The hyperdynamic circulation of cirrhosis and portal hypertension has been postulated to be due to the vasodilatory effects of nitric oxide. However, there have been conflicting results in adults and no studies in children. We aimed to measure the nitric oxide level in serum of pediatric patients with portal hypertension with and without cirrhosis, in order to assess its role in the development of hemodynamic changes. We measured nitric oxide levels in 41 pediatric patients (21 patients with intrahepatic portal hypertension and 20 with extrahepatic portal hypertension). The mean age of the study population was 11.2 +/- 4.6 years; 53 per cent were female. Twenty healthy children were included as a control group. Nitric oxide levels were measured by Boehringer-Mannheim colorimetric assay and the statistical significance was calculated by Kruskal-Wallis one-way ANOVA. Significantly higher nitric oxide levels were found in patients independent of the type of portal hypertension compared with the control group (29.4 +/- 6 in patients with intrahepatic portal hypertension, 29.5 +/- 5.8 in patients with extrahepatic portal hypertension, and 23.6 +/- 6.5 in the control group; p < 0.007). These data showed a difference between the groups and suggest that nitric oxide, predominantly independent of cirrhosis, plays a primary role in the pathogenesis of portal hypertension.
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http://dx.doi.org/10.1093/tropej/49.1.33 | DOI Listing |
Metab Brain Dis
January 2025
Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus N, Denmark.
Background & Aims: Hepatic encephalopathy (HE), one of the most serious prognostic factors for mortality in alcohol-related cirrhosis (ALD cirrhosis), is not recorded in Danish healthcare registries. However, treatment of HE with lactulose, the universal first-line treatment, can be identified through data on filled prescriptions. This study aimed to investigate if lactulose can be used as a surrogate marker of HE.
View Article and Find Full Text PDFAliment Pharmacol Ther
January 2025
Gastro Unit, Copenhagen University Hospital, Hvidovre, Denmark.
Expert Rev Gastroenterol Hepatol
January 2025
Department of Hepatology, Institute of Liver & Biliary Sciences, New Delhi.
Introduction: Acute kidney injury (AKI) in patients with acute-on-chronic liver failure (ACLF) is driven by the severity of systemic inflammation, acute portal hypertension driving circulatory dysfunction, hyperbilirubinemia, and toxicity of bile acids. The spectrum is mostly structural, associated with reduced response to vasoconstrictors. The progression is rapid and need of renal replacement therapy and extracorporeal therapies may be required for the management.
View Article and Find Full Text PDFMetab 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.
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