Literature DB >> 7600081

Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies.

T W Ho1, B Mishu, C Y Li, C Y Gao, D R Cornblath, J W Griffin, A K Asbury, M J Blaser, G M McKhann.   

Abstract

Guillain-Barré syndrome has been considered to be primarily an acute inflammatory demyelinating polyneuropathy (AIDP). Our experience with Guillain-Barré syndrome in northern China differs from the traditional concept. Electrophysiologically and pathologically, most of our patients have motor axonal degeneration with minimal cellular inflammation, which we have termed 'acute motor axonal neuropathy' (AMAN). The current studies were undertaken to characterize prospectively the clinical, electrophysiological, and serological features of Guillain-Barré syndrome, defined clinically, in northern China. In 1991 and 1992, we characterized by electrodiagnostic criteria 129 Chinese patients with Guillain-Barré syndrome. The AMAN form was present in 65% of patients, the AIDP form in 24% and 11% were unclassifiable. For the 38 patients who presented from January to October, 1992, we performed serological assays for antibodies to Campylobacter jejuni and to glycolipids. Of these 38 patients, 55% had AMAN, 32% had AIDP and 13% were unclassifiable. Sixty-six percent of the 38 had serological evidence of recent C. jejuni infection as compared with 16% of village controls (P = 0.001). Seventy-six percent of AMAN patients and 42% of AIDP patients were seropositive. IgG anti-GM1 antibodies were more frequent in Guillain-Barré syndrome patients compared with village controls (42% versus 6%; P < 0.01). However, no statistically significant correlations were found between the pattern of disease, AMAN or AIDP, anti-glycolipid antibodies, or C. jejuni antibodies. Based on electrophysiological criteria, Guillain-Barré syndrome in northern China can be divided into two predominant forms: AIDP and AMAN. The AMAN form is more common and predominates in the yearly summer outbreaks of Guillain-Barré syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1995        PMID: 7600081     DOI: 10.1093/brain/118.3.597

Source DB:  PubMed          Journal:  Brain        ISSN: 0006-8950            Impact factor:   13.501


  123 in total

Review 1.  Guillain-Barré syndrome.

Authors:  U Seneviratne
Journal:  Postgrad Med J       Date:  2000-12       Impact factor: 2.401

2.  Molecular characterization of Campylobacter jejuni from patients with Guillain-Barré and Miller Fisher syndromes.

Authors:  H P Endtz; C W Ang; N van Den Braak; B Duim; A Rigter; L J Price; D L Woodward; F G Rodgers; W M Johnson; J A Wagenaar; B C Jacobs; H A Verbrugh; A van Belkum
Journal:  J Clin Microbiol       Date:  2000-06       Impact factor: 5.948

3.  Guillain-Barré syndrome associated with normal or exaggerated tendon reflexes.

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4.  Pathogenesis and treatment of immune-mediated neuropathies.

Authors:  Helmar C Lehmann; Gerd Meyer Zu Horste; Bernd C Kieseier; Hans-Peter Hartung
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Review 5.  Progress in inflammatory neuropathy -the legacy of Dr Jack Griffin.

Authors:  Eva L Feldman; Richard A C Hughes; Hugh J Willison
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6.  Guillain-Barré syndrome following sepsis after stereotactic aspiration for spontaneous pontine hemorrhage.

Authors:  Wei Song; Yong-Ming Wu; Zhong Ji; Jia-Jia Zhu; Su-Yue Pan
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Review 7.  Guillain-Barré syndrome--a classical autoimmune disease triggered by infection or vaccination.

Authors:  Eitan Israeli; Nancy Agmon-Levin; Miri Blank; Joab Chapman; Yehuda Shoenfeld
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9.  Guillain-Barré syndrome in Taiwan: a clinical study of 167 patients.

Authors:  R K Lyu; L M Tang; S Y Cheng; W C Hsu; S T Chen
Journal:  J Neurol Neurosurg Psychiatry       Date:  1997-10       Impact factor: 10.154

10.  Increased circulating Th17 cell populations and elevated CSF osteopontin and IL-17 concentrations in patients with Guillain-Barré syndrome.

Authors:  Rong Kun Han; Yue Feng Cheng; Shan Shan Zhou; Hong Guo; Rui Dong He; Li Jun Chi; Li Ming Zhang
Journal:  J Clin Immunol       Date:  2013-11-12       Impact factor: 8.317

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