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April 30, 2019; 92 (18) Editorial

Haptoglobin and hemoglobin in subarachnoid hemorrhage

A tale of 2 globins

R. Loch Macdonald, Mira Katan
First published April 5, 2019, DOI: https://doi.org/10.1212/WNL.0000000000007399
R. Loch Macdonald
From the Division of Neurosurgery (R.L.M.), St. Michael's Hospital, Labatt Family Centre of Excellence in Brain Injury and Trauma Research, Keenan Research Centre for Biomedical Research and Li Ka Shing Knowledge Institute, St. Michael's Hospital, Department of Surgery, University of Toronto, Ontario, Canada; and Stroke Center (M.K.), Department of Neurology, University Hospital of Zurich, Switzerland.
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Mira Katan
From the Division of Neurosurgery (R.L.M.), St. Michael's Hospital, Labatt Family Centre of Excellence in Brain Injury and Trauma Research, Keenan Research Centre for Biomedical Research and Li Ka Shing Knowledge Institute, St. Michael's Hospital, Department of Surgery, University of Toronto, Ontario, Canada; and Stroke Center (M.K.), Department of Neurology, University Hospital of Zurich, Switzerland.
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Haptoglobin and hemoglobin in subarachnoid hemorrhage
A tale of 2 globins
R. Loch Macdonald, Mira Katan
Neurology Apr 2019, 92 (18) 831-832; DOI: 10.1212/WNL.0000000000007399

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Although the incidence is declining, subarachnoid hemorrhage (SAH) continues to exact a substantial toll on society, with an estimated 20,000 aneurysmal SAHs (aSAHs) a year in the United States.1 Outcomes have improved, but the mortality remains ≈35%, and half of the survivors cannot return to their previous level of functioning.2 The most important prognostic factors for outcome are the neurologic condition of the patient on admission to hospital, the patient’s age, and preexisting hypertension.3 aSAH has a unique biphasic course, with initial or early brain injury (reflected in the neurologic condition) and a delayed phase of brain injury called delayed cerebral ischemia (DCI). Subarachnoid blood and specifically the erythrocytes and their main content, hemoglobin, appear to mediate DCI in humans. Extravascular free hemoglobin and iron released from it, whether into the CSF or the brain, are highly inflammatory and cytotoxic oxidants.4 The body has developed ways to mitigate this, including synthesis of haptoglobin, which binds free hemoglobin, abrogating its toxicity. Therefore, clearing away the hemoglobin more quickly or preventing its deleterious effects by binding hemoglobin may decrease brain injury and improve patient outcomes from SAH.

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  • Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

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  • © 2019 American Academy of Neurology
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