Purpose: To quantify the accumulation of superparamagnetic iron oxide (SPIO) in patients with and without liver cirrhosis using T2 and T2* mapping.
Materials And Methods: We enrolled 10 patients without liver cirrhosis and 30 patients with liver cirrhosis (Child-Pugh class A, n = 18; and B/C, n = 12). T2 and T2* mapping were performed before and after SPIO administration. The reductions in T2 (DeltaT2) and T2* (DeltaT2*) after SPIO administration were compared between the control and liver cirrhosis groups and the control, Child-Pugh A, and Child Pugh B/C groups.
Results: There were significant differences in DeltaT2 (22.2 +/- 4.4 and 15.1 +/- 7.0) and DeltaT2* values (24.3 +/- 3.3 and 16.8 +/- 8.1) (P = 0.005 and P < 0.001) between the control and the liver cirrhosis groups. There was a significant difference in the DeltaT2* between the Child-Pugh A and Child-Pugh B/C groups (P < 0.001) and in the DeltaT2 and DeltaT2* between the control and Child-Pugh B/C groups (P = 0.018 and P < 0.001).
Conclusion: DeltaT2 and DeltaT2* are significantly larger in patients without liver cirrhosis than those with liver cirrhosis. DeltaT2* is also significantly larger in Child-Pugh class A patients than those in Child-Pugh B/C.
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http://dx.doi.org/10.1002/jmri.22184 | DOI Listing |
Background And Aim: There is paucity of data about the prevalence of cirrhosis and portal hypertension in the US general population.
Methods: We used National Health and Nutrition Examination Surveys (NHANES 2017-2020) to estimate the prevalence of cirrhosis and clinically significant (CS)-portal hypertension in alcoholic liver disease (ALD), MetALD, viral hepatitis (VH) to include chronic hepatitis B (CHB) and chronic hepatitis C (CHC), and metabolic dysfunction-associated steatotic liver disease (MASLD). Cirrhosis was evaluated using liver stiffness measurement (LSM) by transient elastography or FIB-4 score; CS-portal hypertension was defined via LSM and platelet count or the use of non-selective beta-blockers in the presence of cirrhosis.
Hepatology
January 2025
Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA.
Background Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects about a third of adults worldwide and is projected soon to be the leading cause of cirrhosis. It occurs when fat accumulates in hepatocytes and can progress to metabolic dysfunction-associated steatohepatitis (MASH), liver cirrhosis, and hepatocellular carcinoma. MASLD pathogenesis is believed to involve a combination of genetic and environmental risk factors.
View Article and Find Full Text PDFHepatology
January 2025
AP-HP, Sorbonne Université, Liver Intensive Care Unit, Hepatogastroenterology Department, La Pitié-Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris 75013, France.
Background And Aims: In cirrhosis, some patients display acute encephalopathy without hyperammonemia (NonHep E) which is not considered as overt hepatic encephalopathy (OHE). We aimed to assess the prevalence and characteristics of NonHep E and OHE in cirrhotic patients displaying acute encephalopathy, assess their respective prognosis and compare it to other causes of acute decompensation (AD) with/without hyperammonemia.
Approach And Results: We conducted a retrolective analysis from a prospective cohort of patients hospitalized for AD.
Hepatol Commun
February 2025
Department of Anesthesiology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Background: Cell therapy demonstrates promising potential as a substitute therapeutic approach for liver cirrhosis. We have developed a strategy to effectively expand murine and human hepatocyte-derived liver progenitor-like cells (HepLPCs) in vitro. The primary objective of the present study was to apply HepLPCs to the treatment of liver cirrhosis and to elucidate the underlying mechanisms responsible for their therapeutic efficacy.
View Article and Find Full Text PDFHepatol Commun
February 2025
University Grenoble Alpes, Inserm U 1209, CNRS UMR 5309, Institute for Advanced Biosciences, Grenoble, France.
Background: Hepatitis B is a liver infection caused by HBV. Infected individuals who fail to control the viral infection develop chronic hepatitis B and are at risk of developing life-threatening liver diseases, such as cirrhosis or liver cancer. Dendritic cells (DCs) play important roles in the immune response against HBV but are functionally impaired in patients with chronic hepatitis B.
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