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Biomedical subjects

N Yuki

Publications and source records attributed to N Yuki.

At least 19 recordsLinked to original sources
PubMed1999

Subclass distribution and the secretory component of serum IgA anti-ganglioside antibodies in Guillain-Barré syndrome after Campylobacter jejuni enteritis.

Previously, we reported that IgA anti-GM1 antibody is more closely associated with preceding Campylobacter jejuni enteritis in Guillain-Barré syndrome (GBS) than are IgG and IgM antibodies. However, the mechanism of the induction of IgA anti-ganglioside antibodies is not clear. In this study, serum IgA antibodies against GM1, GM1b, and GD1a, and GalNAc-GD1a were examined in 152 GBS patients. In GBS, antecedent C. jejuni infection is closely associated with IgA antibodies, other than GM1, against GM1b. The IgA subclass distribution is completely restricted to IgA1, no secretory IgA anti-ganglioside antibody being detected. This result does not support the hypothesis that the serum IgA antibodies present in GBS after C. jejuni enteritis originate at mucosal sites, such as the gut mucosal immune system. Seventeen (85%) of 20 patients with IgA anti-ganglioside antibodies had serological evidence of C. jejuni infection and/or a history of antecedent diarrhea. Moreover, a motor nerve conduction study showed that patients with IgA antibodies frequently had axonal neuropathy, whereas none had demyelinating neuropathy. This may support the previous report that IgA isotype anti-GM1 antibodies are more closely associated with poor outcome than are the IgG or IgM isotypes. The induction mechanism of IgA anti-ganglioside antibodies must be clarified by determining whether concentrations of cytokines, which increase the IgA class switch, are elevated in patients with GBS after C. jejuni enteritis.

Antibodies↗
PubMed1999

Are Campylobacter curvus and Campylobacter upsaliensis antecedent infectious agents in Guillain-Barré and Fisher's syndromes?

Campylobacter curvus and Campylobacter upsaliensis were isolated from stools of patients with Guillain-Barré (GBS) or Fisher's (FS) syndromes. Whether these microorganisms are pathogens of antecedent diarrhea in GBS and FS is not clear, therefore, we made a serological examination. There were no differences in antibody titer to these organisms among the patients with GBS, FS, and the controls. Some patients had elevated antibodies to the bacteria, but most also had serological evidence of C. jejuni infection. Moreover, the patients from whom C. curvus had been isolated did not have antibodies to the bacterium, indicative that they were healthy carriers of C. curvus or that the isolates were the product of contamination. We conclude that neither C. curvus nor C. upsaliensis is the major agent of antecedent diarrhea in GBS and FS.

Antibodies, Bacterial↗
PubMed1999

The 301 to 314 amino acid residue of beta-tubulin is not a target epitope for serum IgM antibodies in chronic inflammatory demyelinating polyneuropathy.

Connolly et al. [Neurology 48 (1997) 243] reported that IgM M-proteins from three patients selectively binds to an epitope on beta-tubulin that consists of amino acids 301 to 314. We therefore investigated whether these 14 amino acid residues beta301-314 are the target epitope for serum IgMs in sera from 67 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 50 with Guillain-Barré syndrome, 50 with motor neuron diseases, and 50 normal controls. IgM anti-beta301-314 antibodies were not restricted to nor were selectively associated with CIDP. We conclude that beta301-314 is not a target epitope for serum IgMs in CIDP.

Autoantibodies↗
PubMed1999

Special sensory ataxia in Miller Fisher syndrome detected by postural body sway analysis.

To investigate whether ataxia in Miller Fisher syndrome (MFS) is caused by loss of proprioception or cerebellar dysfunction, we studied the power spectrum peak of the body sway frequency in 10 MFS patients, and compared the results with those of patients with cerebellar or sensory ataxia. The cerebellar patients had a peak at 2.4 Hz, whereas sensory ataxia patients had a 1-Hz peak. Nine of the MFS patients had a distinct 1-Hz peak. Clinical sensory loss or abnormal sensory nerve potentials were present in only 3 patients, whereas soleus H-reflexes were absent in all the MFS patients. MFS patients have dysfunction of the proprioceptive afferent system, and the special sensory ataxia may be caused by the selective involvement of muscle spindle afferents.

Adult↗
PubMed1999

Antiganglioside antibody in patients with Guillain-Barré syndrome who show bulbar palsy as an initial symptom.

OBJECTIVES: To identify valuable antiganglioside antibodies that support the diagnosis of Guillain-Barré syndrome (GBS) and its variants in patients showing bulbar palsy as an initial symptom. METHODS: Medical records of 602 patients with GBS or its variants were reviewed. Fifteen patients had bulbar palsy as an initial symptom. Serum antibodies against GM1, GM1b, GD1a, GalNAc-GD1a, GT1a, and GQ1b were examined in 13 of them. RESULTS: Serum antiganglioside antibodies were positive in 11 (85%) patients. IgG anti-GT1a (n=8; 62%) and anti-GM1b (n=7; 54%) antibodies were often present, whereas all the patients had low or no anti-GM1 antibody activity. High anti-GD1a and anti-GQ1b IgG antibody titres were also present in some patients, but most had higher IgG antibody titres to GM1b or GT1a. All five patients with high IgG antibody titre to GM1b or GT1a only had had antecedent diarrhoea. Some patients with pharyngeal-cervical-brachial weakness (PCB) had IgG antibody to GT1a which did not cross react with GQ1b. Other patients with PCB had antibody to GT1a which cross reacted with GQ1b or antibody to GM1b, but anti-GM1b and anti-GT1a antibodies were not associated with the presence of bulbar palsy. All the patients who had no IgG antiganglioside antibodies recovered completely. CONCLUSIONS: Measurement of serum IgG anti-GT1a and anti-GM1b antibodies gives helpful support for the diagnosis of GBS and its variants when there is early involvement of the oropharyngeal function independently of other neurological findings which appear as the illness progresses.

Adolescent↗
PubMed1998

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↗
PubMed1998

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↗
PubMed1998

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↗
PubMed1998

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↗
PubMed1998

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↗
PubMed1998

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↗
PubMed1998

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↗
PubMed1998

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↗