The Lambert-Eaton Myasthenic Syndrome

In this: publication
By this: publisher
In this Subject: <a title="Allergy & Immunology" href="/content/subcat?j_subject=197&j_availability=">Allergy & Immunology
By this author: Antoine F Carpentier ;&nbsp; Jean-Yves Delattre

Authors: Antoine F Carpentier; Jean-Yves Delattre

Source: Clinical Reviews in Allergy and Immunology, Volume 20, Number 1, February 2001 , pp. 155-158(4)

Buy & download fulltext article:

Price: $42.00 plus tax (Refund Policy)

Abstract:

The Lambert-Eaton Myasthenic Syndrome (LEMS) is a disorder of neuromuscular transmission, characterized by reduced release of acetylcholine from the motor nerve terminal (1). LEMS is suspected to be an autoimmune disease. This was first suggested by the association of LEMS with other autoimmune diseases (2) and the clinical response to plasma exchange and immunosuppressive therapy (3,4). Direct evidence of the autoimmune mechanism has been provided by passive transfer experiment in which electrophysiological features of LEMS can be induced in animals after injection of purified IgG from patients with LEMS (5,6). Antibodies against presynaptic voltage-gated calcium channels (VGCC) are believed to play an important role in the pathogenesis of LEMS by inhibiting the calcium currents that trigger acetylcholine release.

Keywords: Lambert-Eaton Myasthenic Syndrome, Small-Cell Lung

Document Type: Miscellaneous

Publication date: 2001-02-01