scholarly journals The role of elastography in the assessment of chronic liver disease in children

2019 ◽  
Vol 19 (3) ◽  
pp. 2806-2311
Author(s):  
Süleyman Sönmez ◽  
Merve Boşat ◽  
Nihal Yurtseven ◽  
Eray Yurtseven

Background: Conventional ultrasonography is a method preferred for the investigation of chronic liver diseases in pediatric groups, as it is non-invasive, cheap, feasible and available. The purpose of this study is to present the role of Share-wave Elastography (SWE) in terms of diagnostic value in children diagnosed with “chronic liver disease.”Methods: We studied patients who had been diagnosed with chronic liver disease between March 2012-September 2015, and who had undergone liver biopsy and had their pathology results, compared with 26 healthy subjects. Statistical analysis was performed with IBM SPSS Statistics for Windows, Version 20.0. “Pearson Correlation Analysis” was performed in order to measure the relationship between elastography values and Brunt level.Results: This study had 107 subjects in total, consisting of 81 patients between 0-204 months of age Pearson correlation coefficient level was determined as r = 0.644. Since the correlation coefficient is positive, there is a same-directional relationship between Elastography level and Brunt degree. This means that while one of the variables is increasing, the other one will also increase.Conclusion: Since it is known that development of hepatic fibrosis is a dynamic process, and that many hepatic fibrosis etiologies are known to continue throughout the course of life, the application of Real time SWE method instead of repeated liver biopsies on patients is a much simpler and smart method. Increasing the clinical use of Real Time SWE method with future studies might provide an opportunity for preventing unnecessary liver biopsies since the patients are evaluated in a shorter time and in a cost-effective manner.Keywords: Shear-Wave Elastography, Brunt degree, chronic liver disease, liver biopsy.

2002 ◽  
Vol 16 (10) ◽  
pp. 722-726 ◽  
Author(s):  
Jacqueline Laurin

Most cases of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are suspected on the basis of the exclusion of viral, autoimmune, metabolic and genetic causes of chronic liver disease in patients with chronic elevation of aminotransferase enzymes. However, the definitive diagnosis of NASH requires liver biopsy. Valuable blood tests include hepatitis B and C serology, iron profile, alpha 1-antitrypsin phenotype, ceruloplasmin, antinuclear antibody and antismooth muscle antibody, and serum protein electrophoresis. If these tests are negative or normal, and if there are no symptoms or signs of chronic liver disease, it is unlikely that a specifically treatable liver disease would be discovered at biopsy. The prevalence of NAFLD in the general population appears to be approximately 20%, and 2% to 3% of people have NASH. There is no proven specific therapy for the spectrum of nonalcoholic liver disease; therefore, the management of the patient with NASH is not likely to be changed after histological assessment. Bleeding, sometimes fatal, and other complications requiring hospitalization can occur, and liver biopsies should not be undertaken without clear clinical indications. The high cost of undertaking histological assessment of all persons with asymptomatic elevations of liver enzymes cannot be justified in view of the risks and limited clinical benefits.


2012 ◽  
Vol 303 (4) ◽  
pp. G498-G506 ◽  
Author(s):  
Jörn M. Schattenberg ◽  
Michael Nagel ◽  
Yong Ook Kim ◽  
Tobias Kohl ◽  
Marcus A. Wörns ◽  
...  

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.


2021 ◽  
Vol 85 (2) ◽  
pp. 3967-3974
Author(s):  
Soumaya E. Hadhod ◽  
Mohamed Z.A. Mourad ◽  
Ashraf M. Radwan ◽  
Omar A.A. Ahmed

2014 ◽  
Vol 146 (5) ◽  
pp. S-737-S-738
Author(s):  
Juan Putra ◽  
Christopher Hartley ◽  
Kirsten J. Pierce ◽  
Christopher H. Chang ◽  
Arifa Toor ◽  
...  

Author(s):  
Hyo Jung Cho ◽  
Jaewon Choi ◽  
Bohyun Kim ◽  
JeongGil Ko ◽  
Joon-Il Choi ◽  
...  

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

2020 ◽  
Vol 40 (02) ◽  
pp. 180-188 ◽  
Author(s):  
Christine E. Dolin ◽  
Gavin E. Arteel

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.


Sign in / Sign up

Export Citation Format

Share Document