Surveillance for early detection of hepatocarcinoma (HCC) in patients with cirrhosis is widely accepted. In a cohort of 141 patients with cirrhosis collected during the year 1995, we conducted a surveillance program by performing liver ultrasonography and blood alpha-foetoprotein measurement every 6 months. The median follow-up was 34 months. This study addressed to two questions: the compliance to the surveillance schedule according to the aetiology of cirrhosis and the results in terms of emergence of HCC and outcome. Aetiology of cirrhosis was alcohol-induced in 86 (61%), HCV-related in 30 (21%) and from other origins in 25 (18%). Compliance to the program schedule was good in patients with HCV-related cirrhosis (29/30--97%) and patients with cirrhosis of "other origins" (20/25--80%) but was poor in patients with alcoholic cirrhosis (45/86--52%). The lack of compliance was significantly linked to the failure to achieve alcohol abstinence. During follow-up, 6 HCC lesions were observed in 6 male patients with median age of 68 years. All 6 HCC were single nodule, less than 4 cm and accessible to percutaneous acetic acid injection. Nevertheless, the outcome was disappointing, four patients dying 3-15 months later (median: 8 months), two of them with extensive HCC. One of the two patients still alive developed extensive HCC, 36 months after percutaneous acetic acid injection.
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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.
Hepatol Commun
February 2025
Department of Surgery, University of California, San Francisco, San Francisco, California, USA.
Background: Rho-associated kinases 1 and 2 (ROCK1 and ROCK2) regulate critical cell functions, including actomyosin contractility, apoptosis, and proliferation. Some studies suggest that ROCK inhibition may serve as a treatment for liver fibrosis. More investigation is needed to understand the role of hepatocyte ROCK signaling in vivo, especially in the context of profibrotic liver injury.
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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January 2025
Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
This study aimed to investigate the correlation of the increased volume index of epicardial adipose tissue (EAT) and left ventricular hypertrophy (LVH) in patients with Hypertension (HTN). A total of 209 HTN patients and 50 healthy controls, who underwent cardiovascular magnetic resonance (CMR) at two medical centers in China between June 2015 and October 2024, were enrolled for this study. Postprocessing and imaging analysis were conducted and EAT measurements were performed.
View Article and Find Full Text PDFBiochem Cell Biol
January 2025
Department of Histology and Embryology, School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, China.
Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible lung disease with high mortality and limited treatment options. While single-dose bleomycin-induced models are commonly used to investigate the pathogenesis of IPF, they fail to adequately replicate the complex pathological features in human patients, thereby hindering comprehensive investigations. Previous studies utilizing repetitive bleomycin injections have demonstrated a closer resemblance to human IPF pathology; however, the time- and resource-intensive nature of this approach presents significant drawbacks.
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