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Calcium Content of RBCs From Patients With Amyotrophic Lateral Sclerosis
Mark T. Felmus, MD, PhD;
Chaudri G. Rasool, PhD;
Walter G. Bradley, DM, FRCP
Arch Neurol. 1982;39(7):454.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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A lthough the cause of amyotrophic lateral sclerosis (ALS) remains unknown, several studies indicate that aberrant calcium metabolism may play a pathogenetic role in some patients.1-4 Theoretically, calcium could exert its deleterious effect on anterior horn cell enzymatic systems that are either deficient in quantity or abnormal in activity. Alternatively, anterior horn cell membrane structure and function may be altered, allowing increased calcium influx into neurons with subsequent cell death.
Neuromuscular syndromes similar to, but not identical to, classic ALS have been described in association with hyperparathyroidism.1,2 Presumably, abnormal calcium metabolism is integrated in the pathogenesis of these neuromuscular complications. Furthermore, Mallette and co-workers3 have found abnormal calcium metabolism in ALS that was not associated with parathyroid disease. Bone disorders also have been noted in association with ALS,3-6 possibly reflecting abnormal sequestration, storage, and release of calcium, as well as other heavy metals, since the major
. . . [Full Text PDF of this Article]
Author Affiliations
From the Department of Neurology, Tufts— New England Medical Center, Boston.
Footnotes
Accepted for publication July 21, 1981.
Reprint requests to Department of Neurology, Tufts—New England Medical Center, 171 Harrison Ave, Boston, MA 02111 (Dr Bradley).
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