Portal hypertensive gastropathy (PHG) is the term used to describe the endoscopic appearance of gastric mucosa seen in patients with cirrhotic or non-cirrhotic portal hypertension with a characteristic mosaic-like pattern with or without red spots. The prevalence of PHG varies from 50% to 98%, this variation of the prevalence being perhaps related to patient selection, inter- and intra-observer variation and absence of uniform criteria and classification. About 8% of the upper digestive hemorrhages in the cirrhotic patients are secondary to PHG. There is no general consensus on the endoscopic classification of PHG (the most New Italian Endoscopy Club). The exact pathogenesis of PHG is not completely understood, but the portal hypertension is the main factor involved in its development and not the severity of the hepatic disease. Gastric Antral Vascular Ectasia (GAVE) is a term used for the typical endoscopic findings of red stripes, separated by normal mucosa, most frequently seen in the gastric antrum or proximal stomach. Current therapy of PHG includes beta blockers, somatostatin and derivates, endoscopic and surgical methods including hepatic transplantation.
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Metab Brain Dis
January 2025
Institute of Liver and Biliary Sciences, New Delhi, India.
Hepatic encephalopathy (HE) is traditionally associated with hepatic parenchymal diseases, such as acute liver failure and cirrhosis. Its prevalence in non-cirrhotic portal hypertension (NCPH) patients, extrahepatic portal vein obstruction (EHPVO), and non-cirrhotic portal fibrosis (NCPF) is less well described. HE in NCPH allows one to study the effect of portosystemic shunting and ammonia without significant hepatic parenchymal injury.
View Article and Find Full Text PDFHepatology
February 2025
Department of Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria.
Background And Aims: Around 750,000 patients per year will be cured of HCV infection until 2030. Those with compensated advanced chronic liver disease remain at risk for hepatic decompensation and de novo HCC. Algorithms have been developed to stratify risk early after cure; however, data on long-term outcomes and the prognostic utility of these risk stratification algorithms at later time points are lacking.
View Article and Find Full Text PDFPNAS Nexus
January 2025
Faculty of Medicine and Dentistry, William Harvey Research Institute, Barts and The London, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Metabolic dysfunction-associated steatotic liver disease (MASLD), hepatic fibrosis, and portal hypertension constitute an increasing public health problem due to the growing prevalence of obesity and diabetes. C-type natriuretic peptide (CNP) is an endogenous regulator of cardiovascular homeostasis, immune cell reactivity, and fibrotic disease. Thus, we investigated a role for CNP in the pathogenesis of MASLD.
View Article and Find Full Text PDFJ Clin Gastroenterol
November 2024
Departments of Gastroenterology.
Introduction And Objectives: The portal vein pressure higher than 10 mm Hg in patients with hepatic cirrhosis is more likely to have serious complications and poor prognosis. Nonselective receptor blockers (NSBBs) can reduce the portal vein pressure; however, the efficacy and safety of different NSBBs in reducing portal vein pressure were unconsistent. A systematic review and meta-analysis was conducted to evaluate the efficacy and safety of carvedilol versus propranolol in reducing portal vein pressure in this study.
View Article and Find Full Text PDFJ Transl Med
January 2025
Department of General Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No.1, Minde Road, Nanchang, 330006, Jiangxi, China.
Background: HCC is characterized by a high interstitial fluid pressure (HIFP) environment, which appears to support cancer cell survival. However, the mechanisms behind this phenomenon are not fully understood.
Methods: This study investigates the role of kinesin family member 11 (KIF11) in HCC under HIFP conditions, using both in vivo and in vitro models.
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