Abstract
The classical findings which Askanazy (1) reported in 1898 continue to stimulate the study of disorders of muscle metabolism associated with Graves’ disease. Askanazy described the widespread degenerative atrophy of muscle cells with fatty infiltration, loss of striation, vacuolization and degeneration of the nuclei confined to striated muscle which included the extrinsic muscles of the eyeball. Confirmation of the disturbance in muscle metabolism associated with the thyrotoxic state was obtained by Shaffer (2), Hunter (3) and Palmer (4, 5) who observed a spontaneous creatinuria in this disease. This was similar to the creatinuria produced by thyroid feeding which was reported as early as 1912 by Krause, and later by Gross and Steenbock (7) and Carson (8). Iodine administration seemed to have little effect upon this artificially produced creatinuria (Carson, 8), although in Graves’ disease iodine treatment reduced the creatinuria (Palmer et al, 5). Asthenia, symptoms of muscular weakness and occasionally ...
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