The Epidemiology of Guillain-Barré Syndrome Worldwide

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Abstract

Background: This systematic literature review of the epidemiology of Guillain-Barré syndrome (GBS) identifies trends in incidence rates by age, study method and cause of disease. It is important to have a reliable estimate of incidence to determine and investigate any changes: no previous systematic reviews of GBS have been found. Methods: After critical assessment of the reliability of the reported data, incidence rates were extracted from all relevant papers published between 1980 and 2008, identified through searches of Medline, Embase and Science Direct. Results: Sixty-three papers were included in this review; these studies were prospective, retrospective reviews of medical records or retrospective database studies. Ten studies reported on the incidence in children (0–15 years old), and found the annual incidence to be between 0.34 and 1.34/100,000. Most studies investigated populations in Europe and North America and reported similar annual incidence rates, i.e. between 0.84 and 1.91/100,000. A decrease in incidence over the time between the 1980s and 1990s was found. Up to 70% of cases of GBS were caused by antecedent infections. Conclusions: Our best estimate of the overall incidence of GBS was between 1.1/100,000/year and 1.8/100,000/year. The incidence of GBS increased with age after 50 years from 1.7/100,000/year to 3.3/100,000/year.

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Most cited references 41

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Guillain-Barré syndrome.

Richard Hughes, David Cornblath (2005)

Guillain-Barré syndrome consists of at least four subtypes of acute peripheral neuropathy. Major advances have been made in understanding the mechanisms of some of the subtypes. The histological appearance of the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) subtype resembles experimental autoimmune neuritis, which is predominantly caused by T cells directed against peptides from the myelin proteins P0, P2, and PMP22. The role of T-cell-mediated immunity in AIDP remains unclear and there is evidence for the involvement of antibodies and complement. Strong evidence now exists that axonal subtypes of Guillain-Barré syndrome, acute motor axonal neuropathy (AMAN), and acute motor and sensory axonal neuropathy (AMSAN), are caused by antibodies to gangliosides on the axolemma that target macrophages to invade the axon at the node of Ranvier. About a quarter of patients with Guillain-Barré syndrome have had a recent Campylobacter jejuni infection, and axonal forms of the disease are especially common in these people. The lipo-oligosaccharide from the C jejuni bacterial wall contains ganglioside-like structures and its injection into rabbits induces a neuropathy that resembles acute motor axonal neuropathy. Antibodies to GM1, GM1b, GD1a, and GalNac-GD1a are in particular implicated in acute motor axonal neuropathy and, with the exception of GalNacGD1a, in acute motor and sensory axonal neuropathy. The Fisher's syndrome subtype is especially associated with antibodies to GQ1b, and similar cross-reactivity with ganglioside structures in the wall of C jejuni has been discovered. Anti-GQ1b antibodies have been shown to damage the motor nerve terminal in vitro by a complement-mediated mechanism. Results of international randomised trials have shown equivalent efficacy of both plasma exchange and intravenous immunoglobulin, but not corticosteroids, in hastening recovery from Guillain-Barré syndrome. Further research is needed to discover treatments to prevent 20% of patients from being left with persistent and significant disability.

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Clinical and epidemiologic features of Guillain-Barré syndrome.

R. Hughes, Jonathan Rees (1997)

Guillain-Barré syndrome (GBS) is defined clinically as a peripheral neuropathy causing limb weakness that progresses for up to 4 weeks before reaching a plateau. The symptoms may be caused by inflammatory demyelination, axonal degeneration, or both. GBS occurs throughout the world, with a median incidence of 1.3 cases/100,000 population (range, 0.4-4.0). Males are more commonly affected than females, and there are peaks in young adults and the elderly. There is no clear seasonal association in Western countries, although this may be because the most frequent antecedent events, respiratory and enteric infections, have opposite seasonality. The most frequently identified cause of GBS is Campylobacter jejuni infection, which has been identified in up to 41% of patients and is associated with more severe disease and prolonged disability. Summer epidemics of GBS occur among children and young adults in Northern China and are particularly likely to be associated with C. jejuni infection.

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Guillain-Barré syndrome: incidence and mortality rates in US hospitals.

Amer Alshekhlee, Zulfiqar Hussain, Badr Sultan … (2008)

To determine the incidence, in-hospital mortality, and predictors of death in Guillain-Barré syndrome (GBS) in a large US cohort. Our cohort was identified from the Nationwide Inpatient Sample database, 2000 through 2004. We excluded patients younger than 18 years and those who presented with rapidly paralyzing conditions due to other causes. GBS patients who were transferred between hospitals were counted once. The incidence rate adjusted for 20% of the US census reported by the Census Bureau. A logistic regression model was used to identify predictors of death. After data cleansing, 4,954 patients were identified with a primary diagnosis of GBS. The adjusted incidence rate varied between 1.65 and 1.79 per 100,000 during the years included in this study. The in-hospital mortality rate was 2.58% (128/4,954) and did not change significantly over the study period. Eleven percent had variable pulmonary complications, and 9.1% received endotracheal intubation, which was a predictor of mortality (adjusted odds ratio 5.09, 95% CI 3.21-8.05). Other predictors of mortality included older age, composite comorbidity index, cardiac complications, and sepsis. The mortality rate in Guillain-Barré syndrome is low, and predictors of death are similar to those predicting poor disability outcome. The disease incidence was stable over the 5 years included in this study.

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Author and article information

Journal

Journal ID (publisher-id): NED

Journal ID (nlm-ta): Neuroepidemiology

Journal ID (doi): 10.1159/issn.0251-5350

Title: Neuroepidemiology

Publisher: S. Karger AG

ISSN (Print): 0251-5350

ISSN (Electronic): 1423-0208

Publication date Subscription-year: 2009

Publication date (Print): February 2009

Publication date (Electronic): 17 December 2008

Volume: 32

Issue: 2

Pages: 150-163

Affiliations

^aDepartment of Pharmacy and Pharmacology, University of Bath, Bath, and ^bDepartment of Pharmacoepidemiology, Postgraduate Medical School, University of Surrey, Guildford, UK

Article

Publisher ID: 184748 Other ID: Neuroepidemiology 2009;32:150–163

DOI: 10.1159/000184748

PubMed ID: 19088488

SO-VID: c1ed4455-0d64-4a40-966b-37f178c03d71

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 02 August 2008

Date accepted : 24 September 2008

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Figures: 1, Tables: 2, References: 74, Pages: 14

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The Epidemiology of Guillain-Barré Syndrome Worldwide

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Abstract

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Karger: Neurology and Neuroscience

Most cited references 41

Guillain-Barré syndrome.

Clinical and epidemiologic features of Guillain-Barré syndrome.

Guillain-Barré syndrome: incidence and mortality rates in US hospitals.

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Cited by 169

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