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Ammonia and beyond - biomarkers of hepatic encephalopathy.
Metab Brain Dis
January 2025
Fundación de Investigación Hospital Clínico Universitario de Valencia-INCLIVA, Valencia, 46010, Spain.
Ammonia is a product of amino acid metabolism that accumulates in the blood of patients with liver cirrhosis, leading to neurotoxic effects and hepatic encephalopathy (HE). HE manifestations can range from mild, subclinical disturbances in cognition, or minimal HE (mHE) to gross disorientation and coma, a condition referred to as overt HE. Many blood-based biomarkers reflecting these neurotoxic effects of ammonia and liver disease can be measured in the blood allowing the development of new biomarkers to diagnose cirrhosis patients at risk of developing HE.
View Article and Find Full Text PDFIntravascular Resuscitation Benefits Compared to Lactulose in Dehydration-Associated Pseudo-Hyperammonemia Causing Altered Mental Status.
Cureus
November 2024
Internal Medicine, Northeast Georgia Medical Center Gainesville, Gainesville, USA.
Article Synopsis
- Hyperammonemia, often caused by liver cirrhosis, is a key factor in encephalopathy cases, affecting patients' mental status.
- Treatment typically involves lactulose and rifaximin to manage ammonia levels.
- In a specific case, a patient with slightly elevated ammonia levels of 39 μmol/L recovered after 30 hours of fluid therapy, without the need for lactulose or rifaximin.
Down the road towards hepatic encephalopathy. Urea synthesis - the liver workhorse of nitrogen metabolism.
Metab Brain Dis
December 2024
Department of Hepatology and Gastroenterology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, Aarhus N, DK-8200, Denmark.
Urea synthesis is an irreversible, essential for maintenance of health and life, and highly regulated liver function with a very high capacity for production of the end-product urea-nitrogen. The set-point of urea synthesis in relation to its overall substrate, the prevailing blood concentration of L-α-amino acids, contributes to determine whole-body nitrogen balance and the size and composition of the plasma free amino acid pool. Ammonia is definitively eliminated from the body by urea synthesis.
View Article and Find Full Text PDFA transient blood IL-17 increase triggers neuroinflammation in cerebellum and motor incoordination in hyperammonemic rats.
J Neuroinflammation
November 2024
Laboratory of Neurobiology, Centro de Investigación Príncipe Felipe, Eduardo Primo-Yufera 3, 46012, Valencia, Spain.
Patients with liver cirrhosis may show minimal hepatic encephalopathy (MHE) with motor incoordination which is reproduced in hyperammonemic rats. Hyperammonemia induces peripheral inflammation which triggers neuroinflammation and enhanced GABAergic neurotransmission in cerebellum and motor incoordination. The mechanisms involved remain unknown.
View Article and Find Full Text PDFBlood ammonia concentration measurement - effects of sampling site and cirrhosis during induced hyperammonaemia.
Metab Brain Dis
November 2024
Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Background: Ammonia is implicated in hepatic encephalopathy (HE) and prognostic in cirrhosis. Venous ammonia concentration, yielding similar correlation with HE grades as arterial, has become the preferred practise but comparative data are limited.
Aim: To quantify effect of sampling site on ammonia concentration in healthy persons and patients with cirrhosis.
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