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Decreased serum hepcidin concentration correlates with brain iron deposition in patients with HBV-related cirrhosis

Dong Lin1, Jing Ding, Jian-Ying Liu

  • 1Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.

Plos One
|June 19, 2013
PubMed

Insights

Decreased serum hepcidin levels in hepatitis B virus (HBV)-related cirrhosis patients correlate with increased brain iron accumulation. This suggests hepcidin may be a biomarker for brain iron deposition.

Area of Science:

  • Neuroscience
  • Hepatology
  • Biochemistry

Background:

  • Excessive brain iron accumulation is linked to cognitive decline in hepatitis B virus (HBV)-related cirrhosis.
  • The precise mechanism behind this iron accumulation is not fully understood.
  • Hepcidin, a peptide hormone produced by the liver, is crucial in regulating systemic iron metabolism and is implicated in iron disorders, particularly liver diseases.

Purpose of the Study:

  • To investigate the relationship between brain iron content and serum hepcidin levels in patients with HBV-related cirrhosis.
  • To explore potential mechanisms linking liver disease, systemic iron regulation, and brain iron deposition.

Main Methods:

  • Quantified brain iron content using susceptibility weighted phase imaging in 70 HBV-related cirrhotic patients and 40 healthy controls.
  • Measured serum hepcidin and other iron parameters (serum iron, transferrin, ferritin, etc.) in a subset of patients and controls.
  • Employed Pearson correlation analysis to assess relationships between brain iron and serum hepcidin/iron parameters.

Main Results:

  • HBV-related cirrhotic patients exhibited increased brain iron in regions including the red nucleus, substantia nigra, thalamus, caudate, and putamen compared to controls.
  • Cirrhotic patients showed significantly lower serum hepcidin, lower transferrin, and higher transferrin saturation.
  • Serum hepcidin negatively correlated with iron in the right caudate, while ferritin positively correlated with iron in the bilateral putamen.

Conclusions:

  • Reduced serum hepcidin levels are associated with excessive iron accumulation in the basal ganglia of HBV-related cirrhotic patients.
  • Systemic iron overload appears to underlie regional brain iron deposition in these patients.
  • Serum hepcidin may serve as a valuable clinical biomarker for detecting brain iron deposition and holds potential therapeutic implications.
Abstract

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