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McArdle's Syndrome with Previously Unreported Electrocardiographic and Serum Enzyme Abnormalities

GERALD RATINOV; WILLIAM P. BAKER; and KENNETH F. SWAIMAN, M.D.
Ann Intern Med. 1965;62(2):328-335. doi:10.7326/0003-4819-62-2-328
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This excerpt has been provided in the absence of an abstract.

In 1951, a metabolic myopathy due to deficient glycogen breakdown in skeletal muscle was described by McArdle (1). The responsible enzymatic deficiency in similar cases was not demonstrated until 1959. Pearson and associates (2-4) and Schmid and associates (5-7) demonstrated an absence of muscle phosphorylase in their cases. Since then several cases have been reported by various authors (8-12).

This inborn error leads to insufficient glycogenosis and relative lack of formation of products of anaerobic metabolism. The serum lactic acid does not increase, and it may even decrease during exercise under these circumstances. This response to exercise is a simple

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Oxidative stress and Nrf2 signaling in McArdle disease. Mol Genet Metab 2013;110(3):297-302.
McArdle's disease: a clinical review and case report. Tenn Med 2013 Nov-Dec;106(10):33, 37.
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