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NEUROLOGY 1983;33:784
© 1983 American Academy of Neurology

Exercising muscle does not produce hypoxanthine in adenylate deaminase deficiency

Victor H. Patterson, MB, MRCP, Kenneth K. Kaiser, BS and Michael H. Brooke, MD

Department of Neurology, Washington University School of Medicine, St. Louis, MO.

The failure of forearm exercise to increase plasma hypoxanthine in subjects with adenylate deaminase deficiency confirms this enzyme's role in hypoxanthine production by normal forearm exercise. The conversion of adenosine monophosphate (AMP) to hypoxanthine may reflect an alternative method of adenosine triphosphate (ATP) regeneration in working muscle.

Address correspondence and reprint requests to Dr. Brooke, Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110.

This work was supported by a Center Grant from the Muscular Dystrophy Association. Dr. Patterson is an MDA Clinical Fellow.

Presented in part at the thirty-fourth annual meeting of the American Academy of Neurology, Washington, DC, April 1982.

Accepted for publication September 14, 1982.