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Manganese and chronic hepatic encephalopathy
D Krieger1, S Krieger, O Jansen
1Department of Neurology, Ruprecht-Karls University of Heidelberg, Germany.
Lancet (London, England)
|July 29, 1995
Summary
Manganese (Mn) accumulates in the basal ganglia of patients with liver failure, potentially causing neurotoxicity. This metal buildup may play a role in chronic hepatic encephalopathy, suggesting new therapeutic avenues.
Area of Science:
- Neuroscience
- Hepatology
- Toxicology
Background:
- Clinical observations and animal studies suggest a link between elevated blood manganese (Mn) and basal ganglia accumulation in end-stage liver disease.
- Chronic hepatic encephalopathy (CHE) is a neuropsychiatric syndrome associated with liver failure, with unclear underlying mechanisms.
Purpose of the Study:
- To investigate manganese (Mn) accumulation in the basal ganglia of patients with liver failure.
- To explore the potential role of Mn in the pathogenesis of chronic hepatic encephalopathy (CHE).
Main Methods:
- Magnetic resonance imaging (MRI) was used to study ten patients with liver failure and ten controls.
- Measurement of Mn concentrations in whole blood and brain tissue samples from patients and controls.
Main Results:
- Significantly increased whole blood Mn concentrations were observed in patients with liver cirrhosis compared to controls (34.4 µg/L vs 10.3 µg/L).
- Pallidal signal intensity on MRI correlated with blood Mn levels (Rs = 0.8, p = 0.0058).
- Brain tissue analysis revealed highest Mn concentrations in the caudate nucleus, followed by the quadrigeminal plate and globus pallidus.
Conclusions:
- Manganese (Mn) demonstrably accumulates within the basal ganglia in patients with liver cirrhosis.
- The findings suggest Mn neurotoxicity may contribute to the pathogenesis of chronic hepatic encephalopathy (CHE).
- Further research into chelating agents as a therapeutic strategy for CHE is warranted.