Ammonia is a byproduct of the metabolism of nitrogen-containing micro and macromolecules. The key source of bodily ammonia in humans is the small intestine, from diet, luminal bacterial activity, and deamination of glutamine in enterocytes. It is disposed of from the system, mainly in the liver, through the urea cycle. Physiologically, ammonia plays a minor role in acid-base homeostasis. It is the critical molecule implicated in the pathogenesis of hepatic encephalopathy. Liver disease is the most common cause of hyperammonemia, while others include urea cycle defects, infections, and drugs. The diagnostic utility of ammonia in liver diseases has met with increasing skepticism but holds good in urea cycle defects. Additionally, the accuracy of ammonia assay depends on a myriad of patient and technical factors, making the test unreliable if not performed meticulously. Most scientific societies currently fall short of recommending ammonia for diagnostic purposes in chronic liver disease. Despite this fact, ammonia continues to be one of the most frequently requested assays in patients with suspected hepatic encephalopathy, contributing to significant non-productive health expenditure. However, ammonia level does have a prognostic role in liver diseases, especially in acute liver failure. Ammonia-lowering strategies are the cornerstone of the management of hepatic encephalopathy. These strategies include medications that attenuate ammoniagenesis and ammonia scavengers. This review examines the role of ammonia in hepatic encephalopathy, its diagnostic and prognostic implications in liver diseases, challenges associated with ammonia assay, and current therapeutic strategies for ammonia-lowering in clinical practice.
Keywords: Ammonia; Cirrhosis; Encephalopathy; Hepatic; Hyperammonemia; Liver.
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