short/2020.06.04.20122457v1?rss=1
doi: 10.1101/2020.06.04.20122457
summary:
  Conclusions UK Biobank data demonstrated an association between pre-existing liver disease and obesity with severe COVID-19, with higher proportions of liver fat in obese individuals a likely risk factor for symptomatic disease and severity. The aim of this study was to test the hypothesis that liver disease, and specifically liver fat accumulation, is a risk factor for developing symptomatic COVID-19. . https://doi.org/10.1101/2020.06.04.20122457 doi: medRxiv preprint Furthermore, the 32.7% of obese patients with liver fat ≥10% had a higher likelihood of being symptomatic and testing positive for COVID-19 (OR: 2.96, p=0.02). Our study demonstrates that in addition to the previouslyreported risk factors of male gender, non-white-British ethnicity, and obesity (1-3), liver fat is also a significant risk factor for having symptomatic COVID-19, with a person testing positive for COVID-19 being 1.85 times more likely to have pre-existing severe fatty liver disease.

title:
  HIGH LIVER FAT ASSOCIATES WITH HIGHER RISK OF DEVELOPING SYMPTOMATIC COVID-19 INFECTION - INITIAL UK BIOBANK OBSERVATIONS

abstract:
  Background A high proportion of COVID-19 patients develop acute liver dysfunction. Early research has suggested that pre-existing fatty liver disease may be a significant risk factor for hospitalisation. Liver fat, in particular, is a modifiable parameter and can be a target for public health policy and individual patient plans. In this study we aimed to assess pre-existing liver disease as a risk factor for developing symptomatic COVID-19. Methods From 502,506 participants from the UK Biobank, 42,146 underwent MRI (aged 45-82), and had measures of liver fat, liver fibroinflammatory disease and liver iron. Patients were censored on May 28th to determine how many had tested for COVID-19 with symptomatic disease. UK testing was restricted to those with symptoms in hospital. COVID-19 symptoms included fever, dry cough, sore throat, diarrhoea and fatigue. Univariate analysis was performed on liver phenotypic biomarkers to determine if these variables increased risk of symptomatic COVID-19, and compared to previously described risk factors associated with severe COVID-19, including to age, ethnicity, gender and obesity, Findings Increased liver fat was associated with a higher risk for symptomatic confirmed COVID-19 in this population in univariate analysis(OR:1.85, p=0.03). In obese participants, only those with concomitant fatty liver([≥]10%) were at increased risk(OR:2.96, p=0.02), with those having normal liver fat (<5%) showing no increased risk(OR:0.36, p=0.09). Conclusions UK Biobank data demonstrated an association between pre-existing liver disease and obesity with severe COVID-19, with higher proportions of liver fat in obese individuals a likely risk factor for symptomatic disease and severity. Public policy measures to protect patients with liver disease who may have almost double the risk of the general population should be considered, especially as dietary and pharmacological strategies to reduce body weight and liver fat already exist. Funding University of Oxford, Innovate UK, UK Biobank. Authors are employees of Perspectum Ltd.


id: cord-277535-u283k70i
title: Drugs and the liver
author: Vaja, Rakesh
date: 2020-09-22
txt: ./txt/cord-277535-u283k70i.txt
cache: ./cache/cord-277535-u283k70i.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/S1472029920301399
doi: 10.1016/j.mpaic.2020.07.001
summary:
  Additionally, drugs can also modify how the liver functions and cause dysfunction or even failure of the organ both by a direct effect on the liver or by alteration in liver blood flow. Furthermore, once a patient has been recognized to be suffering with liver dysfunction or failure drug choice and dosing regime will need to be rationalized. After reading this article you should: C understand the mechanisms of drug metabolism by the liver C have an appreciation of alterations to drug choice and dosing regimens in patients with liver disease due to their altered pharmacokinetics C know the management of a patient with paracetamol overdose There are many different isoforms of CYP450, classified according to their amino acid sequencing into families, subfamilies and individual genes. NSAIDS are contraindicated for systemic use in most liver disease patients, because of increased bioavalibilty, the high risk of precipitating gastrointestinal bleeding and renal failure.

abstract:
  The liver is a major organ with multiple functions. A number of drugs are metabolized by the liver during phase 1 and 2 reactions which include complex processes involving cytochrome P450 enzymes. Genetic and acquired variability in cytochrome P450 activity may have profound effects on pharmacokinetics. Additionally, drugs can also modify how the liver functions and cause dysfunction or even failure of the organ both by a direct effect on the liver or by alteration in liver blood flow. It is important to recognize the signs and symptoms of liver failure in patients and identify possible causes including drug interactions. Furthermore, once a patient has been recognized to be suffering with liver dysfunction or failure drug choice and dosing regime will need to be rationalized. Paracetamol overdose can have severe and life threatening consequences for patients due to its effect on liver function. It is the leading cause of acute liver failure in the UK, 1 Correct and early management is crucial and will be discussed within this article.


id: cord-279667-ikfduu2k
author: Ronnje, Louise
date: 2020-09-04
txt: ./txt/cord-279667-ikfduu2k.txt
cache: ./cache/cord-279667-ikfduu2k.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s12884-020-03172-8
doi: 10.1186/s12884-020-03172-8
summary:
  title: Complicated COVID-19 in pregnancy: a case report with severe liver and coagulation dysfunction promptly improved by delivery Severe COVID-19 promptly improved by the termination of the pregnancy or atypical HELLP (Hemolysis, Elevated Liver Enzymes and Low Platelet Count) exacerbated by concomitant COVID-19 infection could not be ruled out. CONCLUSIONS: This case adds to the growing body of evidence which raises concerns about the possible negative maternal outcomes of COVID-19 infection during pregnancy and advocates for pregnant women to be recognized as a vulnerable group during the current pandemic. We report a case of severe COVID-19 during in third trimester pregnancy, which led to an emergency Caesarean section and preterm delivery at 32 + 6 weeks of gestational age. Atypical presentation of HELLP could not be ruled out and the importance of a multidisciplinary team in the treatment and management of severe COVID-19 during pregnancy is critical for positive patient outcome.

title:
  Complicated COVID-19 in pregnancy: a case report with severe liver and coagulation dysfunction promptly improved by delivery

abstract:
  BACKGROUND: It has been proposed that pregnant women and their fetuses may be particularly at risk for poor outcomes due to the coronavirus (COVID-19) pandemic. From the few case series that are available in the literature, women with high risk pregnancies have been associated with higher morbidity. It has been suggested that pregnancy induced immune responses and cardio-vascular changes can exaggerate the course of the COVID-19 infection. CASE PRESENTATION: A 26-year old Somalian woman (G2P1) presented with a nine-day history of shortness of breath, dry cough, myalgia, nausea, abdominal pain and fever. A nasopharyngeal swab returned positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Her condition rapidly worsened leading to severe liver and coagulation impairment. An emergency Caesarean section was performed at gestational week 32 + 6 after which the patient made a rapid recovery. Severe COVID-19 promptly improved by the termination of the pregnancy or atypical HELLP (Hemolysis, Elevated Liver Enzymes and Low Platelet Count) exacerbated by concomitant COVID-19 infection could not be ruled out. There was no evidence of vertical transmission. CONCLUSIONS: This case adds to the growing body of evidence which raises concerns about the possible negative maternal outcomes of COVID-19 infection during pregnancy and advocates for pregnant women to be recognized as a vulnerable group during the current pandemic.


id: cord-280234-anlytu3q
author: Memar, Elmira Haji Esmaeil
date: 2020-09-29
txt: ./txt/cord-280234-anlytu3q.txt
cache: ./cache/cord-280234-anlytu3q.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/33069564/
doi: 10.1016/j.arcped.2020.09.009
summary:
  Although several typical manifestation of novel coronavirus disease 2019 (COVID-19) including respiratory symptoms, weakness, fever, and fatigue have been reported, some rare and novel manifestations have also been observed, particularly in children. In this study, we report a novel pediatric case of fulminant hepatic failure associated with COVIDAlthough there have been a significantly smaller number of reported cases of COVID-19 in the pediatric population compared with the adults, the number of infected children has seen a moderate increase [2, 7] . Owing to the acute fulminant hepatic failure in our patient, the only treatment option was liver transplantation; however, because of the progressive course of the disease and its rapid progression to stage 4 with encephalopathy and brain death, he died. In conclusion, in patients with fulminant hepatic failure, especially in cases with symptoms including fever, respiratory distress, and diarrhea, we should rule out COVID-19 infection as the underlying cause.

title:
  Fulminant hepatic failure: a rare and devastating manifestation of Coronavirus disease 2019 in an 11-year-old boy

abstract:
  Although several typical manifestation of novel coronavirus disease 2019 (COVID-19) including respiratory symptoms, weakness, fever, and fatigue have been reported, some rare and novel manifestations have also been observed, particularly in children. We report a pediatric case of fulminant hepatic failure associated with COVID-19. Although the patient was treated for acute fulminant hepatic failure in the context of COVID-19, he died following the progression of the disease to stage 4 hepatic failure with encephalopathy and brain death.


id: cord-283120-hyzk59qv
author: Sharma, Ashish
date: 2020-10-16
txt: ./txt/cord-283120-hyzk59qv.txt
cache: ./cache/cord-283120-hyzk59qv.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/33075578/
doi: 10.1016/j.aohep.2020.10.001
summary:
  In this meta-analysis, we aim to study the occurrence and association of liver injury, comorbid liver disease and elevated liver enzymes in COVID-19 confirmed hospitalizations with outcomes. MATERIALS AND METHODS: Data from observational studies describing comorbid chronic liver disease, acute liver injury, elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels and outcomes of COVID-19 hospitalized patients from December 1, 2019, to June 30, 2020 was extracted following PRISMA guidelines. The aim of the study is to evaluate the role of the comorbid chronic liver disease (CM-CLD), elevated liver enzymes and COVID-19 associated acute liver injury (COVID-19 ALI) in predicting the outcomes in confirmed COVID-19 hospitalized patients. The Maentel-Haenszel formula was used to calculate dichotomous variables to obtain odds ratios (ORs) along with its 95% confidence intervals to describe the association of comorbid liver disease, elevated liver enzymes, acute liver injury and outcomes of COVID-19 patients in each study.

title:
  Liver disease and outcomes among COVID-19 hospitalized patients- a systematic review and meta-analysis

abstract:
  INTRODUCTION AND OBJECTIVES: The coronavirus disease 2019 (COVID-19) pandemic has been a challenge globally. In severe acute respiratory syndrome (SARS) epidemic 60% of patients had hepatic injury, due to phylogenetic similarities of the viruses it is assumed that COVID-19 is associated with acute liver injury. In this meta-analysis, we aim to study the occurrence and association of liver injury, comorbid liver disease and elevated liver enzymes in COVID-19 confirmed hospitalizations with outcomes. MATERIALS AND METHODS: Data from observational studies describing comorbid chronic liver disease, acute liver injury, elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels and outcomes of COVID-19 hospitalized patients from December 1, 2019, to June 30, 2020 was extracted following PRISMA guidelines. Adverse outcomes were defined as admission to intensive care unit (ICU), oxygen saturation <90%, invasive mechanical ventilation (IMV), severe disease and in-hospital mortality. Odds ratio (OR) and 95% confidence interval (95%CI) were obtained. RESULTS: 24 studies with 12882 confirmed COVID-19 patients were included. Overall prevalence of CM-CLD was 2.6%, COVID-19-ALI was 26.5%, elevated AST was 41.1% and elevated ALT was 29.1%. CM-CLD had no significant association with poor outcomes (pooledOR:0.96;95%CI:0.71–1.29; p = 0.78). COVID-19-ALI (1.68;1.04–2.70; p = 0.03), elevated AST (2.98;2.35–3.77; p < 0.00001) and elevated ALT (1.85;1.49–2.29; p < 0.00001) were significantly associated with higher odds of poor outcomes. CONCLUSION: Our meta-analysis suggests that acute liver injury and elevated liver enzymes were significantly associated with COVID-19 severity. Future studies should evaluate changing levels of biomarkers amongst liver disease patients to predict poor outcomes of COVID-19 and causes of liver injury during COVID-19 infection.


id: cord-284693-mgpxnnk0
title: Post Liver transplant recurrent and de novo viral infections
author: Jothimani, Dinesh
date: 2020-09-26
txt: ./txt/cord-284693-mgpxnnk0.txt
cache: ./cache/cord-284693-mgpxnnk0.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1016/j.bpg.2020.101689
doi: 10.1016/j.bpg.2020.101689
summary:
  Advanced recipient age, diabetes mellitus, severe liver disease (Child Pugh >10), IL-28B polymorphism, high HCV RNA >10 7 IU/ml, ischemic/reperfusion injury, CMV, donor age >65 years, cold ischaemic time over 8 hours and warm ischemia over 90 minutes, marginal graft, DCD donor, higher immunosuppression in particular high dose corticosteroids for acute cellular rejection, use of anti-thymocyte globulin were significantly associated with rHCV in the liver allograft 15, 16 . Initial studies with sofosbuvir and ribavirin combination therapy for post-transplant rHCV showed poor drug tolerance, however, the main adverse event was anaemia related to ribavirin in 62% of patients, and subsequent hepatic decompensation related to the low haemoglobin 38 . A study by Pellicelli et al., showed significant adverse events including hepatic decompensation and 25% mortality in those with advanced disease following treatment with daclatasvir and sofosbuvir for post-transplant rHCV 51 .

abstract:
  Survival following liver transplantation has changed dramatically owing to improvement in surgical techniques, peri-operative care and optimal immunosuppressive therapy. Post-Liver transplant (LT) de novo or recurrent viral infection continues to cause major allograft dysfunction, leading to poor graft and patient survival in untreated patients. Availability of highly effective antiviral drugs has significantly improved post-LT survival. Patients transplanted for chronic hepatitis B infection should receive life-long nucleos(t)ide analogues, with or without HBIg for effective viral control. Patients with chronic hepatitis C should be commenced on directly acting antiviral (DAA) drugs prior to transplantation. DAA therapy for post-LT recurrent hepatitis C infection is associated with close to 100% sustained virological response (SVR), irrespective of genotype. De novo chronic Hepatitis E infection is an increasingly recognised cause of allograft dysfunction in LT recipients. Untreated chronic HEV infection of the graft may lead to liver fibrosis and allograft failure. Similarly, CMV and EBV can reactivate leading to systemic illness following liver transplantation. With COVID-19 pandemic, post-transplant patients are at risk of SARS-Co-V2 infection. Majority of the LT recipients require hospitalisation, and the mortality in this population is around 20%. Early recognition of allograft dysfunction and identification of viral aetiology is essential in the management of post-LT de novo or recurrent infections. Optimising immunosuppression is an important step in reducing the severity of allograft damage in the treatment of post-transplant viral infections. Viral clearance or control can be achieved by early initiation of high potency antiviral therapy.


id: cord-288721-3bv3aak6
author: Schneider, Annika
date: 2019-06-11
txt: ./txt/cord-288721-3bv3aak6.txt
cache: ./cache/cord-288721-3bv3aak6.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/31186476/
doi: 10.1038/s41598-019-44922-9
summary:
  Thus, single-organelle and multi-parameter resolution allows to explore altered energy metabolism and antiviral defence by tagged mitochondria selectively in virus-infected cells and will be instrumental to identify viral immune escape and to develop and monitor novel mitochondrial-targeted therapies. When challenged with high concentrations of calcium (100 µM), mitochondria isolated from virus-infected livers are much more fragile shown by time-dependent loss of membrane potential and change of their morphology indicated by decrease in side-scatter (Fig. 2F ). Number of viable mitochondria detected per second by flow-cytometry declined after calcium challenge, consistent with loss of mitochondrial integrity, and did so much faster in samples from virus-infected livers (Fig. 2F ). In order to further evaluate mitochondrial functionality, we challenged mitochondria with Ca 2+ as stress test and performed time kinetic measurements of DilC 1 (5) fluorescence and side-scatter of mito-DsRed + and mito-DsRed − mitochondria isolated from Ad-CMV-mitoRL infected livers.

title:
  Single organelle analysis to characterize mitochondrial function and crosstalk during viral infection

abstract:
  Mitochondria are key for cellular metabolism and signalling processes during viral infection. We report a methodology to analyse mitochondrial properties at the single-organelle level during viral infection using a recombinant adenovirus coding for a mitochondrial tracer protein for tagging and detection by multispectral flow cytometry. Resolution at the level of tagged individual mitochondria revealed changes in mitochondrial size, membrane potential and displayed a fragile phenotype during viral infection of cells. Thus, single-organelle and multi-parameter resolution allows to explore altered energy metabolism and antiviral defence by tagged mitochondria selectively in virus-infected cells and will be instrumental to identify viral immune escape and to develop and monitor novel mitochondrial-targeted therapies.


id: cord-290412-m6fesoyb
author: Zhao, Chang-qing
date: 2014-09-30
txt: ./txt/cord-290412-m6fesoyb.txt
cache: ./cache/cord-290412-m6fesoyb.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/S209549641460039X
doi: 10.1016/s2095-4964(14)60039-x
summary:
  In this article, we introduce TCM herbal preparations from the Chinese materia medica (such as Fuzheng Huayu) that are typically used for the treatment of liver diseases. TCM is widely applied in the treatment of liver diseases in China by both Chinese medicine doctors and Western medicine doctors because its ability to protect hepatocytes, inhibit hepatic inflammation and reduce fibrosis in the liver. Several patent drugs (Chinese herbal formulas) for treatment Clinical observations showed that FZHYC can effectively improve liver function and decrease the expression of fibrosis biomarkers such as serum hyaluronic acid, collagen type IV, procollagen type III and laminin, in chronic liver disease patients with fibrosis or cirrhosis [43, 44] . Randomized controlled multicenter clinical trial for integrated treatment of community-acquired pneumonia based on traditional Chinese medicine syndrome differentiation Optimized project of traditional Chinese medicine in treating chronic kidney disease stage 3: a multicenter double-blinded randomized controlled trial

title:
  Traditional Chinese medicine for treatment of liver diseases: progress, challenges and opportunities

abstract:
  Abstract Traditional Chinese medicine (TCM) is commonly used in treating liver diseases worldwide, especially in China. The advantages of using TCM for treatment of liver diseases include: protecting hepatocytes, inhibiting hepatic inflammation and antifibrosis in the liver. In this article, we introduce TCM herbal preparations from the Chinese materia medica (such as Fuzheng Huayu) that are typically used for the treatment of liver diseases. Literature surrounding the mechanisms of TCM therapy for treatment of liver diseases is presented and discussed. We propose that side effects of herbal compounds are often under-appreciated, and that more care should be taken in the prescription of potentially hepatotoxic medicines. Further, to deepen the understanding of TCM mechanisms, new techniques and methodologies must be developed. Future studies will lead to the enhancement of clinical outcomes of TCM. As complementary and alternative therapies, TCMs will play an expanding role in the future of liver disease treatment.


id: cord-291851-xesef17i
title: A systematic review and meta-analysis of the COVID-19 associated liver injury
author: Wong, Yu-Jun
date: 2020-08-31
txt: ./txt/cord-291851-xesef17i.txt
cache: ./cache/cord-291851-xesef17i.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/S1665268120301617
doi: 10.1016/j.aohep.2020.08.064
summary:
  Our meta-analysis aims to compare the risks and clinical outcomes of COVID-19 associated liver injury among adults with severe and non-severe COVID-19. The objective of this meta-analysis is to compare the risk and clinical outcome of COVID-19 associated liver injury between COVID-19 patients with severe and non-severe COVID-19. In this meta-analysis, we included all studies that met the following inclusion criteria: (1) population: adult patients infected with the COVID-19, (2) reported outcome data on liver enzymes derangement (3) reported outcome data on the risk or severity of liver injury between severe and non-severe COVID-19. We extracted data on the demographic of study populations (age, gender, sample size, the proportion of subjects with baseline chronic liver disease and the use of Lopinavir/ritonavir) as well as the pattern of COVID-19 associated liver injury (ALT, AST, bilirubin, albumin and GGT) from all included studies. and performed a meta-analysis on the severity and risk of COVID-19 associated liver injury in these patients.

abstract:
  INTRODUCTION AND OBJECTIVES: The novel coronavirus disease 2019 (COVID-19) has affected more than 5 million people globally. Data on the prevalence and degree of COVID-19 associated liver injury among patients with COVID-19 remain limited. We conducted a systematic review and meta-analysis to assess the prevalence and degree of liver injury between patients with severe and non-severe COVID-19. METHODS: We performed a systematic search of three electronic databases (PubMed/MEDLINE, EMBASE and Cochrane Library), from inception to 24(th) April 2020. We included all adult human studies (>20 subjects) regardless of language, region or publication date or status. We assessed the pooled odds ratio (OR), mean difference (MD) and 95% confidence interval (95%CI) using the random-effects model. RESULTS: Among 1543 citations, there were 24 studies (5961 subjects) which fulfilled our inclusion criteria. The pooled odds ratio for elevated ALT (OR = 2.5, 95%CI: 1.6-3.7, I(2) = 57%), AST (OR = 3.4, 95%CI: 2.3-5.0, I(2) = 56%), hyperbilirubinemia (OR = 1.7, 95%CI: 1.2-2.5, I(2) = 0%) and hypoalbuminemia (OR = 7.1, 95%CI: 2.1-24.1, I(2) = 71%) were higher subjects in critical COVID-19. CONCLUSION: COVID-19 associated liver injury is more common in severe COVID-19 than non-severe COVID-19. Physicians should be aware of possible progression to severe disease in subjects with COVID-19-associated liver injury.


id: cord-292501-2jv7xkfn
author: Jiang, Saiping
date: 2020-06-23
txt: ./txt/cord-292501-2jv7xkfn.txt
cache: ./cache/cord-292501-2jv7xkfn.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32656222/
doi: 10.3389/fmed.2020.00347
summary:
  Multivariable regression showed that the number of concomitant medications (odds ratio [OR]: 1.12, 95% confidence interval [CI]: 1.05-1.21) and the combination treatment of lopinavir/ritonavir and arbidol (OR: 3.58, 95% CI: 1.44-9.52) were risk factors for liver injury in non-critically ill patients. Multivariable regression showed that the number of concomitant medications (odds ratio [OR]: 1.12, 95% confidence interval [CI]: 1.05-1.21) and the combination treatment of lopinavir/ritonavir and arbidol (OR: 3.58, 95% CI: 1.44-9.52) were risk factors for liver injury in non-critically ill patients. In the non-critically ill group, the univariate logistic analyses showed that the combination treatment of lopinavir/ritonavir and arbidol and the number of concomitant medications were significantly associated with liver injury ( Table 4) . Drug factors, including the combination treatment of lopinavir/ritonavir and arbidol and the number of concomitant medications were independent risk factors for liver injury in non-critically ill patients with COVID-19, which may be due to drug interactions at the metabolic level.

title:
  Liver Injury in Critically Ill and Non-critically Ill COVID-19 Patients: A Multicenter, Retrospective, Observational Study

abstract:
  Background: Liver injury commonly occurs in patients with COVID-19. There is limited data describing the course of liver injury occurrence in patients with different disease severity, and the causes and risk factors are unknown. We aim to investigate the incidence, characteristics, risk factors, and clinical outcomes of liver injury in patients with COVID-19. Methods: This retrospective observational study was conducted in three hospitals (Zhejiang, China). From January 19, 2020 to February 20, 2020, patients confirmed with COVID-19 (≥18 years) and without liver injury were enrolled and divided into non-critically ill and critically ill groups. The incidence and characteristics of liver injury were compared between the two groups. Demographics, clinical characteristics, treatments, and treatment outcomes between patients with or without liver injury were compared within each group. The multivariable logistic regression model was used to explore the risk factors for liver injury. Results: The mean age of 131 enrolled patients was 51.2 years (standard deviation [SD]: 16.1 years), and 70 (53.4%) patients were male. A total of 76 patients developed liver injury (mild, 40.5%; moderate, 15.3%; severe, 2.3%) with a median occurrence time of 10.0 days. Critically ill patients had higher and earlier occurrence (81.5 vs. 51.9%, 12.0 vs. 5.0 days; p < 0.001), greater injury severity (p < 0.001), and slower recovery (50.0 vs. 61.1%) of liver function than non-critically ill patients. Multivariable regression showed that the number of concomitant medications (odds ratio [OR]: 1.12, 95% confidence interval [CI]: 1.05–1.21) and the combination treatment of lopinavir/ritonavir and arbidol (OR: 3.58, 95% CI: 1.44–9.52) were risk factors for liver injury in non-critically ill patients. The metabolism of arbidol can be significantly inhibited by lopinavir/ritonavir in vitro (p < 0.005), which may be the underlying cause of drug-related liver injury. Liver injury was related to increased length of hospital stay (mean difference [MD]: 3.2, 95% CI: 1.3–5.2) and viral shedding duration (MD: 3.0, 95% CI: 1.0–4.9). Conclusions: Critically ill patients with COVID-19 suffered earlier occurrence, greater injury severity, and slower recovery from liver injury than non-critically ill patients. Drug factors were related to liver injury in non-critically ill patients. Liver injury was related to prolonged hospital stay and viral shedding duration in patients with COVID-19. Clinical Trial Registration: World Health Organization International Clinical Trials Registry Platform, ChiCTR2000030593. Registered March 8, 2020.


id: cord-300187-fr6tme32
title: Infectious Hepatopathies in Dogs and Cats
author: Kearns, Shawn
date: 2009-11-26
txt: ./txt/cord-300187-fr6tme32.txt
cache: ./cache/cord-300187-fr6tme32.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/19945087/
doi: 10.1053/j.tcam.2009.06.004
summary:
  Although bacterial infections are probably the most common cause of infectious hepatitis, the clinician should be aware of other potential organisms and other commonly involved systems. Therefore, this article includes a description of common bacterial, mycobacterial, viral, fungal, protozoal, parasitic, and rickettsial diseases in dogs and cats. Mycobacterial disease is often subclinical in dogs and cats, but signs may be associated with granuloma formation in various organs. 39, 40 Nontuberculous mycobacterium, including those in the Mycobacterium avium complex, are saprophytic opportunistic organisms primarily implicated in disseminated disease in cats [41] [42] [43] [44] [45] and occasionally in dogs. No clear dissemination pattern has been identified because of low case numbers, but affected organs include the internal lymph nodes, liver, lungs, eyes, bone, muscles, and CNS. Infection results in disseminated disease, including protozoal hepatitis. Bacterial culture results from liver, gallbladder, or bile in 248 dogs and cats evaluated for hepatobiliary disease: 1998-2003

abstract:
  This article serves to review the various infectious diseases that affect the liver primarily or as a part of systemic infection. Although bacterial infections are probably the most common cause of infectious hepatitis, the clinician should be aware of other potential organisms and other commonly involved systems. Therefore, this article includes a description of common bacterial, mycobacterial, viral, fungal, protozoal, parasitic, and rickettsial diseases in dogs and cats.


id: cord-303046-unksl7p4
title: COVID-19 and the liver-related deaths to come
author: Pawlotsky, Jean-Michel
date: 2020-06-11
txt: ./txt/cord-303046-unksl7p4.txt
cache: ./cache/cord-303046-unksl7p4.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32528138/
doi: 10.1038/s41575-020-0328-2
summary:
  As a result of lockdowns and suspension of usual clinical care activities for the benefit of patients with COVID-19, the SARS-CoV-2 pandemic is having a major effect on the management of patients with chronic liver diseases, in particular those with cirrhosis, hepatocellular carcinoma and in liver transplantation programmes. The COVID-19 pandemic will also negatively affect the care and management of patients with hepatocellular carcinoma, generating delayed diagnosis, deferred treatment (including medical and surgical, such as access to liver transplantation), loss to follow-up and, ultimately, increased mortality. Most COviD-19-induced liver-mortality will be delayed, resulting from deferred care for liver diseases, reduced funding for public health interventions and the global economic crisis, which will lead to increases in alcohol and drug use and in blood-borne virus transmissions, while access to care and funding are reduced.

abstract:
  Coronavirus disease 2019 (COVID-19) itself and/or the use of hepatotoxic drugs might negatively affect the course and management of patients with pre-existing chronic liver diseases. However, the greatest effect of COVID-19 on liver diseases will be indirect and delayed, resulting from the impending global economic crisis.


id: cord-305956-l02xdq87
title: Liver injury in COVID-19: The current evidence
author: Alqahtani, Saleh A
date: 2020-05-26
txt: ./txt/cord-305956-l02xdq87.txt
cache: ./cache/cord-305956-l02xdq87.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1177/2050640620924157
doi: 10.1177/2050640620924157
summary:
  These reports highlighted that beyond severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a complicated course of the disease or even viral infection itself can lead to involvement of other organs and multiorgan failure. The current review summarizes the pathophysiology and potentially specific role of COVID-19 in liver disease based on the available data and case series published, ahead of print and non-peer-reviewed preprints as of 2 April. In this study, 47.3% of the discharged patients showed elevated LFTs at baseline, and 23.7% developed abnormalities during hospitalization, suggesting emerging liver injury from drugs or during the course of the infection. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: A single-centered, retrospective, observational study Clinical findings in a group of patients infected with the 2019 novel coronavirus (SARS-Cov-2) outside of Wuhan, China: Retrospective case series

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


id: cord-309795-2kozsv4z
title: Metabolic liver disease in diabetes – from mechanisms to clinical trials
author: Dewidar, Bedair
date: 2020-06-20
txt: ./txt/cord-309795-2kozsv4z.txt
cache: ./cache/cord-309795-2kozsv4z.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/S0026049520301633?v=s5
doi: 10.1016/j.metabol.2020.154299
summary:
  NAFLD, which affects about 25% of the population [3] , comprises a broad range of abnormalities ranging from simple fatty liver (steatosis) to non-alcoholic steatohepatitis (NASH), characterized by inflammation, necrosis, and hepatocellular ballooning, and progression to liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) [2] . In general, both hyperglycemia and toxic lipids such as ceramides, DAG, FFA, and cholesterol can induce deleterious effects on liver cells (glucolipotoxicity), which might initiate NAFLD progression from simple steatosis to NASH and fibrosis via various mechanisms, including cell death, oxidative stress, endoplasmic reticulum (ER) stress and mitochondrial disorders [46] . BL, baseline; CCR2/5, C-C chemokine receptors type 2 and type 5; FXR, farnesoid X receptor; HbA 1c , glycated haemoglobin; LXR, Liver X receptor; MPC, mitochondrial pyruvate carrier; NA, data not available; NAFLD, non-alcoholic fatty liver disease; NFS, NAFLD fibrosis score; PPAR, peroxisome proliferator-activated receptor; NASH, non-alcoholic steatohepatitis; SCD, stearoyl-CoA desaturase; SGLT, sodium-glucose cotransporter; THR, thyroid hormone receptor; T2DM, type 2 diabetes. Potential Nexus of Non-alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus: Insulin Resistance Between Hepatic and Peripheral Tissues

abstract:
  Abstract Non-alcoholic fatty liver disease (NAFLD) comprises fatty liver (steatosis), non-alcoholic steatohepatitis (NASH) and fibrosis/cirrhosis and may lead to end-stage liver failure or hepatocellular carcinoma. NAFLD is tightly associated with the most frequent metabolic disorders, such as obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM). Both multisystem diseases share several common mechanisms. Alterations of tissue communications include excessive lipid and later cytokine release by dysfunctional adipose tissue, intestinal dysbiosis and ectopic fat deposition in skeletal muscle. On the hepatocellular level, this leads to insulin resistance due to abnormal lipid handling and mitochondrial function. Over time, cellular oxidative stress and activation of inflammatory pathways, again supported by multiorgan crosstalk, determine NAFLD progression. Recent studies show that particularly the severe insulin resistant diabetes (SIRD) subgroup (cluster) associates with NAFLD and its accelerated progression and increases the risk of diabetes-related cardiovascular and kidney diseases, underpinning the critical role of insulin resistance. Consequently, lifestyle modification and certain drug classes used to treat T2DM have demonstrated effectiveness for treating NAFLD, but also some novel therapeutic concepts may be beneficial for both NAFLD and T2DM. This review addresses the bidirectional relationship between mechanisms underlying T2DM and NAFLD, the relevance of novel biomarkers for improving the diagnostic modalities and the identification of subgroups at specific risk of disease progression. Also, the role of metabolism-related drugs in NAFLD is discussed in light of the recent clinical trials. Finally, this review highlights some challenges to be addressed by future studies on NAFLD in the context of T2DM.


id: cord-318755-fip8wj6y
title: Liver transplantation in the era of COVID-19
author: El Kassas, Mohamed
date: 2020-05-12
txt: ./txt/cord-318755-fip8wj6y.txt
cache: ./cache/cord-318755-fip8wj6y.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1016/j.ajg.2020.04.019
doi: 10.1016/j.ajg.2020.04.019
summary:
  Management of immunosuppressive therapy and drug-drug interactions in liver transplant recipients infected with COVID-19 should be cautiously practiced to prevent rejection and effectively treat the underlying infection. Although healthcare facilities are overwhelmed with management of COVID-19 patients & health resources are being rapidly consumed, the American Association for the Study of Liver Diseases (AASLD), recommended against postponing transplantation. Patients with advanced liver disease and those after LTX represent vulnerable patient cohorts with an increased risk of infection and/or a severe course of COVID-19 Because of the immunosuppressed state they have [59] . Available data on coronavirus before and during outbreaks suggest that immunosuppressed patients are not at increased risk of severe pulmonary disease compared to the general population; however, immunosuppression may prolong viral shedding in post-transplant patients with COVID-19 if they are already infected [36, 60] .

abstract:
  Liver transplantation is considered the ultimate solution for patients with end-stage chronic liver disease or acute liver failure. Patients with liver transplant need special care starting from preoperative preparation, surgical intervention ending with postoperative care. Transplanted patients have to receive immunosuppressive therapy to prevent rejection. Such a state of immune suppression could predispose to different types of infections in liver transplant recipients. Currently, the world is suffering a pandemic caused by a new strain of the coronavirus family called COVID-19. Certain infection control precautions are needed to protect immunocompromised and vulnerable patients, including liver transplant candidates and recipients from acquiring COVID-19 infection. Restricting non-transplant elective surgical procedures, managing transplant patients in separate outpatient clinics, and in-patient wards can prevent transmission of infection both to patients and healthcare workers. Telemedicine can help in the triage of patients to screen for symptoms of COVID-19 before their regular appointment. Management of immunosuppressive therapy and drug-drug interactions in liver transplant recipients infected with COVID-19 should be cautiously practiced to prevent rejection and effectively treat the underlying infection. In this report, we are trying to summarize available evidence about different aspects of the management of liver transplant candidates and recipients in the era of COVID-19.


id: cord-323736-zup9cp6s
author: Ko, Sheung‐Fat
date: 2020-07-21
txt: ./txt/cord-323736-zup9cp6s.txt
cache: ./cache/cord-323736-zup9cp6s.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32691975/
doi: 10.1111/jcmm.15617
summary:
  This study tested the hypothesis that (31)P‐magnetic resonance spectroscopy ((31)P‐MRS) findings could provide reliable living images to accurately identify the degree of acute liver IRI and melatonin‐pretreated mitochondria was an innovative treatment for protecting the liver from IRI in rat. [1] [2] [3] Studies have further displayed that several key factors contribute to the hepatic injury at the initiation and during the progression of liver IRI, including those of elevation of anaerobic metabolism, dysfunction of mitochondria, insult of oxidative stress, overload of intracellular calcium, activation of liver Kupffer cells, infiltration of immune cells and release of inflammatory cytokines. Additionally, this study further tested whether the 31 P-MRS examination could provide reliable living images to accurately identify the degree of ATP consumption/depletion in hepatocytes, that is an indicator of acute liver ischaemia-reperfusion in rodent. Melatonin-pretreated mitochondria effectively protected liver against IRI and 31 P-MRS was a reliable tool for measuring the mitochondrial/ATP consumption in living animals. Hepatic 31 P-magnetic resonance spectroscopy identified the impact of melatonin-pretreated mitochondria in acute liver ischaemia-reperfusion injury

title:
  Hepatic (31)P‐magnetic resonance spectroscopy identified the impact of melatonin‐pretreated mitochondria in acute liver ischaemia‐reperfusion injury

abstract:
  Acute liver ischaemia‐reperfusion injury (IRI), commonly encountered during liver resection and transplantation surgery, is strongly associated with unfavourable clinical outcome. However, a prompt and accurate diagnosis and the treatment of this entity remain formidable challenges. This study tested the hypothesis that (31)P‐magnetic resonance spectroscopy ((31)P‐MRS) findings could provide reliable living images to accurately identify the degree of acute liver IRI and melatonin‐pretreated mitochondria was an innovative treatment for protecting the liver from IRI in rat. Adult male SD rats were categorized into group 1 (sham‐operated control), group 2 (IRI only) and group 3 (IRI + melatonin [ie mitochondrial donor rat received intraperitoneal administration of melatonin] pretreated mitochondria [10 mg/per rat by portal vein]). By the end of study period at 72 hours, (31)P‐MRS showed that, as compared with group 1, the hepatic levels of ATP and NADH were significantly lower in group 2 than in groups 1 and 3, and significantly lower in group 3 than in group 1. The liver protein expressions of mitochondrial‐electron‐transport‐chain complexes and mitochondrial integrity exhibited an identical pattern to (31)P‐MRS finding. The protein expressions of oxidative stress, inflammatory, cellular stress signalling and mitochondrial‐damaged biomarkers displayed an opposite finding of (31)P‐MRS, whereas the protein expressions of antioxidants were significantly progressively increased from groups 1 to 3. Microscopic findings showed that the fibrotic area/liver injury score and inflammatory and DNA‐damaged biomarkers exhibited an identical pattern of cellular stress signalling. Melatonin‐pretreated mitochondria effectively protected liver against IRI and (31)P‐MRS was a reliable tool for measuring the mitochondrial/ATP consumption in living animals.


id: cord-324509-5c6fzdjm
author: Huang, Haijun
date: 2020-07-22
txt: ./txt/cord-324509-5c6fzdjm.txt
cache: ./cache/cord-324509-5c6fzdjm.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32697870/
doi: 10.1111/apt.15962
summary:
  7 Some studies have reported the clinical characteristics of patients with coronavirus disease 2019 (COVID19) , including some factors that may lead to COVID-19-related liver damage and the relationship between liver function damage and disease prognosis. Therefore, we retrospectively analysed the clinical characteristics and dynamic changes in liver function based on different liver function levels at admission and different prognosis, in the purpose of finding out risk factors related to liver injury, and associations between markers of liver injury and clinical outcomes in COVID-19, including mortality and mechanical ventilation. 13, 17 One study had suggested that the dynamic changes in liver enzyme levels in severe patients were more significant, and AST was the parameter most correlated with mortality. In our study, the dynamic changes of ALT and AST levels were more significant in patients with liver injury and in the fatal group.

title:
  The association between markers of liver injury and clinical outcomes in patients with COVID‐19 in Wuhan

abstract:
  BACKGROUND: The outbreak of coronavirus disease 2019 (COVID‐19) is a critical challenge for public health. The effect of COVID‐19 on liver injury has not been fully presented. AIMS: To evaluate the dynamic changes in liver function and the relationship between liver function damage and prognosis in patients with COVID‐19. METHODS: Retrospective analysis of clinical data of 675 patients with COVID‐19 in Zhongnan Hospital of Wuhan University from January 3 to March 8, 2020. Patients were classified as normal, abnormal liver function and liver injury. RESULTS: Of 675 patients, 253 (37.5%) had abnormal liver function during hospitalisation, and 52 (7.7%) had liver injury. The dynamic changes of ALT and AST levels were more significant in patients with liver injury and in those who died. AST >3‐fold ULN had the highest risk of death and mechanical ventilation. Compared to patients with normal AST levels, mortality and risk of mechanical ventilation significantly increased 19.27‐fold (95% confidence interval [CI], 4.89‐75.97; P < 0.0001) and 116.72‐fold (95% CI, 31.58‐431.46; P < 0.0001), respectively, in patients with AST above 3‐fold ULN. Increased leucocytes, decreased lymphocytes and female sex were independently associated with liver injury. CONCLUSIONS: The dynamic changes in liver function may have a significant correlation with the severity and prognosis of COVID‐19. Increased index of liver injury was closely related to mortality and need for mechanical ventilation. Therefore, these indicators should be closely monitored during hospitalisation.


id: cord-324529-xbrdtxnz
author: Wang, Ming
date: 2020-10-07
txt: ./txt/cord-324529-xbrdtxnz.txt
cache: ./cache/cord-324529-xbrdtxnz.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1007/s12072-020-10075-5
doi: 10.1007/s12072-020-10075-5
summary:
  title: Clinical characteristics and risk factors of liver injury in COVID-19: a retrospective cohort study from Wuhan, China This study was designed to evaluate the clinical characteristics and risk factors of COVID-19-associated liver injury. extracted the currently largest cohort regarding 1099 mainly moderate SARS-CoV-2 infected patients and showed 39.4% with severe disease had elevated AST and 28.1% had elevated ALT, and the proportion was 18.2% and 19.8% in patients with non-severe disease [6] .Given that the number of patients in these studies is relatively small, information about the clinical characteristics of liver injury in these patients is scarce. The present study showed that liver injury was more prevalent in male, severe or critically ill patients with percutaneous oxygen saturation ≤ 93% or peak temperature ≥ 38.5 °C on admission, and comprehensively delineated the risk factors for COVID-19-associated liver injury.

title:
  Clinical characteristics and risk factors of liver injury in COVID-19: a retrospective cohort study from Wuhan, China

abstract:
  BACKGROUND: Coronavirus disease 2019 (COVID-19) has rapidly become a major international public health concern. This study was designed to evaluate the clinical characteristics and risk factors of COVID-19-associated liver injury. METHODS: A fraction of 657 COVID-19 patients were retrospectively analyzed. Clinical and laboratory data were derived from electronic medical records and compared between patients with or without liver injury. Multivariate logistic regression method was used to analyze the risk factors for liver injury. RESULTS: Among 657 patients, 303 (46.1%) patients had liver injury with higher rate in severe/critically ill patients [148/257 (57.6%)] than those in moderate cases [155/400 (38.8%)]. The incidence of liver injury was much higher in male [192/303 (63.4%)] than female [111/303 (36.6%)], and in severe/critical patients [148/303 (48.8%)] with percutaneous oxygen saturation ≤ 93% [89/279 (31.9%)] or peak body temperature ≥ 38.5 °C [185/301 (61.5%)] on admission. Liver injury-related inflammations included increased white blood cells, neutrophils and decreased lymphocytes. More patients with liver injury than without had increased serum IL-2R, TNFα, ferritin, hsCRP, PCT, ESR, γ-GT, and LDH. Multivariate regression analysis revealed that increasing odds of liver injury were related to male, higher serum hsCRP (≥ 10 mg/L), and neutrophil-to-lymphocyte ratio (NLR) (≥ 5). Moreover, more deceased patients (14/82 (17%)) had significantly elevated serum TBIL than discharged patients [25/532 (4.7%)]. CONCLUSION: Liver injury is a common complication in COVID-19 patients. The potential risk factors of liver injury include male, hsCRP and NLR score. A close monitor of liver function should be warned in COVID-19 patients, especially in severe/critical individuals. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s12072-020-10075-5) contains supplementary material, which is available to authorized users.


id: cord-327601-4uqgwlnx
title: SARS-CoV-2: is the liver merely a bystander to severe disease?
author: Bangash, Mansoor N.
date: 2020-06-02
txt: ./txt/cord-327601-4uqgwlnx.txt
cache: ./cache/cord-327601-4uqgwlnx.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/S016882782030355X?v=s5
doi: 10.1016/j.jhep.2020.05.035
abstract: nan
summary:
  1 Their study shows SARS-CoV-2 positive patients with ≥1 week history of increased aminotransferases have worse acute pulmonary disease (radiological and physiological) than those without. Considering that Interleukin (IL)-6 and C-reactive protein (CRP) are similar between patients with normal and prolonged abnormal liver aminotransferases, the authors speculate that liver injury is a direct effect of SARS-CoV-2 viral hepatitis rather than an indirect immune mediated injury. The fact that increases in liver aminotransferases occur and tend to parallel the severity of pulmonary disease remains unquestioned 2 , however, whether the liver injury is a true viral hepatitis rather than a bystander to the multi-organ pathophysiology of critical illness requires further discussion. Based on the above perspectives, we feel that raised liver aminotransferases associated with SARS-CoV-2 positivity are more likely attributable to illness severity, in which host response and iatrogenic harm (i.e. drugs, ventilation) drive bystander liver injury, thus explaining its association with mortality and in an analogous fashion to patterns seen in sepsis.


id: cord-328147-61gtx2h2
author: Lopez-Mendez, Ivan
date: 2020-10-21
txt: ./txt/cord-328147-61gtx2h2.txt
cache: ./cache/cord-328147-61gtx2h2.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/S1665268120301861
doi: 10.1016/j.aohep.2020.09.015
summary:
  In Mexico, 72.5% of the adult population is overweight and 9.4% have T2DM(4) Additionally, the prevalence of hepatic steatosis in Mexico ranges from 14 .4% to 62.9%, (5) and he prevalence of liver fibrosis has been reported in 8.1% (noninvasive assessment).(6) Currently, Mexico City is one of the most affected regions in the world with rising numbers of cases and deaths caused by COVID-19, and we have very few data regarding GI symptoms and LFT abnormalities and their prognostic value in Mexican patients. They also represent a challenge for therapeutic maneuvers such as imaging diagnosis, intubation, mechanical ventilation, and pronation, among others.(11) A meta-analysis including 3,207 patients with COVID-19 described that underlying chronic conditions such as hypertension, diabetes, and cardiovascular and respiratory diseases were higher in critical/non-surviving patients; clinical manifestations such as fever and dyspnea were also associated with the progression of the disease.(12) We found similar results in our study, with dyspnea as the most important associated symptom for ICU admission with OR 4.07 (CI95% 1.6-9.86).

title:
  Association of liver steatosis and fibrosis with clinical outcomes in patients with SARS-CoV-2 infection (COVID-19)

abstract:
  INTRODUCTION AND OBJECTIVES: Liver function tests (LFT) abnormalities are reported in up to 50% of COVID-19 patients, metabolic comorbidities are associated with poorer outcomes. The aim of the study is to determine prevalence of liver steatosis and fibrosis in patients with COVID-19 and their association with clinical outcomes. MATERIAL AND METHODS: Retrospective study in hospitalized COVID-19 patients. Risk for liver steatosis was estimated by HSI > 36, and risk for advanced liver fibrosis with APRI > 1.0, NAFLD FS > 0.675 and/or FIB-4 > 3.25. Clinical outcomes were admission to Intensive Care Unit (ICU) and mortality. RESULTS: Of 155 patients, 71.6% were male (n = 111), and 28.4% (n = 44) were obese. Abnormal LFT were present in 96.8% (n = 150), prevalence of steatosis was 42.6% (n = 66) and of significative liver fibrosis was 44.5% (n = 69). Liver fibrosis by FIB-4 was associated with risk of ICU admission (OR 1.74 [95%CI 1.74-2.68; p = 0.023]) and mortality (OR 6.45 [95%CI 2.01-20.83, p = 0.002]), no independent associations were found. CONCLUSIONS: The prevalence of steatosis and significant liver fibrosis was high in COVID-19 patients but was not associated with clinical outcomes.


id: cord-332827-gll4nqdd
title: Hepatology in the COVID Era: Another C Virus, again Challenging the Liver
author: Peixe, Paula
date: 2020-04-30
txt: ./txt/cord-332827-gll4nqdd.txt
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mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32775544/
doi: 10.1159/000508116
abstract: nan
summary:
  In published series, liver disease was not identified as a risk factor for SARS-Cov2 infection [11] [12] [13] [14] [15] . The authors state that NAFLD patients also had a higher risk of progression to severe COVID-19 and present an increased viral clearance time. Immune-mediated liver diseases, particularly autoimmune hepatitis, have not been mentioned as risk factors for COVID-19, but the immunosuppressive treatment required has triggered fears about the risk of infection in patients. Extensive records and targeted studies are needed to explore multiple open-ended questions such as the severity and mortality of COVID-19 and episodes of acute-on-chronic or decompensation associated with the presence of this disease (ascites, hepatic encephalopathy, digestive bleeding, kidney dysfunction, and the risk of infection) or the response to treatment [25, 26] . However, it is not yet possible to say whether transplantation-associated immunosuppression can alter the predisposition for the acquisition of SARS-Cov2 infection or how COVID-19 evolves in these patients.


id: cord-339786-elrzlbsg
title: Acute Liver Failure in a COVID-19 Patient Without any Preexisting Liver Disease
author: Gurala, Dhineshreddy
date: 2020-08-26
url: https://doi.org/10.7759/cureus.10045
doi: 10.7759/cureus.10045
abstract:
  In December 2019, an outbreak of novel coronavirus started in Wuhan, China, which gradually spread to the entire world. The World Health Organization (WHO) on February 11, 2020, officially announced the name for the disease as coronavirus disease 2019, abbreviated as COVID-19. It is caused by severe respiratory distress syndrome coronavirus 2 (SARS-CoV-2). The WHO declared SARS-CoV-2 as a pandemic on March 11, 2020. SARS-CoV-2 mainly causes fever as well as respiratory symptoms such as cough and shortness of breath. Gastrointestinal/hepatic sequelae such as diarrhea, nausea, vomiting, and elevated liver enzymes have been reported as well. Studies and data so far on coronavirus infections from China, Singapore, and other countries showed that liver enzymes elevation could be seen in 20-50% of cases. More severe disease can correlate with the worsening of liver enzymes. However, acute liver failure in patients with COVID-19 has not been described. Herein we report a case of acute liver failure in an elderly patient with COVID-19 infection who did not have a history of preexisting liver disease.


id: cord-340325-0oh40b6r
title: Lipid nanoparticle technology for therapeutic gene regulation in the liver
author: Witzigmann, Dominik
date: 2020-07-02
url: https://www.sciencedirect.com/science/article/pii/S0169409X20300727?v=s5
doi: 10.1016/j.addr.2020.06.026
abstract:
  Hereditary genetic disorders, cancer, and infectious diseases of the liver affect millions of people around the globe and are a major public health burden. Most contemporary treatments offer limited relief as they generally aim to alleviate disease symptoms. Targeting the root cause of diseases originating in the liver by regulating malfunctioning genes with nucleic acid-based drugs s holds great promise as a therapeutic approach. However, employing nucleic acid therapeutics in vivo is challenging due to their unfavorable characteristics. Lipid nanoparticle (LNP) delivery technology is a revolutionary development that has enabled clinical translation of gene (editing) therapies. LNPs can deliver siRNA, mRNA, DNA, or gene-editing complexes, providing opportunities to treat hepatic diseases by silencing pathogenic genes, expressing therapeutic proteins, or correcting genetic defects. Here we discuss the state-of-the-art LNP technology for hepatic gene therapy including formulation design parameters, production methods, preclinical development and clinical translation.


id: cord-340576-dabcs3w5
title: Liver Cirrhosis and Sarcopenia from the Viewpoint of Dysbiosis
author: Nishikawa, Hiroki
date: 2020-07-24
txt: ./txt/cord-340576-dabcs3w5.txt
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mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32722100/
doi: 10.3390/ijms21155254
summary:
  In individuals with chronic liver diseases (CLDs), metabolic or nutritional dysfunctions including protein-energy malnutrition (PEM) or muscle abnormalities are frequently found, which can be related to disabilities, poor quality of life, or mortality [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] . LC-related complications themselves such as hepatocellular carcinoma (HCC), ascites, spontaneous bacterial peritonitis (SBP), varices, hepatic encephalopathy (HE), and acute or chronic liver failure (ACLF) can cause sarcopenia [22, 40] . LC-related complications themselves such as hepatocellular carcinoma (HCC), ascites, spontaneous bacterial peritonitis (SBP), varices, hepatic encephalopathy (HE), and acute or chronic liver failure (ACLF) can cause sarcopenia [22, 40] . Cumulative evidence has highlighted the relevance of increase in intestinal permeability (i.e., leaky gut syndrome) and consequent bacterial translocation in the development of CLDs. Particularly, in recent hypotheses regarding patients with non-alcoholic fatty liver disease (NAFLD), intestinal permeability impairment, dietary habits, and gut dysbiosis are considered to be the main pathogenic triggers [85] [86] [87] .

abstract:
  Sarcopenia in patients with liver cirrhosis (LC) has been attracting much attention these days because of the close linkage to adverse outcomes. LC can be related to secondary sarcopenia due to protein metabolic disorders and energy metabolic disorders. LC is associated with profound alterations in gut microbiota and injuries at the different levels of defensive mechanisms of the intestinal barrier. Dysbiosis refers to a state in which the diversity of gut microbiota is decreased by decreasing the bacterial species and the number of bacteria that compose the gut microbiota. The severe disturbance of intestinal barrier in LC can result in dysbiosis, several bacterial infections, LC-related complications, and sarcopenia. Here in this review, we will summarize the current knowledge of the relationship between sarcopenia and dysbiosis in patients with LC.


id: cord-340710-dmow5p7k
author: Lagana, Stephen M.
date: 2020-08-13
txt: ./txt/cord-340710-dmow5p7k.txt
cache: ./cache/cord-340710-dmow5p7k.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1038/s41379-020-00649-x
doi: 10.1038/s41379-020-00649-x
summary:
  title: Hepatic pathology in patients dying of COVID-19: a series of 40 cases including clinical, histologic, and virologic data Here we report the clinical and histologic findings related to the liver in 40 patients who died of complications of COVID-19. In conclusion, we found patients dying of COVID-19 had biochemical evidence of hepatitis (of variable severity) and demonstrated histologic findings of macrovesicular steatosis and mild acute hepatitis (lobular necroinflammation) and mild portal inflammation. A more recent study performed core needle biopsies on the livers of four patients and reported nonspecific findings, attributed to preexisting disease or perimortem injury [4] . Histologically, the most frequently encountered findings were macrovesicular steatosis, mild acute hepatitis, and minimal-to-mild portal inflammation. Nonetheless, based on the pattern of injury observed and the results of the PCR analysis, SARS-CoV-2 seems to involve the liver, and is associated with, possibly causal of, macrovesicular steatosis and acute hepatitis.

title:
  Hepatic pathology in patients dying of COVID-19: a series of 40 cases including clinical, histologic, and virologic data

abstract:
  The novel coronavirus SARS-CoV-2 (coronavirus disease 19, or COVID-19) primarily causes pulmonary injury, but has been implicated to cause hepatic injury, both by serum markers and histologic evaluation. The histologic pattern of injury has not been completely described. Studies quantifying viral load in the liver are lacking. Here we report the clinical and histologic findings related to the liver in 40 patients who died of complications of COVID-19. A subset of liver tissue blocks were subjected to polymerase chain reaction (PCR) for viral ribonucleic acid (RNA). Peak levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were elevated; median ALT peak 68 U/l (normal up to 46 U/l) and median AST peak 102 U/l (normal up to 37 U/l). Macrovesicular steatosis was the most common finding, involving 30 patients (75%). Mild lobular necroinflammation and portal inflammation were present in 20 cases each (50%). Vascular pathology, including sinusoidal microthrombi, was infrequent, seen in six cases (15%). PCR of liver tissue was positive in 11 of 20 patients tested (55%). In conclusion, we found patients dying of COVID-19 had biochemical evidence of hepatitis (of variable severity) and demonstrated histologic findings of macrovesicular steatosis and mild acute hepatitis (lobular necroinflammation) and mild portal inflammation. We also identified viral RNA in a sizeable subset of liver tissue samples.


id: cord-342930-f7cw2ca6
title: Hepatic consequences of COVID-19 infection. Lapping or biting?
author: Portincasa, Piero
date: 2020-06-01
txt: ./txt/cord-342930-f7cw2ca6.txt
cache: ./cache/cord-342930-f7cw2ca6.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1016/j.ejim.2020.05.035
doi: 10.1016/j.ejim.2020.05.035
summary:
  Although the most frequent and critical clinical 15 presentation is secondary to the involvement of the lung (fever, cough), the infection by SARS16 CoV-2 virus may lead to a systemic and multi-organ disease [10] , also involving the gastrointestinal 17 tract (nausea/vomiting, or diarrhea) [11, 12] . Although the level of serum transaminases could be already elevated before the onset of COVID-14 19, results from clinical reports and autopsy studies [26, 49, 50] suggest that liver dysfunction can 15 be an expression of a worse disease evolution, and that an isolated elevation of transaminases alone 16 is likely to be the indirect expression of a systemic inflammation. In one study, patients 17 developing abnormal liver tests had higher risks of progressing to severe disease [51] , and the 18 finding is associated with longer hospital stay [62] . Non-alcoholic fatty liver diseases in patients with 19 COVID-19: A retrospective study

abstract:
  The outbreak of coronavirus disease 2019 (COVID-19) starting last December in China placed emphasis on liver involvement during infection. This review discusses the underlying mechanisms linking COVID-19 to liver dysfunction, according to recent available information, while waiting further studies. The manifestations of liver damage are usually mild (moderately elevated serum aspartate aminotransferase activities), and generally asymptomatic. Few patients can still develop severe liver problems, and therapeutic options can be limited. Liver dysfunction may affect about one-third of the patients, with prevalence greater in men than women, and in elderly. Mechanisms of damage are complex and include direct cholangiocyte damage and other coexisting conditions such as the use of antiviral drugs, systemic inflammatory response, respiratory distress syndrome-induced hypoxia, sepsis, and multiple organ dysfunction. During new COVID-19 infections, liver injury may be observed. If liver involvement appears during COVID-19 infection, however, attention is required. This is particularly true if patients are older or have a pre-existing history of liver diseases. During COVID-19 infection, the onset of liver damage impairs the prognosis, and hospital stay is longer.


id: cord-348024-n8wn4och
title: Longitudinal association between markers of liver injury and mortality in COVID‐19 in China
author: Lei, Fang
date: 2020-05-02
url: https://doi.org/10.1002/hep.31301
doi: 10.1002/hep.31301
abstract:
  Coronavirus disease 2019 (COVID‐19) is a new infectious disease. To reveal the hepatic injury related to this disease and its clinical significance, we conducted a multicenter retrospective cohort study that included 5,771 adult patients with COVID‐19 pneumonia in Hubei Province. We reported the distributional and temporal patterns of liver injury indicators in these patients and determined their associated factors and death risk. Longitudinal liver function tests were retrospectively analyzed and correlated with the risk factors and death. Liver injury dynamic patterns differed in alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin (TBIL). AST elevated first, followed by ALT, in severe patients. ALP modestly increased during hospitalization and largely remained in the normal range. The fluctuation in TBIL levels was mild in the non‐severe and the severe group. AST abnormality was associated with the highest mortality risk compared to other indicators of liver injury during hospitalization. Common factors associated with elevated liver injury indicators were lymphocyte count decrease, neutrophil count increase, and male gender. CONCLUSION: The dynamic patterns of liver injury indicators and their potential risk factors may provide an important explanation for the COVID‐19‐associated liver injury. Because elevated liver injury indicators, particularly AST, are strongly associated with the mortality risk, our study indicates that these parameters should be monitored during hospitalization.


id: cord-353633-a4pu6rlu
author: Perakakis, Nikolaos
date: 2020-07-23
txt: ./txt/cord-353633-a4pu6rlu.txt
cache: ./cache/cord-353633-a4pu6rlu.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1016/j.metabol.2020.154320
doi: 10.1016/j.metabol.2020.154320
summary:
  Non-alcoholic fatty liver disease (NAFLD) is a multifaceted metabolic disorder, whose spectrum covers clinical, histological and pathophysiological developments ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and liver fibrosis, potentially evolving into cirrhosis, hepatocellular carcinoma and liver failure. The disease is characterized initially by hepatic lipid accumulation (nonalcoholic fatty liver; NAFL), that can often progress to non-alcoholic steatohepatitis (NASH), liver fibrosis or cirrhosis, as outlined in detail elsewhere in this special issue [1] . Several studies have assessed the impact of epigenetic modifications in the development and progress of NAFLD ( Figure 2 ) as well as in the association of NAFLD with other metabolic diseases by focusing on DNA methylation, histone modifications and miRNA expression profiles that can significantly affect transcriptional activity. Proteomic analysis to identify differentially expressed proteins between subjects with metabolic healthy obesity and non-alcoholic fatty liver disease

title:
  The role of omics in the pathophysiology, diagnosis and treatment of non-alcoholic fatty liver disease

abstract:
  Non-alcoholic fatty liver disease (NAFLD) is a multifaceted metabolic disorder, whose spectrum covers clinical, histological and pathophysiological developments ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and liver fibrosis, potentially evolving into cirrhosis, hepatocellular carcinoma and liver failure. Liver biopsy remains the gold standard for diagnosing NAFLD, while there are no specific treatments. An ever-increasing number of high-throughput Omics investigations on the molecular pathobiology of NAFLD at the cellular, tissue and system levels produce comprehensive biochemical patient snapshots. In the clinical setting, these applications are considerably enhancing our efforts toward obtaining a holistic insight on NAFLD pathophysiology. Omics are also generating non-invasive diagnostic modalities for the distinct stages of NAFLD, that remain though to be validated in multiple, large, heterogenous and independent cohorts, both cross-sectionally as well as prospectively. Finally, they aid in developing novel therapies. By tracing the flow of information from genomics to epigenomics, transcriptomics, proteomics, metabolomics, lipidomics and glycomics, the chief contributions of these techniques in understanding, diagnosing and treating NAFLD are summarized herein.


id: cord-355395-rckzi8vz
title: Hepatic complications of COVID‐19 and its treatment
author: Tian, Dandan
date: 2020-05-21
url: https://www.ncbi.nlm.nih.gov/pubmed/32437004/
doi: 10.1002/jmv.26036
abstract:
  COVID‐19 is highly contagious and has a variety of clinical manifestations, it can affect a number of other organs in addition to the lungs, and liver injury may occur. SARS‐CoV‐2 can cause liver injury through systemic inflammatory response syndrome (SIRS), cytokine storms, ischemia‐reperfusion injury, side effects of treatment drugs, and underlying liver disease and can attack liver cells directly via ACE2. Clinical studies have found that liver injury in COVID‐19 patients mainly manifests as abnormal liver biochemical indicators, but there have been no reports of liver failure caused by this disease. The number of COVID‐19 patients with liver injury is increasing, and the incidence of liver injury in COVID‐19 patients with severe disease are higher than in patients with mild disease. Liver injury may be a risk factor for progresses and worsens in patients with COVID‐19, and it is necessary to pay attention to the occurrence of liver injury in the diagnosis and treatment of COVID‐19. This article is protected by copyright. All rights reserved.


