Hepatic small vessel neoplasia (HSVN) is a recently recognized hemangioma of the liver with uncertain malignant potential. Almost all the patients are asymptomatic. Budd-Chiari syndrome (BCS) is a rare disorder characterized by noncardiogenic hepatic venous outflow obstruction. Benign hepatocellular nodules have been acknowledged for a long time in the liver with the chronic BCS. However, there has been no case report of BCS associated with HSVN. The patient was diagnosed with BCS 13 years ago. The imaging test initially displayed multiple hepatic nodules that were suspected of benign hepatocellular nodules. They gradually increased in size and number in the course of the disease. At an autopsy, these nodules were confirmed to be multifocal HSVN. The tumor of the present case could not be proved to have GNAQ and GNQ14 mutations. We describe the case focusing on the chronological imaging changes and discuss on the relationship between BCS and HSVN.
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http://dx.doi.org/10.1007/s00428-023-03505-w | DOI Listing |
Ann Surg Oncol
January 2025
Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The Jikei University School of Medicine, Tokyo, Japan.
Background: AT-rich interaction domain 4B (ARID4B) is a transcriptional activator that regulates the phosphatidylinositol 3-kinase (PI3K)/AKT pathway in prostate cancer. However, the role of ARID4B in hepatocellular carcinoma (HCC) has remained unclear.
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Curr Atheroscler Rep
January 2025
Carbohydrate and Lipid Metabolism Research Unit, Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa.
Purpose Of Review: Homozygous familial hypercholesterolaemia (HoFH) is characterized by marked elevation of low-density lipoprotein cholesterol (LDLC) and premature atherosclerotic cardiovascular disease. This is a review of novel pharmacological therapies to lower LDLC in patients with HoFH.
Recent Findings: Novel therapies can be broadly divided by whether their efficacy is dependent or independent of residual low-density lipoprotein receptor (LDLR) function.
Nat Commun
January 2025
Department of General Surgery, West China Hospital, Sichuan University, Chengdu, China.
Metabolic reprogramming fuels cancer cell metastasis and remodels the immunosuppressive tumor microenvironment (TME). We report here that circPETH, a circular RNA (circRNA) transported via extracellular vesicles (EVs) from tumor-associated macrophages (TAMs) to hepatocellular carcinoma (HCC) cells, facilitates glycolysis and metastasis in recipient HCC cells. Mechanistically, circPETH-147aa, encoded by circPETH in an m6A-driven manner, promotes PKM2-catalyzed ALDOA-S36 phosphorylation via the MEG pocket.
View Article and Find Full Text PDFAm J Pathol
December 2024
The Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical Science, Changsha, Hunan, 410013 China. Electronic address:
The pathogenesis of Alcohol-associated liver disease (ALD) is complex, involving ethanol-induced enhancement of gut permeability results in the release of bacterial products from the intestine. This triggers intrahepatic inflammation and liver damage, with hepatic macrophages playing key roles in the inflammatory response to alcohol. SIRT7 a NAD-dependent type III histone deacetylase, is being recognized as a potential therapeutic target in various human diseases including cancer.
View Article and Find Full Text PDFJ Agric Food Chem
January 2025
College of Food Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.
The effect of konjac glucomannan (KGM) on lipid absorption is related to the viscosity effect and hepatic lipid synthesis. However, the molecular mechanism of regulation of intestinal lipid absorption by KGM and its correlation with gut microbiota have not been studied. This study explored the effects of KGM and degradation products of KGM (DKGM) on intestinal lipid absorption and output in obese mice and their potential mechanisms.
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