Literature DB >> 2189179

Lambert-Eaton syndrome.

R M Pascuzzi1, Y I Kim.   

Abstract

LES is an autoimmune disorder of the neuromuscular junction in which autoantibodies directed against voltage-dependent Ca2+ channels block nerve-evoked Ca2+ entry at the motor nerve terminal. The pathogenic IgG is likely to produce a similar inhibitory effect on the Ca2+ channel function in other cholinergic synapses of the autonomic nervous system. This pathophysiology is sufficient to account for the distinctive clinical, immunologic, and electrophysiologic manifestations in patients with LES. Etiology of this disease is uncertain but in view of its frequent association with small cell lung cancer, this specific type of neoplasm may be implicated in the initiation of autoimmune response. Recent studies indeed support the possibility that the antigenic stimulus in the neoplastic form of LES may arise from voltage-dependent Ca2+ channels found in the lung cancer cells.

Entities:  

Mesh:

Year:  1990        PMID: 2189179     DOI: 10.1055/s-2008-1041251

Source DB:  PubMed          Journal:  Semin Neurol        ISSN: 0271-8235            Impact factor:   3.420


  1 in total

1.  A case of Addison's disease associated with the Lambert-Eaton myasthenic syndrome.

Authors:  M Ozata; Z Odabasi; U Musabak; A Corakci; M A Gundogan
Journal:  J Endocrinol Invest       Date:  1997-06       Impact factor: 4.256

  1 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.