This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on Web of Science (32)  • Contact me when this article is cited  Related Content  • Related article  • Similar articles in this journal  Topic Collections  • Neurology, Other  • Alert me on articles by topic  Social Bookmarking   What's this?

Åse Mygland, MD; Angela Vincent, MB, FRCPath; John Newsom-Davis, MD; Henry Kaminski, MD; Francesco Zorzato, MD; Mark Agius, MD; Nils E. Gilhus, MD; Johan A. Aarli, MD

Arch Neurol. 2000;57:527-531.

Background  About 50% of patients with thymoma have paraneoplastic myasthenia gravis (MG). Myositis and myocarditis or neuromyotonia (NMT) will also develop in some. Patients with thymoma-associated MG produce autoantibodies to a variety of neuromuscular antigens, particularly acetylcholine receptor (AChR), titin, skeletal muscle calcium release channel (ryanodine receptor [RyR]), and voltage-gated potassium channels (VGKC).

Objective  To examine whether neuromuscular autoantibodies in patients with thymoma correlate with specific clinical syndromes.

Methods  Serum and plasma samples from 19 patients with thymoma-associated MG, of whom 5 had myositis and 6 had NMT, underwent testing for antibodies to AChR, titin, RyR, and VGKC.

Results  Antibodies to AChR and titin were found in 19 and 17 patients, respectively. Antibodies to RyR correlated with the presence of myositis (P=.03); they were found in all 5 patients with myositis and in only 1 patient with NMT, but also in 4 of 8 patients with neither disease. Antibodies to VGKC were found in 4 patients with NMT, 1 of 3 patients undergoing testing for myositis, and 2 of 7 patients undergoing testing with neither comorbidity. Presence of RyR antibodies correlated with high levels of titin antibodies.

Conclusions  The results appear to distinguish partially between 3 groups of patients with thymoma-associated MG: the first with RyR antibodies and myositis or myocarditis, the second with NMT without RyR antibodies, and the third without RyR antibodies, myositis, or NMT. Differences in the thymoma may underlie these pathologic associations.

From the Departments of Neurology, University of Bergen, Bergen, Norway (Drs Mygland, Gilhus, and Aarli), Vest-Agder Central Hospital, Kristiansand, Norway (Dr Mygland), Case Western Reserve School of Medicine, Cleveland, Ohio (Dr Kaminski), and University of California–Davis (Dr Agius); the Neuroscience Group, Institute of Molecular Medicine, John Radcliff Hospital, Oxford, England (Drs Vincent and Newsom-Davis); and the Institute of Pathology, University of Ferrara, Ferrara, Italy (Dr Zorzato).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

RELATED ARTICLE

Archives of Neurology Reader's Choice: Continuing Medical Education
Arch Neurol. 2000;57(4):613-614.
FULL TEXT  

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Autoimmune Targets of Heart and Skeletal Muscles in Myasthenia Gravis
Suzuki et al.
Arch Neurol 2009;66:1334-1338.
ABSTRACT | FULL TEXT  

Cerebellar ataxia associated with neuroendocrine thymic carcinoma and GAD antibodies
Bataller et al.
J. Neurol. Neurosurg. Psychiatry 2009;80:696-697.
FULL TEXT  

Classification of Myasthenia Gravis Based on Autoantibody Status
Suzuki et al.
Arch Neurol 2007;64:1121-1124.
ABSTRACT | FULL TEXT  

Lambert-Eaton myasthenic syndrome associated with thymitis
Warren et al.
Neurology 2005;64:168-169.
FULL TEXT  

The occurrence of anti-titin antibodies and thymomas: A population survey of MG 1970-1999
Somnier and Engel
Neurology 2002;59:92-98.
ABSTRACT | FULL TEXT