ArticleHepatology communications2024
Activation of the kynurenine pathway identified in individuals with covert hepatic encephalopathy.
Article in Hepatology communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Serotonin, Kynurenine, and Indole Pathways of Tryptophan Metabolism in Humans in Health and Disease.Nutrients · 2026Review
- Development of a tryptophan metabolomics-based diagnostic model for hepatic encephalopathy in liver cirrhosis.European journal of medical research · 2026Article
- Modulation of the Kynurenine Pathway in Obese Mexican Navy Women Following a Structured Weight Loss Program: A Pre-Post-Intervention Study.Nutrients · 2026Article
- Gut microbiome and its metabolites in liver cirrhosis: mechanisms and clinical implications.Frontiers in cellular and infection microbiology · 2025Review
- Renal and hepatic function is preserved following inducible knockout of kynurenine pathway enzymes KMO or QPRT in adult mice.PloS one · 2025Article
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12 authors.
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Abstract
backgroundHE is a neuropsychiatric complication of liver disease characterized by systemic elevation in ammonia and proinflammatory cytokines. These neurotoxins cross the blood-brain barrier and cause neuroinflammation, which can activate the kynurenine pathway (KP). This results in dysregulated production of neuroactive KP metabolites, such as quinolinic acid, which is known to cause astrocyte and neuronal death. Our aim was to compare KP activity between patients with covert HE (CHE), patients without encephalopathic cirrhosis (NHE), and healthy controls (HCs).
methodsThis was a single-center prospective cohort study conducted between 2018 and 2021 at St Vincent's Hospital, Sydney. Overall, 13 patients with CHE, 10 patients with NHE, and 12 with HC were recruited. Patients with cirrhosis were diagnosed with CHE if they scored ≤-4 on the Psychometric Hepatic Encephalopathy Score. KP metabolite levels were quantified on plasma samples via HPLC and gas chromatography/mass spectrometry. One-way Kruskal-Wallis test was used to compare the expression levels of KP enzymes.
resultsKP was highly activated in patients with cirrhosis, demonstrated by higher levels of activity in the rate-limiting enzymes, indoleamine 2,3-dioxygenase, and tryptophan-2,3-dioxygenase in both CHE (65.04±20.72, p=0.003) and patients with NHE (64.85±22.10, p=0.015) compared to HC (40.95±7.301). Higher quinolinic acid concentrations were demonstrated in CHE (3726 nM±3385, p<0.001) and patients with NHE (1788 nM±632.3, p=0.032) compared to HC (624 nM±457). KP activation was positively correlated with inflammatory marker C-reactive protein in patients with CHE (Rs=0.721, p≤0.01).
conclusionsKP is highly activated in patients with CHE, resulting in heightened production of neurotoxic metabolites. Dysregulation of the pathway is demonstrable in patients who do not yet show clinical signs of neurocognitive impairment. Therapeutic agents that modulate KP activity may be able to alleviate symptoms of patients with CHE.
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