Severe myopathy in patients with thyrotoxicosis.

Myopathy, including muscle weakness, is not rare in patients with thyrotoxicosis ( 1 ). While the precise mechanism of the myopathy associated with Graves' disease is not known, several hypotheses are reported. Some patients show myoskeletal disorders from an autoimmune mechanism. One of the most important states is disorder of neuromuscular junction, observed in the patients with myasthenia gravis and EatonLamburt syndrome. It is reported that the anti-acetylcholine receptor antibodies that occur in myasthenia gravis are comparable to the anti-TSH receptor antibodies found in Graves' disease. It has been found that thyroglobulin and acetylcholinesterase share epitopes recognized by B cells, and that antibodies to either antigen cross-react with the other. Somepatients whosuffer from non-organ-specific autoimmunediseases , such as systemic lupus erythematosus (SLE) and progressive systemic sclerosis (PSS), show inflammatory damages of neural junctions in central nervous system, resulting in the neurological asthenia, which is accentuated in the presence of Graves ' hyperthyroidism (2). However, whether the anti-TSH receptor antibodies, immunoglobulins which interact not only with TSH receptor but also with other componentsof nervous system, directly affect the neuronal and neuro-muscular junction is not known (3). Another mechanism of abnormal muscle function is a setting disorder of cell membranepotential, which comes from an abnormalelectrolyte metabolismin the patients with Graves' disease. In Asia, periodic paralysis observed in patients with Graves' disease is lmore common(4). It has been speculated that the augmentation of synthesis of membraneNa+-K+ activated ATPase is related to the mechanism of paralytic myopathy. However, the exact mechanismof this type of myopathy is not certain(5). Some patients with Graves' hyperthyroidism showhypercalcemia and hypomagnessemia.These electrolyte disorders may also be related to the occurrence of muscle weakness and myopathy through the disturbance of cell membrane potential setting. However, the patients who have abnormal levels of these electrolytes do not necessarily showmyopathy. Thus, the mechanism of this myopathy could be induced by the combination of other factors which are generated in Graves ' hyperthyroidism. As is well known, neurological disturbances are frequently observed in patients with thyrotoxicosis. Myopathy, independent from neurological disorder, also is knownas one of the symptomsof thyrotoxicosis. Noto and his coworkers reported a case with dysphagia associated with thyrotoxicosis (6). See also p 472.