Incidence of serum anti-P/Q-type and anti-N-type calcium channel autoantibodies in the Lambert-Eaton myasthenic syndrome

Motomura, Masakatsu; Lang, Bethan; Johnston, Irene; Palace, J; Vincent, Angela; Newsom‐Davis, John

doi:10.1016/s0022-510x(96)05303-8

Cited by 230 publications

(148 citation statements)

References 19 publications

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“…The underlying pathophysiology of LEMS is impaired calcium-dependent release of acetylcholine from motor nerve terminals (Elmqvist et al 1968). Circulating antibodies against voltage-gated calcium channels (VGCCs) are found in around 90% of LEMS patients (Lennon et al 1995;Motomura et al 1997) and result in the down-regulation of functional VGCCs (Pinto et al 1998). VGCCs are composed of a number of pharmacologically and electrophysiologically distinct subtypes.…”

Section: Lambert Eaton Myasthenic Syndromementioning

confidence: 99%

“…Results have previously been shown to be comparable using human and rabbit cerebellar extracts as an antigenic source for potassium (unpublished data), and calcium channels (Motomura et al, 1997). For use in the assay, the membrane preparation was diluted 1:5 in 2% digitonin solubilisation buffer, incubated for 1 h at 4 ºC and centrifuged at 13,000 rpm for 15 min.…”

Section: Preparation Of Channel Extractsmentioning

confidence: 99%

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The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

Hubball

Martin

Lang

et al. 2009

Progress in Neurobiology

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Dysfunction of the gastrointestinal neuromuscular apparatus (including interstitial cells ofCajal) is presumed to underlie a heterogeneous group of disorders collectively termed gastrointestinal neuromuscular diseases (GINMDs). Humoral (antibody)-mediated autoimmunity directed against ligand-or voltage-gated ion channels or associated proteins involved in neuromuscular transmission is associated with several acquired neuromuscular diseases of the periphery and is now implicated in an increasing number of less well-characterised diseases. Anti-channel antibodies have been reported in small numbers of patients with GINMD, particularly in those with GI dysfunction secondary to an underlying disease such as neoplasia or infection. However, little is known of humoral autoimmunity in primary GINMDs.This thesis investigated the association between anti-channel antibodies and GINMD, and the human GI tract as a potential target of anti-channel antibodies. The presence of antivoltage-and ligand-gated antibodies was investigated in the serum of patients with primary achalasia, enteric dysmotility and intestinal pseudo-obstruction, and in those with GINMD secondary to Chagas' disease. The functional effect of sera from some of these patients on colonic smooth muscle contractility was also characterised. Finally, the distribution of six voltage-gated potassium channels (VGKCs), which serve essential roles in the peripheral and central nervous systems and are known targets of pathological autoantibodies, were investigated in all layers of the human GI tract.Our findings suggest that currently recognised anti-channel antibodies are not a common pathogenic factor in primary GINMDs. Anti-channel antibodies, in particular anti-VGKC antibodies, were however found in a significant number of individuals with Chagas' disease. Furthermore, circulating factors in patients with chagasic GI disease altered GI smooth muscle contractility in vitro which may have pathological relevance to GI

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Section: Lambert Eaton Myasthenic Syndromementioning

confidence: 99%

Section: Preparation Of Channel Extractsmentioning

confidence: 99%

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

Hubball

Martin

Lang

et al. 2009

Progress in Neurobiology

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“…Their titers of AChR Ab were measured by immunoprecipitation assay using 125 I-α-bungarotoxin labeled AChR from TE671 (Lindstrom et al, 1976). Their titers of anti-P/Q-type voltage-gated calcium channel (VGCC) antibody (P/Q-VGCC Ab) were measured by immunoprecipitation assay using 125 I-ω-conotoxin MVIIC labeled P/Q-type VGCC from rat cerebellum (Motomura et al, 1997).…”

Section: Patientsmentioning

confidence: 99%

Autoantibody to dihydropyridine receptor in myasthenia gravis

Maruta

Yoshikawa

Fukasawa

et al. 2009

Journal of Neuroimmunology

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To investigate autoantibodies related to excitation-contraction (E-C) coupling in patients with myasthenia gravis (MG), we developed a novel method to detect autoantibodies against dihydropyridine receptor (DHPR). Using this method, we detected DHPR antibody in 37% (11 out of 30) of MG patients with thymoma.Antibodies were not detected in normal nor disease controls. The titer of DHPR antibodies showed no significant correlation with autoantibodies to acetylcholine nor ryanodine receptors. The DHPR antibody is another marker for thymoma in MG, and it might have some role in clinical symptoms related to E-C coupling.

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“…5 A link between paraneoplastic and genetic cerebellar ataxia is also illustrated by voltage-gated calcium channel antibodies (VGCC-Ab). VGCC-Ab, especially those directed against the P/Q type VGCC, are mainly associated with Lambert-Eaton myasthenic syndromes (LEMS), 7 which are paraneoplastic in .70% of the patients. Studies have shown that the frequency of cerebellar ataxia in patients with LEMS is higher than that expected by chance, and that LEMS with ataxia is usually associated with cancer.…”

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confidence: 99%

Understanding the physiopathology of paraneoplastic and genetic cerebellar ataxia

Honnorat

2006

Journal of Neurology, Neurosurgery & Psychiatry

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Incidence of serum anti-P/Q-type and anti-N-type calcium channel autoantibodies in the Lambert-Eaton myasthenic syndrome

Cited by 230 publications

References 19 publications

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

Autoantibody to dihydropyridine receptor in myasthenia gravis

Understanding the physiopathology of paraneoplastic and genetic cerebellar ataxia

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