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Biomedical subjects

N Yuki

Publications and source records attributed to N Yuki.

At least 19 recordsLinked to original sources
PubMed2001

Features of sensory ataxic neuropathy associated with anti-GD1b IgM antibody.

Some reports have called sensory ataxic neuropathy (SAN) associated with IgM antibody against b-series gangliosides a chronic form of Miller Fisher syndrome (MFS), but this has yet to be established. We examined five patients with SAN and eight patients with IgG anti-GQ1b-positive MFS. Only one patient with SAN complained of diplopia, whose ocular movement was not limited. The other four patients had neither diplopia nor limitation of ocular movement. All the SAN patients had severe deep sense impairment, whereas one patient with MFS showed only mild vibratory sense impairment. All sera from the SAN patients had remarkably high IgM antibody titers to the b-series gangliosides GD3, GD2, GD1b, GT1b, GQ1b, GQ1b alpha, fucosyl-GD1b, and alpha galactosyl [alpha fucosyl] GD1b. An absorption study confirmed that the anti-GQ1b antibodies cross-reacted with GD3, GD2, GD1b, and GT1b. In contrast, only two samples from the MFS patients had IgG antibody to GD3, and no sample reacted with GD2, GD1b, or GT1b. SAN has different clinical or serological features from MFS, and therefore is not a chronic form of it.

Adult↗
PubMed2001

Intravenous immunoglobulin therapy for Guillain-Barré syndrome with IgG anti-GM1 antibody.

To compare the effects of intravenous immunoglobulin (IVIg) therapy and plasmapheresis for the IgG anti-GM1-positive subtype of Guillain-Barré syndrome (GBS), clinical and electrophysiological recoveries were analyzed in 24 patients treated with IVIg (n = 10) or plasmapheresis (n = 14). At entry, there were no significant differences between the two patient groups in age, sex, clinical severity (Hughes grade), sum scores of distally evoked amplitudes of compound muscle action potentials (CMAPs), and frequency of Campylobacter jejuni infection. The patients treated with IVIg had significantly lower Hughes grade scores 1, 3, and 6 months after onset (P = 0.03), and a higher probability to regain independent locomotion at 6 months [P(logrank) = 0.044]. In the IVIg group, markedly rapid recovery (improvement by two or more Hughes grade scores within 4 weeks) was more frequent (6 of 10 vs. 3 of 14, P = 0. 03), and delayed recovery (unable to walk independently at 6 months) was less frequent (0 of 10 vs. 4 of 14, P = 0.06). CMAP sum score at 6 months tended to be greater for the IVIg group (P = 0.07). For the IgG anti-GM1-positive subgroup of GBS patients, IVIg therapy may be a more efficacious treatment than plasmapheresis.

Action Potentials↗
PubMed2001

Acute ophthalmoparesis (without ataxia) associated with anti-GQ1b IgG antibody: clinical features.

OBJECTIVE: To examine the clinical features of acute ophthalmoparesis (AO) (without ataxia) associated with anti-GQ1b immunoglobulin G (IgG) antibody. DESIGN: Retrospective observational case series. PARTICIPANTS: Twenty-one subjects with AO (without ataxia) who had anti-GQ1b IgG. METHODS: Clinical features of 21 subjects with AO were analyzed. RESULTS: Seventeen had symptoms of antecedent infection. Gaze limitation was bilateral in 16 subjects and unilateral in five, indicative that laterality does not always negate AO. Nine subjects showed abducens paresis, and two limitation of abduction and adduction. Eight, who initially had bilateral abducens palsy, subsequently had impairment of adduction and vertical movement. These showed that bilateral abducens palsy followed by oculomotor nerve involvement is characteristic of AO. Muscle stretch reflexes were normal in nine subjects, hypoactive in eight, absent in three, and brisk in one. Distal paresthesias were present in seven subjects. Acellular cerebrospinal fluid (CSF) associated with raised protein concentration was detected in three. CONCLUSIONS: Antecedent infectious symptoms, characteristic limitation of ocular movement, areflexia, distal paresthesias, and CSF albuminocytologic dissociation are useful markers for diagnosing AO as well as anti-GQ1b IgG. AO can be considered a mild form of Miller Fisher syndrome or a regional variant of Guillain-Barré syndrome.

Abducens Nerve Diseases↗
PubMed2001

Anti-GQ1b IgG antibody syndrome: clinical and immunological range.

OBJECTIVES: To clarify the nosological relation among Miller Fisher syndrome (MFS), Guillain-Barré syndrome (GBS) with ophthalmoplegia, Bickerstaff's brain stem encephalitis (BBE), and acute ophthalmoparesis without ataxia. Serum samples from patients with each condition often have anti-GQ1b IgG antibody. METHODS: Information on antecedent illness, initial symptoms, neurological signs during the illness, and CSF findings were reviewed in 194 patients with anti-GQ1b IgG. It was determined whether overlapping MFS and GBS (MFS/GBS), as well as overlapping BBE and GBS (BBE/GBS), is explained by the combined action of anti-GQ1b IgG and anti-GM1 or anti-GD1a IgG, serological markers of GBS. RESULTS: Based on the diagnostic criteria, all the patients with acute ophthalmoparesis, MFS, MFS/GBS, BBE/GBS, and BBE had external ophthalmoplegia; all the patients with MFS, MFS/GBS, or GBS had hyporeflexia or areflexia; and all those with MFS and BBE showed ataxia. Tendon reflexes were decreased or absent in 91% of those with BBE/GBS, 67% of those with BBE, and 53% of those with acute ophthalmoparesis. Ataxia was present in 68% of the patients with MFS/GBS and 45% of those with BBE/GBS. Antecedent illness caused by upper respiratory tract infection had occurred in 60% to 80% of these patients, and CSF albuminocytological dissociation in 25% to 75%. Anti-GM1 or anti-GD1a IgG was present in 50% of those with GBS, 35% of those with MFS/GBS, 27% of those with BBE/GBS, 16% of those with MFS, and 8% of those with BBE. CONCLUSIONS: These findings together with the common autoantibody (anti-GQ1b IgG) suggest that a common autoimmune mechanism functions in the pathogenesis of these illnesses. In a larger study, it was confirmed clinically that MFS, GBS, BBE, and acute ophthalmoparesis are closely related, forming a continuous range. This is supported by the immunological findings. The term "anti-GQ1b IgG antibody syndrome" is not intended to be used as a clinical diagnosis, but recognition of this syndrome is useful for understanding the aetiological relation among the various illnesses and for introducing the established treatments of GBS for use with other conditions.

Adolescent↗
PubMed2000

Ataxic Guillain-Barré syndrome with anti-GQ1b antibody: relation to Miller Fisher syndrome.

The authors reviewed the medical records of seven patients with anti-GQ1b immunoglobulin G (IgG) who had no or minimal external ophthalmoplegia but showed ataxia. The clinical features of the patients were consistent with the ataxic form of Guillain-Barré syndrome (GBS). Anti-GQ1b IgG antibodies from the patients, as well as from those with Miller Fisher syndrome (MFS), were absorbed by GT1a. The finding that ataxic GBS and MFS have in common an autoantibody with the same fine specificity suggests that they form a continuous spectrum.

Adult↗
PubMed2000

Antibodies to GM1(NeuGc) in Guillain-Barré syndrome after ganglioside therapy.

N-Glycolylneuraminic acid-containing GM1 [GM1(Gc)] is a molecule for serum antibodies in patients with Guillain-Barré syndrome (GBS). To clarify the pathogenesis of GBS after treatment with bovine brain ganglioside, we investigated the presence of anti-GM1(Gc) antibody in patients who developed GBS after ganglioside injection. Serum samples were taken from nine Italian patients with GBS after ganglioside therapy as well as from untreated Italian (n=30) and Japanese (n=131) GBS patients. Bovine brain gangliosides fractionated in a column were used as antigens, and binding of serum IgG or IgM was examined. An absorption study of IgG anti-GM1(Gc) antibody was made with GM1, asialo-GM1, GM2, GD1a, and GD1b. Four of the nine patients who developed GBS after being administered gangliosides had IgG anti-GM1(Gc) antibodies. Anti-GM1(Gc) IgG antibody frequencies were higher in patients with GBS after ganglioside therapy than in those who were untreated. Rates of absorption of IgG anti-GM1(Gc) antibodies by GM1 were significantly higher (except for asialo-GM1 and GD1b) than by GM2 and GD1a. The presence of GM1(Gc) was confirmed in bovine brain immunochemically using cholera toxin and Hanganutziu-Deicher antibody. Secondary ion mass spectra showed that the structure of the ganglioside was consistent with that of GM1(Gc). GM1(Gc) was recognized more frequently in sera from patients who developed GBS after ganglioside therapy than in sera from untreated GBS patients. Because N-glycolylneuraminic acid-containing gangliosides seem to be highly immunogenic in humans, GM1(Gc) may act as an immunogen in some patients who develop GBS following ganglioside therapy.

Animals↗
PubMed2000

Anti-SGPG antibody in CIDP: nosological position of IgM anti-MAG/SGPG antibody-associated neuropathy.

Polyneuropathy with monoclonal gammopathy usually is considered a nosological entity different from chronic inflammatory demyelinating polyneuropathy (CIDP). Criteria proposed by the American Academy of Neurology AIDS Task Force (1991), however, show monoclonal gammopathy to be a condition concurrent with CIDP. The purpose of this study was to clarify the nosological relationship between CIDP and IgM anti-myelin-associated glycoprotein (MAG)/sulfated glucuronyl paragloboside (SGPG)-associated polyneuropathy. We investigated IgM anti-MAG/SGPG antibody in 85 CIDP patients by various methods, then examined the relation of M-protein to the presence of IgM anti-MAG/SGPG antibody. In our large study, 17 (20%) of 85 CIDP patients had high IgM anti-SGPG antibody titers in the enzyme-linked immunosorbent assay. This was confirmed by thin-layer chromatography-immunostaining for IgM anti-SGPG antibody and immunoblotting for IgM anti-MAG antibody. Immunoelectrophoresis and immunofixation, respectively, detected IgM M-protein in 6 (35%) and 13 (76%) of the 17 CIDP patients. We conclude that some patients with IgM anti-MAG/SGPG antibody with or without monoclonal gammopathy may be diagnosed as having CIDP, when patients are diagnosed according to the current CIDP criteria.

Adult↗
PubMed2000

Current cases in which epitope mimicry is considered a component cause of autoimmune disease: Guillain-Barré syndrome.

Some patients develop 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. Molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from patients with GBS, and between GQ1b and C. jejuni lipopolysaccharides from patients with MFS have been demonstrated. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies. This sugar mimicry is one possible cause of the Guillain-Barré and Miller Fisher syndromes; however, unidentified host factors may contribute to the development of these syndromes.

Animals↗
PubMed2000

Is Campylobacter lipopolysaccharide bearing a GD3 epitope essential for the pathogenesis of Guillain-Barré syndrome?

The hypothesis has been proposed that the GD3 ganglioside-like lipopolysaccharide (LPS) is essential for and functions in the development of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) subsequent to Campylobacter jejuni enteritis. Our study showed that patients with GBS or MFS who had previously suffered diarrhea had anti-GD3 antibodies less often than those who had not had diarrhea. Sera from patients who showed GBS or MFS with the serologic evidence of prior C. jejuni infection had anti-GD3 antibodies less frequently than sera from those without evidence of infection. Statistical analysis showed that anti-GD3 antibodies were less frequent in patients with GBS or MFS from whom C. jejuni had been isolated than were other antiganglioside antibodies, such as anti-GM1 antibodies. These results could not support the above hypothesis.

Acute Disease↗
PubMed2000

Reappraisal of biochemical hepatitis C activity in hemodialysis patients.

We reappraised biochemical hepatitis C activity in hemodialysis patients in comparison with normal controls. A total of 111 hemodialysis patients and 66 healthy volunteer blood donors with hepatitis C virus (HCV) infection were consecutively enrolled. Serum alanine aminotransferase (ALT) levels were normal (< or =45 U/L) in 103 (93%) hemodialysis patients and 34 (52%) donors (p < 0.001). HCV viremic levels were lower in the hemodialysis group (p = 0.044), with no difference in the HCV genotype prevalence. During two-year follow-up, 60 (67%) of 90 hemodialysis patients and 13 (26%) of 50 donors showed persistently normal ALT levels (p < 0.001). For hemodialysis patients, however, the upper normal limit of ALT activity was reset at 25 U/L corresponding to the mean + 2 x SD for the normalized ALT distribution in 400 control patients. The adjusted ALT levels were initially normal in 73 (66%) hemodialysis patients and persistently normal in 19 (21%). Thus, ALT levels were the same for the two groups. GB virus C (GBV-C)/hepatitis G virus (HGV) coinfection found only in the hemodialysis group (10/111) had no influence on the disease. A relationship was noted between low disease activity and female gender in both groups. These findings indicate that biochemical hepatitis C activity in hemodialysis patients is similar to that in normal controls and should be monitored based on adjusted ALT levels.

Alanine Transaminase↗
PubMed2000

Retreatment with interferon for chronic hepatitis C after transient response.

Approximately half of all patients with chronic hepatitis C show an initial biochemical response to interferon, but only 15% to 20% of patients achieve a sustained response. We studied the efficacy of retreatment with interferon for patients with chronic hepatitis C who showed transient biochemical responses to initial treatment. Thirty patients who relapsed were retreated 1 to 52 months (median 14) after the end of initial treatment, according to the previously used regimens. The responses were correlated with the pre-retreatment patient data. The liver histologic grades, compared with those found before the initial treatment, were better in eight (27%) patients but worse in six (20%), whereas the fibrosis stage was improved in five (17%) but worsened in eight (27%). All patients displayed end-of-retreatment biochemical responses. Of the 30 patients, 10 (33%) achieved sustained aminotransferase normalization and serum hepatitis C virus (HCV) RNA clearance, but the remaining 20 patients showed relapse within 1 year after cessation of retreatment. Univariate analysis associated the sustained response with low pre-retreatment viral loads (0.8 +/- 0.7 MEq/mL vs. 9.1 +/- 6.5 MEq/mL; p = 0.006), short treatment intervals (13 +/- 13 months vs. 22 +/- 14 months; p = 0.031), and low histologic grades (1.3 +/- 0.7 vs. 1.9 +/- 0.7; p = 0.039). However, multivariate analysis indicated that only the pre-retreatment viral load was predictive of the sustained response (p = 0.049). These findings suggest that transient responders to interferon are likely to respond to retreatment but the achievement of a sustained response depends on the HCV viral load before retreatment.

Adult↗
PubMed2000

Colonization of the stratified squamous epithelium of the nonsecreting area of horse stomach by lactobacilli.

Selective adhesion to only certain epithelia is particularly common among the bacterial members of the indigenous microflora of mammals. We have found that the stratified squamous epithelium of the nonsecreting area of horse stomach is colonized by gram-positive rods. The microscopic features of a dense layer of these bacteria on the epithelium were found to be similar to those reported in mice, rats, and swine. Adhering microorganisms were isolated and identified as Lactobacillus salivarius, L. crispatus, L. reuteri, and L. agilis by DNA-DNA hybridization and 16S rRNA gene sequencing techniques. These lactobacilli associated with the horse, except for L. reuteri, were found to adhere to horse epithelial cells in vitro but not to those of rats. A symbiotic relationship of these lactobacilli with the horse is suggested.

Animals↗
PubMed2000

Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barré syndrome with antiganglioside antibodies.

OBJECTIVES: To investigate the pathophysiology of selective absence of F waves and its relation with antiganglioside antibodies in Guillain-Barré syndrome (GBS). Some patients with GBS show the absence of F waves as an isolated conduction abnormality, which has been interpreted as demyelination in the proximal nerve segments. METHODS: In 62 consecutive patients with GBS, sequential nerve conduction and F wave studies were reviewed, and antibodies against ganglioside GM1, GM1b, GD1a, GalNAc-GD1a, GD1b, and GQ1b were measured by an enzyme linked immunosorbent assay. RESULTS: In the first electrophysiological studies, isolated absence of F waves was found in 12 (19%) patients. Sequential studies in 10 of these patients showed two electrophysiological sequel patterns; rapid restoration of F waves (six patients), and persistent absence of F waves with distal motor nerve degeneration (acute motor axonal neuropathy, four patients). None of the 10 patients showed evidence of demyelination in the proximal, intermediate, or distal nerve segments throughout the course. Of the 62 patients, IgG antibodies against GM1, GM1b, GalNAc-GD1a, or GD1b were significantly associated with the electrodiagnosis of acute motor axonal neuropathy, and patients with these antibodies more often had isolated absence of F waves than patients without them (11 of 36 (31%) v one of 26 (4%); p<0.01). Eleven of the 12 patients with isolated absence of F waves had positive serology for one or more antiganglioside antibodies. CONCLUSIONS: In GBS with antiganglioside antibodies, isolated absence of F waves is a frequent conduction abnormality especially in the early phase of the disease, and may be caused by axonal dysfunction, such as physiological conduction block or axonal degeneration at the nerve roots.

Adolescent↗