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Guillain-Barré syndrome and related diseases after influenza virus infection
OBJECTIVE: We examined the clinical and serologic features of Guillain-Barré syndrome (GBS)-related diseases (GBSRDs), including GBS, Fisher syndrome (FS), and Bickerstaff brainstem encephalitis (BBE), after influenza virus infection (GBSRD-I) to reveal potential underlying autoimmune mechanisms. ME...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6624088/ https://www.ncbi.nlm.nih.gov/pubmed/31355311 http://dx.doi.org/10.1212/NXI.0000000000000575 |
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author | Yamana, Masaki Kuwahara, Motoi Fukumoto, Yuta Yoshikawa, Keisuke Takada, Kazuo Kusunoki, Susumu |
author_facet | Yamana, Masaki Kuwahara, Motoi Fukumoto, Yuta Yoshikawa, Keisuke Takada, Kazuo Kusunoki, Susumu |
author_sort | Yamana, Masaki |
collection | PubMed |
description | OBJECTIVE: We examined the clinical and serologic features of Guillain-Barré syndrome (GBS)-related diseases (GBSRDs), including GBS, Fisher syndrome (FS), and Bickerstaff brainstem encephalitis (BBE), after influenza virus infection (GBSRD-I) to reveal potential underlying autoimmune mechanisms. METHODS: We retrospectively investigated the presence of antiglycolipid antibodies against 11 glycolipids and the clinical features of 63 patients with GBSRD-I. Autoantibody profiles and clinical features were compared with those of 82 patients with GBSRDs after Campylobacter jejuni infection (GBSRD-C). RESULTS: The anti-GQ1b seropositivity rate was significantly higher, whereas the GM1 and GD1a seropositivity rates were significantly lower in GBSRD-I compared with GBSRD-C. Anti-GQ1b and anti-GT1a were the most frequently detected antiglycolipid antibodies in GBSRD-I (both 15/63, 24%). Consequently, FS was more frequent in GBSRD-I than GBSRD-C (22% vs 9%, p < 0.05). In addition, as for GBS, cranial nerve deficits, sensory disturbances, and ataxia were more frequent in the cases after influenza infection (GBS-I) than in those after C. jejuni infection (GBS-C) (46% vs 15%, 75% vs 46%, and 29% vs 4%, respectively; all p < 0.01). Nerve conduction studies revealed acute inflammatory demyelinating polyneuropathy (AIDP) in 60% of patients with GBS-I but only 25% of patients with GBS-C (p < 0.01). CONCLUSIONS: Anti-GQ1b antibodies are the most frequently detected antibodies in GBSRD-I. Compared with GBS-C, GBS-I is characterized by AIDP predominance and frequent presence of cranial nerve involvement and ataxia. |
format | Online Article Text |
id | pubmed-6624088 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-66240882019-07-26 Guillain-Barré syndrome and related diseases after influenza virus infection Yamana, Masaki Kuwahara, Motoi Fukumoto, Yuta Yoshikawa, Keisuke Takada, Kazuo Kusunoki, Susumu Neurol Neuroimmunol Neuroinflamm Article OBJECTIVE: We examined the clinical and serologic features of Guillain-Barré syndrome (GBS)-related diseases (GBSRDs), including GBS, Fisher syndrome (FS), and Bickerstaff brainstem encephalitis (BBE), after influenza virus infection (GBSRD-I) to reveal potential underlying autoimmune mechanisms. METHODS: We retrospectively investigated the presence of antiglycolipid antibodies against 11 glycolipids and the clinical features of 63 patients with GBSRD-I. Autoantibody profiles and clinical features were compared with those of 82 patients with GBSRDs after Campylobacter jejuni infection (GBSRD-C). RESULTS: The anti-GQ1b seropositivity rate was significantly higher, whereas the GM1 and GD1a seropositivity rates were significantly lower in GBSRD-I compared with GBSRD-C. Anti-GQ1b and anti-GT1a were the most frequently detected antiglycolipid antibodies in GBSRD-I (both 15/63, 24%). Consequently, FS was more frequent in GBSRD-I than GBSRD-C (22% vs 9%, p < 0.05). In addition, as for GBS, cranial nerve deficits, sensory disturbances, and ataxia were more frequent in the cases after influenza infection (GBS-I) than in those after C. jejuni infection (GBS-C) (46% vs 15%, 75% vs 46%, and 29% vs 4%, respectively; all p < 0.01). Nerve conduction studies revealed acute inflammatory demyelinating polyneuropathy (AIDP) in 60% of patients with GBS-I but only 25% of patients with GBS-C (p < 0.01). CONCLUSIONS: Anti-GQ1b antibodies are the most frequently detected antibodies in GBSRD-I. Compared with GBS-C, GBS-I is characterized by AIDP predominance and frequent presence of cranial nerve involvement and ataxia. Lippincott Williams & Wilkins 2019-05-21 /pmc/articles/PMC6624088/ /pubmed/31355311 http://dx.doi.org/10.1212/NXI.0000000000000575 Text en Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND) (http://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. |
spellingShingle | Article Yamana, Masaki Kuwahara, Motoi Fukumoto, Yuta Yoshikawa, Keisuke Takada, Kazuo Kusunoki, Susumu Guillain-Barré syndrome and related diseases after influenza virus infection |
title | Guillain-Barré syndrome and related diseases after influenza virus infection |
title_full | Guillain-Barré syndrome and related diseases after influenza virus infection |
title_fullStr | Guillain-Barré syndrome and related diseases after influenza virus infection |
title_full_unstemmed | Guillain-Barré syndrome and related diseases after influenza virus infection |
title_short | Guillain-Barré syndrome and related diseases after influenza virus infection |
title_sort | guillain-barré syndrome and related diseases after influenza virus infection |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6624088/ https://www.ncbi.nlm.nih.gov/pubmed/31355311 http://dx.doi.org/10.1212/NXI.0000000000000575 |
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