Non-hepatic Hyperammonemia: A Potential Therapeutic Target for Sepsis-associated Encephalopathy.

Abstract

Sepsis-Associated Encephalopathy (SAE) is a common complication in the acute phase of sepsis, and patients who develop SAE have a higher mortality rate, longer hospital stay, and worse quality of life than other sepsis patients. Although the incidence of SAE is as high as 70% in sepsis patients, no effective treatment is available for this condition. To develop an effective treatment for SAE, it is vital to explore its pathogenesis. It is known that hyperammonemia is a possible factor in the pathogenesis of hepatic encephalopathy as ammonia is a potent neurotoxin. Furthermore, our previous studies indicate that non-hepatic hyperammonemia seems to occur more often in sepsis patients; it was also found that >50% of sepsis patients with non-hepatic hyperammonemia exhibited encephalopathy and delirium. Substatistical analyses indicate that non-hepatic hyperammonemia is an independent risk factor for SAE. This study updates the definition, clinical manifestations, and diagnosis of SAE; it also investigates the possible treatment options available for non-hepatic hyperammonemia in patients with sepsis and the mechanisms by which non-hepatic hyperammonemia causes encephalopathy.

• Authors: Lina Zhao, Yun Li, Yunying Wang, Zengzheng Ge, Huadong Zhu, Xiuhua Zhou, Yi Li
• Journal: CNS & neurological disorders drug targets (CNS Neurol Disord Drug Targets) Vol. 21 Issue 9 Pg. 738-751 ( 2022) ISSN: 1996-3181 [Electronic] United Arab Emirates
• PMID: 34939553 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright© Bentham Science Publishers; For any queries, please email at [email protected].

Topics

• Hepatic Encephalopathy (complications, therapy)
• Humans
• Hyperammonemia (complications)
• Quality of Life
• Sepsis (complications, pathology)
• Sepsis-Associated Encephalopathy (complications, therapy)