Serum Ferritin and Metal Levels as Risk Factors for Amyotrophic Lateral Sclerosis



Muddasir Qureshi*, 1, 2, Robert H Brown Jr2, 3, Jack T Rogers4, Merit E Cudkowicz1, 2
1 Neurology Clinical Trials Unit; Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA
2 Department of Neurology; Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA
3 Day Neuromuscular Research Laboratory; Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA
4 Department of Psychiatry-Neuroscience, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA


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© Qureshi et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/ which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Massachusetts General Hospital, Building 149, 13th Street, Room 2274, Charlestown, MA 02129, USA; Tel: 617-726-9095; E-mail: mqureshi@partners.org


Abstract

Metal toxicity has been identified as a possible risk factor for amyotrophic lateral sclerosis (ALS) and other neurodegenerative disorders. We conducted a retrospective chart review of urinary, hair and blood metal levels and serum ferritin in 321 people with ALS seen over a ten-year period at the Massachusetts General Hospital (MGH). We found that hair lead levels and serum ferritin levels were elevated in ALS patients compared to published normal values. Metal levels of arsenic, lead, mercury, cadmium, thallium, cobalt and aluminum in 24-hour urine specimens and lead, mercury and arsenic in serum were within the normal range. We conclude that twenty-four hour urine or blood testing for metals is not warranted as part of the evaluation of ALS. Elevated levels of serum ferritin in ALS population could reflect an underlying perturbation in iron metabolism.