Role of platelets in chronic liver disease and acute liver injury

2013 ◽  
Vol 44 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Takeshi Nowatari ◽  
Soichiro Murata ◽  
Kiyoshi Fukunaga ◽  
Nobuhiro Ohkohchi
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Chronic Liver Disease ◽  
Acute Liver Injury ◽  
Chronic Liver

Increased hepatic fibrosis and JNK2-dependent liver injury in mice exhibiting hepatocyte-specific deletion of cFLIP

2012 ◽  
Vol 303 (4) ◽  
pp. G498-G506 ◽  
Author(s):  
Jörn M. Schattenberg ◽  
Michael Nagel ◽  
Yong Ook Kim ◽  
Tobias Kohl ◽  
Marcus A. Wörns ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Chronic Liver Disease ◽  
Hepatic Fibrosis ◽  
Chronic Liver ◽  
Hepatocellular Injury ◽  
Inhibitory Protein ◽  
Hepatocellular Apoptosis ◽  
Specific Deletion

Chronic liver disease promotes hepatocellular injury involving apoptosis and triggers compensatory regeneration that leads to the activation of quiescent stellate cells in the liver. The deposition of extracellular matrix from activated myofibroblasts promotes hepatic fibrosis and the progression to cirrhosis with deleterious effects on liver physiology. The role of apoptosis signaling pathways in the development of fibrosis remains undefined. The aim of the current study was to determine the involvement of the caspase-8 homologue cellular FLICE-inhibitory protein (cFLIP) during the initiation and progression of fibrosis. Liver injury and fibrosis from carbon tetrachloride (CCl4) and thioacetamide (TAA) were examined in mice exhibiting a hepatocyte-specific deletion of cFLIP ( flip −/−). Acute liver injury from CCl4 and TAA were enhanced in flip −/− mice. This was accompanied by increased activation of caspase-3 and -9, pronounced phosphorylation of JNK, and decreased phosphorylation of Erk. Deletion of the cJun NH2-terminal kinase 2 (JNK2) in flip −/− mice protected from injury. Hepatic fibrosis was increased at baseline in 12-wk-old flip −/− mice, and progression of fibrosis from TAA was accelerated compared with the wild type. In conclusion, deletion of cFLIP in hepatocytes leads to increased fibrosis and accelerated fibrosis progression. This is accompanied by increased injury involving the activation of caspases and JNK2. Thus predisposition to liver injury involving increased hepatocellular apoptosis is a critical mediator of accelerated fibrogenesis, and prevention of liver injury will be a most important measure for patients with chronic liver disease.

scholarly journals Risk factors and severity of acute liver injury in non-chronic liver disease and chronic liver disease patients

2021 ◽  
Vol 60 (2) ◽  
Author(s):  
S Kerdsin ◽  
◽  
R Norasetkun ◽  
W Khamwang ◽  
A Phensombun ◽  
...  
Keyword(s):  
Risk Factors ◽  
Liver Disease ◽  
Liver Injury ◽  
Chronic Liver Disease ◽  
Acute Liver Injury ◽  
Dengue Infection ◽  
Chronic Liver ◽  
Disease Group ◽  
Bacterial Peritonitis ◽  
Complications And Mortality

Objectives To study factors related to acute liver injury and compare the severity and risk of those factors in patients with and without chronic liver disease. Methods This cross-sectional study of 323 patients admitted to Somdejphrajaotaksin Maharaj Hospital between 1 January and 30 September 2019, analyzing data collected on the clinical background, signs and symptoms, and laboratory results of those patients. Results Of the 323 patients in the study, 188 did not have chronic liver disease (58.2%) and 135 had chronic liver disease (41.8%). Risk factors for acute liver injury in the chronic liver disease group included bacterial infection (33.3%) and spontaneous bacterial peritonitis (4.4%), much significantly higher than the rates in the no chronic disease group. However, the risk factors excessive consumption of alcohol (30.3%) and dengue infection (11.2%) in the no chronic liver disease group were significantly higher than in the chronic disease group. Both groups had a high incidence of disease severity as well as a high incidence of complications and mortality, although the mortality rate was higher in the chronic liver disease group (15.0% vs. 6.9%). Conclusions The types and frequencies of risk factors for acute liver injury in patients with chronic liver disease and those with no chronic liver disease groups are different. The incidence of bacterial infection and spontaneous bacterial peritonitis is higher in patients with chronic liver disease. The incidence of excessive alcohol consumption and dengue infection is much higher in patients without chronic liver disease. Both groups have high levels of disease severity, complications and mortality. Sepsis is the major cause of mortality, especially in patients with chronic liver disease.

scholarly journals Oral Azole Antifungal Medications and Risk of Acute Liver Injury, Overall and by Chronic Liver Disease Status

2016 ◽  
Vol 129 (3) ◽  
pp. 283-291.e5 ◽  
Author(s):  
Vincent Lo Re ◽  
Dena M. Carbonari ◽  
James D. Lewis ◽  
Kimberly A. Forde ◽  
David S. Goldberg ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Chronic Liver Disease ◽  
Acute Liver Injury ◽  
Disease Status ◽  
Chronic Liver

scholarly journals Possible unrecognised liver injury is associated with mortality in critically ill COVID-19 patients

2021 ◽  
Vol 14 ◽  
pp. 175628482110234
Author(s):  
Mario Romero-Cristóbal ◽  
Ana Clemente-Sánchez ◽  
Patricia Piñeiro ◽  
Jamil Cedeño ◽  
Laura Rayón ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Chronic Liver Disease ◽  
Critically Ill ◽  
Cox Regression ◽  
Chronic Liver ◽  
Cox Regression Analysis ◽  
Risk Of Death ◽  
The Impact

Background: Coronavirus disease (COVID-19) with acute respiratory distress syndrome is a life-threatening condition. A previous diagnosis of chronic liver disease is associated with poorer outcomes. Nevertheless, the impact of silent liver injury has not been investigated. We aimed to explore the association of pre-admission liver fibrosis indices with the prognosis of critically ill COVID-19 patients. Methods: The work presented was an observational study in 214 patients with COVID-19 consecutively admitted to the intensive care unit (ICU). Pre-admission liver fibrosis indices were calculated. In-hospital mortality and predictive factors were explored with Kaplan–Meier and Cox regression analysis. Results: The mean age was 59.58 (13.79) years; 16 patients (7.48%) had previously recognised chronic liver disease. Up to 78.84% of patients according to Forns, and 45.76% according to FIB-4, had more than minimal fibrosis. Fibrosis indices were higher in non-survivors [Forns: 6.04 (1.42) versus 4.99 (1.58), p < 0.001; FIB-4: 1.77 (1.17) versus 1.41 (0.91), p = 0.020)], but no differences were found in liver biochemistry parameters. Patients with any degree of fibrosis either by Forns or FIB-4 had a higher mortality, which increased according to the severity of fibrosis ( p < 0.05 for both indexes). Both Forns [HR 1.41 (1.11–1.81); p = 0.006] and FIB-4 [HR 1.31 (0.99–1.72); p = 0.051] were independently related to survival after adjusting for the Charlson comorbidity index, APACHE II, and ferritin. Conclusion: Unrecognised liver fibrosis, assessed by serological tests prior to admission, is independently associated with a higher risk of death in patients with severe COVID-19 admitted to the ICU.

scholarly journals Chronic liver disease not a significant comorbid condition for COVID-19

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jiahao Lin ◽  
Bingting Bao ◽  
Nigar Anjuman Khurram ◽  
Kasey Halsey ◽  
Ji Whae Choi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Chronic Liver Disease ◽  
The United States ◽  
Postmortem Examination ◽  
Chronic Liver ◽  
Critical Groups ◽  
Comorbid Condition ◽  
Central Vein ◽  
Significant Difference

AbstractTo explore the role of chronic liver disease (CLD) in COVID-19. A total of 1439 consecutively hospitalized patients with COVID-19 from one large medical center in the United States from March 16, 2020 to April 23, 2020 were retrospectively identified. Clinical characteristics and outcomes were compared between patients with and without CLD. Postmortem examination of liver in 8 critically ill COVID-19 patients was performed. There was no significant difference in the incidence of CLD between critical and non-critical groups (4.1% vs 2.9%, p = 0.259), or COVID-19 related liver injury between patients with and without CLD (65.7% vs 49.7%, p = 0.065). Postmortem examination of liver demonstrated mild liver injury associated central vein outflow obstruction and minimal to moderate portal lymphocytic infiltrate without evidence of CLD. Patients with CLD were not associated with a higher risk of liver injury or critical/fatal outcomes. CLD was not a significant comorbid condition for COVID-19.

scholarly journals The Role of Iron and Iron Overload in Chronic Liver Disease

2016 ◽  
Vol 22 ◽  
pp. 2144-2151 ◽  
Author(s):  
Sandra Milic ◽  
Ivana Mikolasevic ◽  
Lidija Orlic ◽  
Edita Devcic ◽  
Nada Starcevic-Cizmarevic ◽  
...  
Keyword(s):  
Liver Disease ◽  
Iron Overload ◽  
Chronic Liver Disease ◽  
Chronic Liver

scholarly journals The Matrisome, Inflammation, and Liver Disease

2020 ◽  
Vol 40 (02) ◽  
pp. 180-188 ◽  
Author(s):  
Christine E. Dolin ◽  
Gavin E. Arteel
Keyword(s):  
Extracellular Matrix ◽  
Liver Disease ◽  
Fatty Liver ◽  
Chronic Liver Disease ◽  
Fatty Liver Disease ◽  
Chronic Liver ◽  
Disease Development ◽  
Disease States ◽  
Ecm Proteins

AbstractChronic fatty liver disease is common worldwide. This disease is a spectrum of disease states, ranging from simple steatosis (fat accumulation) to inflammation, and eventually to fibrosis and cirrhosis if untreated. The fibrotic stage of chronic liver disease is primarily characterized by robust accumulation of extracellular matrix (ECM) proteins (collagens) that ultimately impairs the function of the organ. The role of the ECM in early stages of chronic liver disease is less well-understood, but recent research has demonstrated that several changes in the hepatic ECM in prefibrotic liver disease are not only present but may also contribute to disease progression. The purpose of this review is to summarize the established and proposed changes to the hepatic ECM that may contribute to inflammation during earlier stages of disease development, and to discuss potential mechanisms by which these changes may mediate the progression of the disease.

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