Myasthenia gravis (MG) and its animal model experimental autoimmune myasthenia gravis (EAMG) are caused by autoantibodies against nicotinic acetylcholine receptor (AChR) in skeletal muscle. The production of anti-AChR antibodies is mediated by cytokines produced by CD4+ and CD8+ T helper (Th) cells.
1999 Scientific session of the Myasthenia Gravis Foundation
β Scribed by Robert L. Ruff
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 96 KB
- Volume
- 23
- Category
- Article
- ISSN
- 0148-639X
No coin nor oath required. For personal study only.
β¦ Synopsis
The annual scientific session of the Myasthenia Gravis Foundation of America (MGFA) was held on October 9, 1999 in Seattle, Washington. Dr. James F. Howard, Jr. organized the meeting which contained 17 international presentations that covered six topics: 1) autoantibodies in myasthenia gravis (MG); 2) the role of the thymus gland in MG; 3) ocular MG; 4) immunology related to MG; 5) molecular/electrical properties of the acetylcholine receptor (AChR); and 6) treatment of MG.
Drs. Steven Vernino and Vanda Lennon from the Mayo Clinic described 6 patients who had MG plus another muscle disorder associated with autoantibodies. Three patients had cramp-fasiculation syndrome, 2 had rippling muscle syndrome, and 1 had neuromyotonia. Four patients had a thymoma. All patients had anti-AChR antibodies. Five patients had antibodies against voltage-gated potassium channels. Consequently, some MG patients have additional muscle problems due to antibodies that alter release of ACh from motor nerve terminals or that compromise the electrical stability of muscle membranes. Thomas C. Watkins and colleagues from Youngstown State University discussed the possible autoimmune pathogenesis of rippling muscle disease. They described 3 patients with rippling muscle disease; 1 patient also had MG and a thymoma. All patients
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