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3-Methylhistidhe excretion in myotonic dystrophy

From the Departments of Neurology and Medicine (Drs. Griggs and Moxley), Pediatrics (Drs. Griggs, Moxley, and Forbes), and Radiation Biology and Biophysics (Dr. Forbes), University of Rochester School of Medicine and Dentistry, Rochester, NY.

3-Methylhistidine (3-MH) excretion reflects the rate of muscle protein catabolism, since 3-MH occurs almost exclusively in muscle actin and myosin and is not reutilized or catabolized. We studied 3-MH excretion in 9 patients with myotonic dystrophy, 8 normals, and 10 disease controls with Duchenne dystrophy and other disorders. 3-MH excretion was expressed relative to muscle mass as determined by both urinary creatinine and total body potassium (⁴⁰K method). Absolute 3-MH excretion was decreased in myotonic dystrophy patients but was normal when related to muscle mass. The finding of normal 3-MH excretion in myotonic dystrophy suggests that the muscle wasting in this disorder results from impaired anabolic processes rather than accelerated muscle destruction.

Address correspondence and reprint requests to Dr. Griggs, Department of Neurology, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, P.O. Box 673, Rochester, NY 14642.

Accepted for publication February 21, 1980.

Supported in part by grants from the Muscular Dystrophy Association, US. Public Health Service Grant RR 00044 from the Division of Research Resources of the National Institutes of Health, and by grants from the NIH, National Institute of Arthritis, Metabolism, and Digestive Diseases AM 22048; and NICHHD 18454. A portion of this work was performed under contract number DE-AC02–76EVO3490 with the U.S. Department of Energy at the University of Rochester, Department of Radiation Biology and Biophysics, and has been assigned report number UR 3490–1820.

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