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Nobuhiro Yuki

Publications and source records attributed to Nobuhiro Yuki.

61 records · Page 4Linked to original sources
PubMed2002

Peripheral neuropathies and anti-glycolipid antibodies.

This review charts the progress of anti-glycolipid antibodies in neuropathy, from their original discovery 20 years ago in immunoglobulin M paraproteinaemic neuropathy through to current discoveries mapping their relationship to subtypes of Guillain-Barré syndrome. Antibodies to >20 different glycolipids have now been associated with a wide range of clinically identifiable acute and chronic neuropathy syndromes. Particular progress has been achieved in understanding the link between acute motor axonal neuropathy and antibodies to GM1, GD1a, GM1b and GalNAc-GD1a, and between the cranial, bulbar and sensory variants of GBS and antibodies to the disialylated gangliosides GQ1b, GT1a, GD1b and GD3. In addition to clinical and serological studies, the origins and measurement of anti-glycolipid antibodies and their relationships to similar carbohydrate structures on infectious organisms, particularly Campylobacter jejuni, are discussed in the context of a molecular mimicry hypothesis. The structure and nomenclature of relevant glycolipids are outlined, along with information on their localization in nerve, and the influence this has on clinical phenotypes. Major advances have been made in animal modelling of anti-glycolipid antibody-associated diseases, both in vitro and in vivo. This has advanced our understanding of the role of anti-GQ1b antibodies in Miller Fisher syndrome with particular respect to the motor nerve terminal as a potential site of injury, and led to the creation of rabbit models of anti-GD1b and anti-GM1 antibody-mediated sensory and motor neuropathy, respectively. With such information in place, it will now be possible to determine the precise mechanisms by which antibodies injure the different compartments of peripheral nerve and establish how a range of immunomodulating therapies, including current treatments, exert their therapeutic effects. Despite these very significant advances, considerable gaps in our knowledge persist, and it is likely that other pathogenic pathways operate in inflammatory neuropathy that are unrelated to glycolipid antibodies, although these are outside the scope of this review.

Animals↗
PubMed2002

Fulminant Guillain-Barré syndrome after Campylobacter jejuni enteritis and monospecific anti-GT1a IgG antibody.

A 21-year-old man developed rapid progression of tetraplegia, bulbar palsy, and respiratory paralysis after Campylobacterjejuni enteritis. Based on the diagnosis of Guillain-Barré syndrome, he received plasmapheresis and intravenous immunoglobulin. Serum anti-GT1a IgG antibody which lacked cross-reactivity with GQ1b was detected. Four months after the onset, the patient still had severe muscle weakness of the lower limbs. This case suggests that anti-GT1a IgG antibody can be associated with severe paralysis in Guillain-Barré syndrome after C. jejuni enteritis.

Adult↗
PubMed2002

[A case of Fisher's syndrome after Haemophilus influenzae infection].

We report a case of Fisher's syndrome with serological evidence of antecedent Haemophilus influenzae infection. A 66-year-old woman developed unsteady gait and multiple cranial nerve palsies after upper respiratory infection. Serum anti-GQ 1 b and anti-GT 1 a IgG antibodies were positive. In the acute phase of the illness, her serum had high titers of IgM, IgG and IgA anti-H. influenzae antibodies, which significantly decreased during the clinical course. Further study is needed to clarify the clinical and immunological features of Fisher's syndrome after H. influenzae infection.

Aged↗
PubMed2002

[A case of pharyngeal-cervical-brachial weakness suggestive of the nosological continuity between acute oropharyngeal palsy].

A 68-year-old man without history of antecedent infection experienced nasal voice (day 1), and the developed dysphagia on day 9. Eleven days after the onset, he developed ophthalmoplegia, and on day 13 mild weakness in the neck and the upper limbs. Cerebrospinal fluid examination revealed albuminocytologic dissociation on day 19. Motor nerve conduction velocities and compound muscle action potentials were normal, but terminal latency was slightly prolonged in the median nerve. Enzyme-linked immunosorbent assay showed that the patient's anti-GT1 a IgG antibody fiter was high and that the antibody cross-reacts with GQ1b. We considered that this patient showed acute oropharyngeal palsy at the onset, and then evolved into pharyngeal-cervical-brachial weakness. The presence of this case suggested the nosological continuity between acute oropharyngeal palsy and pharyngeal-cervical-brachial weakness in both clinical and serological aspects.

Aged↗