[Miller Fisher syndrome].
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Autoantibodies↗
Biomedical subjects
N Yuki
Publications and source records attributed to N Yuki.
Pathogenesis of Guillain-Barré and Miller Fisher syndromes subsequent to Campylobacter jejuni enteritis.
Some patients developed Guillain-Barré syndrome (GBS) after the administration of bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. We showed the existence of molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from patients with GBS, and that between GQ1b and C. jejuni lipopolysaccharides from patients with MFS. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies. This sugar mimicry is one possible cause for GBS and MFS, and unidentified host factor may contribute to the development of these syndromes.
Autoantibodies↗
[Campylobacter jejuni enteritis and Guillain-Barré syndrome].
Some patients developed Guillain-Barré syndrome after the administration of bovine brain ganglioside. Patients with Guillain-Barré syndrome subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Miller Fisher syndrome, a variant of Guillain-Barré syndrome, is associated with IgG antibody to GQ1b ganglioside. My colleagues and I showed the existence of molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from a patient with Guillain-Barré syndrome, and that between GQ1b and C. jejuni lipopolysaccharides from patients with Miller Fisher syndrome. The glycotope mimicry between infectious agents and gangliosides may function in the production of antiganglioside antibodies and the development of Guillain-Barré syndrome and Miller Fisher syndrome.
Campylobacter Infections↗
[Chronic sensory ataxic neuropathy associated with IgM antibody against b-series gangliosides including GD1b].
We described a 62-year-old man with a 10 years history of chronic sensory ataxic neuropathy. His laboratory investigations revealed elevated serum IgM with IgM kappa paraproteinemia, IgM antibody against b-series gangliosides including GD3, GD2, GD1b, GT1b, GQ1b, GQ1b alpha, and high titer of cold agglutinin. The clinical and serological features in our patient were compatible with the diagnosis of CANOMAD (chronic ataxic neuropathy with ophthalmoplegia, M-protein, agglutination, and disialosyl antibodies), proposed by Willison et al. IgM antibody against b-series gangliosides including GD1b appeared to play an essential role in developing autoimmune sensory ataxic neuropathy.
Ataxia↗
[A case of Bickerstaff's brainstem encephalitis during pregnancy].
Here we present a case of 23-year-old woman with Bickerstaff's brainstem encephalitis (BBE) during 13 weeks of pregnancy. After symptoms of the upper respiratory tract infection, she developed somnolence, marked disturbance of extraocular eye movements, cerebellar ataxia, hyperreflexia and spasticity of the lower limbs. An electroencephalogram revealed slow waves and brainstem auditory evoked potential disclosed prolongation of III-V interpeak intervals. Serum IgG anti-GQ1b antibody was detected. Plasma exchanges (PE) were performed four times. Although no patient with BBE during pregnancy has ever been reported, in the literatures the pregnant patients with Guillain-Barré syndrome had four sessions of plasmapheresis with safe. Neurological symptoms gradually improved after the PE. No serious adverse effects were noted. Although no definite therapy for BBE has been established, PE may be one of the selections even if the patients is pregnant.
Adult↗
[Treatment of anti-glycolipid antibody-associated neuropathy].
The therapeutic effect of plasma exchange in Guillain-Barré syndrome (GBS) is related to the removal of circulating factors. Plasma concentrations of interleukin and other cytokines are elevated in GBS, but because their circulating half-lives are only a few hours, the effect of plasma exchange on their plasma levels would be short term. In contrast, the half-life of IgG is 3 weeks, much longer than that of other plasma proteins. This indicates that IgG is the most important factor in the development of GBS. Results of a large clinical study suggest that 2 exchanges are sufficient for mild cases of GBS, and for all others 4 exchanges are optimal. We showed that a significant IgG decrease was obtained in the first 2 sessions. Our result supports that at least 2 exchanges are needed for treating GBS. In Japan, patients with GBS often receive not only plasma exchange but also double-filtration plasmapheresis or immunoadsorption. We compared their abilities to remove immunoglobulins and anti-ganglioside antibodies. Plasma exchange decreased the IgG concentration much more than double-filtration plasmapheresis. The ability to remove IgG anti-ganglioside antibodies in plasma exchange was significantly superior to that of the other plasmaphereses.
Gangliosides↗
Fisher's syndrome and group A streptococcal infection.
Group A beta-hemolytic streptococcus causes immune-mediated disorders such as acute rheumatic fever and acute glomerulonephritis. We describe a second patient with Fisher's syndrome (FS) from whom beta-hemolytic streptococcus was isolated. We performed a study of the antecedent pharyngeal symptoms in FS and Guillain-Barré syndrome. Sore throat was statistically more frequent in FS (18/24 cases, 75%) than in Guillain-Barré syndrome (29/58 cases, 50%). In a series, however, the association of FS with group A streptococcal infection was not shown. Some patients may develop FS after group A streptococcal infection, but the bacterium is not a major antecedent agent in FS.
Adolescent↗
Guillain-Barré and Fisher's syndromes subsequent to Campylobacter jejuni enteritis are associated with HLA-B54 and Cw1 independent of anti-ganglioside antibodies.
The frequencies of human leukocyte antigens (HLA)-class I (A, B and Cw) were determined serologically and those of HLA-class II (DRB1 and DQB1) at the genomic level in 35 Japanese patients with Guillain-Barré syndrome (GBS), 58 with Fisher's syndrome (FS), and 112 healthy controls. HLA-B54 and -Cw1 antigens were found in GBS and FS patients from whom Campylobacter jejuni had been isolated more often than found in the healthy controls. No HLA types were related to GBS or FS as a whole, except for the B54 antigen which often was significant in the entire GBS group. This relation, however, may depend on the high population of C. jejuni-isolate patients in our GBS group. There were no relationships between the frequencies of HLA types and the presence of serum IgG antibodies to GM1, GQ1b, GD1a, or GalNAc-GD1a. Our findings suggest that HLA types are associated with the onset of GBS and FS after C. jejuni enteritis and that the HLA types in distinct GBS and FS subgroups of a single etiological origin need to be examined.
Antibodies↗
Guillain-Barré syndrome and Fisher's syndrome following Campylobacter jejuni infection.
The patients with Guillain-Barré Syndrome (GBS) subsequent to Campylobacter jejuni enteritis showed axonal degeneration and had IgG anti-GM1 antibody. The most frequently isolated C. jejuni from the patients was specific serotype of Penner's 19 in Japan. In the lipopolysaccharide (LPS) in C. jejuni of this serotype, the same oligosaccharide structure as GM1 ganglioside existed, suggesting the molecular mimicry between GM1 in nervous tissue and C. jejuni LPS. IgG anti-GM1 antibody may bind the nodes of Ranvier and axon terminals and causes degeneration of the motor axon. Some patients develop Fisher's syndrome following C. jejuni infection. C. jejuni strains from the patients who had IgG anti-GQ1b antibody in the acute phase had GQ1b epitope in their LPS, and the molecular mimicry between GQ1b in nervous tissue and an antecedent infectious agent was clarified.
Adult↗
Is IgG anti-GT1a antibody associated with pharyngeal-cervical-brachial weakness or oropharyngeal palsy in Guillain-Barré syndrome?
The pharyngeal-cervical-brachial variant (PCB) of Guillain-Barré syndrome (GBS) has clinical features similar to those of botulism and diphtheria. Mizoguchi et al. (1994) [Mizoguchi, K., Hase, A., Obi, T., Matsuoka, H., Takatsu, M., Nishimura, Y., Irie, F., Seyama, Y., Hirabayashi, Y., 1994. Two species of antiganglioside antibodies in a patient with a pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. J. Neurol. Neurosurg. Psychiatry 57, 1121-1123] reported a patient with PCB-like symptoms who had serum IgG anti-GT1a antibodies which did not cross-react with GQ1b. We assumed that PCB is associated with anti-GT1a antibodies that do not have reactivity to GQ1b and made a serological study of a PCB patient. We searched for PCB patients prospectively and found one with PCB. This patient had IgG anti-GT1a antibodies which were not absorbed with GQ1b in an absorption study, whereas IgG anti-GT1a antibodies from Fisher's syndrome patients were. The frequency of positive IgG anti-GT1a antibody did not differ in patients with and without bulbar palsy. Our findings indicate that IgG anti-GT1a antibodies which do not cross-react with GQ1b are specifically detectable in PCB and can be used as a diagnostic marker of PCB.
Adult↗
Ability to remove immunoglobulins and anti-ganglioside antibodies by plasma exchange, double-filtration plasmapheresis and immunoadsorption.
In Japan, patients with Guillain-Barré (GBS) and Fisher's (FS) syndromes often receive plasma exchange (PE), double-filtration plasmapheresis (DFPP), or immunoadsorption (IA). To determine whether DFPP and IA are as effective as PE, we compared their abilities to remove immunoglobulins and anti-ganglioside antibodies. Plasma samples were obtained from 55 GBS patients and 53 FS patients, before and after each session of the treatments. PE decreased the IgG concentration more than DFPP did, its abilities to remove anti-ganglioside IgG antibodies in PE markedly being superior to the abilities of the other plasmaphereses. IA on a tryptophan-immobilized column adsorbed anti-ganglioside IgG antibodies more effectively than IA on other affinity columns.
Adult↗
[Etiological mechanism and treatment of Guillain-Barre syndrome-- Campylobacter jejuni enteritis and the development of anti-ganglioside antibody preceding the syndrome].
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Autoantibodies↗
Acute cytomegalovirus infection and IgM anti-GM2 antibody.
Guillain-Barré syndrome (GBS) sometimes is preceded by cytomegalovirus (CMV) infection. Irie et al. (J. Neuroimmunol. 1996;68:19-26) reported that three patients with GBS subsequent to CMV infection had IgM and IgG anti-GM2 antibodies. In our larger study, the IgMs from the CMV-associated GBS patients showed significantly higher anti-GM2 antibody titers than anti-GM3, anti-GD1a, anti-GD1b, anti-GD2, anti-GD3, anti-GT1b, anti-GQ1b, and anti-SGPG antibody titers. None of the anti-glycosphingolipid antibody titers differed significantly from the others in the IgGs from the CMV-associated GBS patients. However, IgM anti-GM2 antibody frequently was present in GBS patients who were not preceded by CMV infection and non-GBS patients with acute CMV infection. Our results did not support the conclusion of Irie et al. that anti-GM2 antibodies were closely associated with acute CMV infection in GBS, but acute CMV infection, with and without GBS, was associated with IgM anti-GM2 antibody.
Acute Disease↗
Preserved tendon reflexes in Campylobacter neuropathy.
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Adult↗
Postinfection sensory neuropathy associated with IgG anti-GD1b antibody.
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Adult↗
N-glycolylneuraminic acid-containing GM1 is a new molecule for serum antibody in Guillain-Barré syndrome.
To clarify the pathogenesis of Guillain-Barré syndrome (GBS) after parenteral injections of bovine brain gangliosides, we searched for new molecules in bovine brain gangliosides recognized by sera from GBS patients. Gangliosides fractionated in a Q-Sepharose column were used as the antigens, and the binding of serum IgG or IgM was examined by thin-layer chromatography/immunostaining. Fourteen of 175 serum samples from the patients reacted with the monosialoganglioside fraction 2. In the neutral solvent system, a band in this fraction migrated with N-acetylneuraminic acid-containing GM1 [GM1(NeuAc)], whereas in the alkaline solvent system it migrated slower. This suggested that the band was N-glycolylneuraminic acid-containing GM1 [GM1(NeuGc)]. In both solvent systems, its mobility was almost the same as that of authentic GM1(NeuGc) from mouse liver. Secondary ion mass spectrometry showed that the ganglioside's structure was consistent with that of GM1(NeuGc). IgG anti-GM1(NeuGc) antibodies in sera from the GBS patients were significantly absorbed by GM1(NeuAc), indicative that the anti-GM1(NeuGc) antibodies cross-react with GM1(NeuAc). N-Glycolylneuraminic acid-containing gangliosides are so highly immunogenic in humans that the injection of GM1(NeuGc) could induce the production of IgG anti-GM1(NeuGc) antibody, which cross-reacts with GM1(NeuAc).
Animals↗
IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome.
To investigate the pathophysiological role of anti-GM1 antibody in Guillain-Barré syndrome (GBS), we reviewed sequential nerve conduction studies of 345 nerves in 34 GBS patients. Statistically significant correlation between IgG anti-GM1 antibodies and electrodiagnoses was found. Sixteen IgG anti-GM1-positive patients were classified as having acute motor or acute motor sensory axonal neuropathy (AMAN or AMSAN) (12 patients), as having acute inflammatory demyelinating polyneuropathy (AIDP) (3 patients), or as undetermined (1 patient) by electrodiagnostic criteria. Besides axonal features, there was rapid resolution of conduction slowing and block. In 3 patients initially diagnosed as having AIDP, conduction slowing was resolved within days, and 1 of them and 3 AMAN patients showed markedly rapid increases in amplitudes of distal compound muscle action potentials that were not accompanied by prolonged duration and polyphasia. The time courses of conduction abnormalities were distinct from those in IgG anti-GM1-negative AIDP patients. Rapid resolution of conduction slowing and block, and the absence of remyelinating slow components, suggest that conduction failure may be caused by impaired physiological conduction at the nodes of Ranvier. Reversible conduction failure as well as axonal degeneration constitutes the pathophysiological mechanisms in IgG anti-GM1-positive GBS. In both cases, immune-mediated attack probably occurs on the axolemma of motor fibers.
Adult↗
Correlation between cytomegalovirus infection and IgM anti-MAG/SGPG antibody-associated neuropathy.
IgM anti-myelin-associated glycoprotein (anti-MAG)/sulfated glucuronyl paragloboside (SGPG) antibody is found in some patients with chronic polyneuropathy (CP). An antigen-driven process is considered to induce this autoantibody, but the agent has yet to be identified. It has been reported that sera from cytomegalovirus (CMV)-infected patients contained anti-SGPG antibody. To clarify the mechanism of the production of the anti-MAG/SGPG antibody, we investigated CMV DNA in sera from 26 patients with IgM anti-MAG/SGPG antibody-positive CP. Twenty-three (88%) had CMV DNA. The positive frequency was significantly higher than the frequencies in sera from patients with IgM anti-MAG/SGPG-negative CP, the other disease controls, and the normal control subjects. There were no statistical differences in the frequencies of Epstein-Barr virus DNA between anti-MAG/SGPG-positive and anti-MAG/SGPG-negative CP and between anti-MAG/SGPG-positive CP and each disease control. Moreover, no herpes simplex virus 1 DNA was detected in the sera from patients with anti-MAG/SGPG-positive CP. The strong correlation of anti-MAG/SGPG-positive CP with the presence of serum CMV DNA suggests that CMV infection induces the IgM anti-MAG/SGPG antibody.
Autoantibodies↗