Iron In Intracerebral Injury

[ironjustice]

Thrombin and hemin as central factors in the mechanisms of
intracerebral hemorrhage-induced secondary brain injury and as
potential targets for intervention.
Babu R, Bagley JH, Di C, Friedman AH, Adamson C.
Neurosurg Focus. 2012 Apr
32(4):E8. doi: 10.3171/2012.1.FOCUS11366.
Division of Neurosurgery, Department of Surgery,
Duke University Medical Center, Durham, NC, USA.

Abstract
Intracerebral hemorrhage (ICH) is a subtype of stoke that may cause
significant morbidity and mortality.
Brain injury due to ICH initially occurs within the first few hours as
a result of mass effect due to hematoma formation.
However, there is increasing interest in the mechanisms of secondary
brain injury as many patients continue to deteriorate clinically
despite no signs of rehemorrhage or hematoma expansion.
This continued insult after primary hemorrhage is believed to be
mediated by the cytotoxic, excitotoxic, oxidative, and inflammatory
effects of intraparenchymal blood.
The main factors responsible for this injury are thrombin and
erythrocyte contents such as hemoglobin.
Therapies including thrombin inhibitors, N-methyl-D-aspartate
antagonists, chelators to bind free iron, and antiinflammatory drugs
are currently under investigation for reducing this secondary brain
injury.
This review will discuss the molecular mechanisms of brain injury as a
result of intraparenchymal blood, potential targets for therapeutic
intervention, and treatment strategies currently in development.

PMID:22463118


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