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Antibodies against saline-soluble components of skeletal muscle in myasthenia gravis

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Summary

Antibodies against phosphate-buffered-saline extracts (SE) of non-acetylcholine receptor (AChR) skeletal muscle antigens were found in patients with myasthenia gravis (MG). The antigenicity of SE was distributed in three fractions with molecular masses of over 200 kDa, 90–150 kDa and 7–14 kDa on gel filtration. These fractions shared common antigenicities. Further analysis of 90–150 kDa fractions on sodium dodecyl sulphate polyacrylamide gel electrophoresis showed five major bands, ranging from 105 kDa to 275 kDa. The antibodies against SE were detected in 52% (58/112) of the MG patients; incidence and titres were higher in the thymoma group (n=21; 90% and 0.872 respectively) than in the non-thymoma group (n=91; 43% and 0.200, P<0.001). In patients without a thymoma, these antibodies were frequently observed in late-onset disease and the severe generalized form (P<0.01). In 4 of 7 ocular MG patients without anti-AChR antibodies, low but appreciable levels of anti-SE antibodies were found. In 73% (11/15) of generalized MG patients treated with prednisolone and thymectomy, anti-SE antibody titres changed in association with those of anti-AChR antibodies and with the clinical course. Both antibody titres increased synchronously in patients who developed crises.

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Article 02 May 2019

Nils Erik Gilhus, Socrates Tzartos, … Jan J. G. M. Verschuuren

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Authors and Affiliations

  1. Department of Neurology, Brain Research Institute, Chiba University School of Medicine, 1-8-1 Inohona, 280, Chiba, Japan

    A. Komiyama & K. Hirayama

  2. National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan

    A. Komiyama, I. Kamo, S. Furukawa, S. Akazawa & E. Satoyoshi

Authors
  1. A. Komiyama
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  2. I. Kamo
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  3. S. Furukawa
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  4. S. Akazawa
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  5. K. Hirayama
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  6. E. Satoyoshi
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Komiyama, A., Kamo, I., Furukawa, S. et al. Antibodies against saline-soluble components of skeletal muscle in myasthenia gravis. J Neurol 235, 207–213 (1988). https://doi.org/10.1007/BF00314348

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  • DOI: https://doi.org/10.1007/BF00314348

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