Guillain-Barré syndrome related to Zika virus infection: A systematic review and meta-analysis of the clinical and electrophysiological phenotype
The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all pu...
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| Vydáno v: | PLoS neglected tropical diseases Ročník 14; číslo 4; s. e0008264 |
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| Hlavní autoři: | , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Public Library of Science
01.04.2020
Public Library of Science (PLoS) |
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| ISSN: | 1935-2735, 1935-2727, 1935-2735 |
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| Abstract | The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS.
We searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated.
Thirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15-47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93-99), diminished/absent reflexes 96% (95%CI 88-100), sensory symptoms 82% (95%CI 76-88), and facial palsy 51% (95%CI 44-58). Median time between infectious and neurological symptoms was 5-12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables.
The clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959). |
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| AbstractList | Background
The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS.
Methods
We searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated.
Results
Thirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15–47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93–99), diminished/absent reflexes 96% (95%CI 88–100), sensory symptoms 82% (95%CI 76–88), and facial palsy 51% (95%CI 44–58). Median time between infectious and neurological symptoms was 5–12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables.
Conclusions
The clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959). Guillain-Barré syndrome (GBS) is a rare but severe neurological disease, characterized by an acute onset flaccid paralysis. GBS is thought to be caused by an exaggerated immune response to common infections that damages the peripheral nerves. The Zika virus (ZIKV) is the most recent pathogen to be connected to GBS, when large outbreaks of ZIKV infection in French Polynesia and Latin America were followed by an increased incidence of GBS patients. To better understand the clinical features and outcome of ZIKV-related GBS, we have performed a systematic review and meta-analysis of all published studies on GBS related to ZIKV. We identified 35 studies, reporting on a total of 601 patients with GBS and a suspected, probable or confirmed Zika virus infection, and were able to summarize data of 587 patients from 21 studies in a pooled analysis. Our study shows that published cases with ZIKV-related GBS generally have both sensory and motor symptoms, facial palsy, demyelination on electrophysiological examination, and a severe disease course that often necessitates ICU admittance. The relatively long time between infectious and neurologic symptoms and the lack of detection of viral particles in bodily fluids in most patients suggest a post-infectious rather than an infectious pathogenesis. However, these results should be interpreted taking into account the heterogeneity between studies, which was considerable for many variables, and a possible reporting bias of more severe cases. Outbreaks of ZIKV and GBS may appear in the future and our study can help clinicians in diagnosing and managing GBS patients in ZIKV endemic areas, and increases our understanding of the neuropathology of ZIKV. The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS. We searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated. Thirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15-47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93-99), diminished/absent reflexes 96% (95%CI 88-100), sensory symptoms 82% (95%CI 76-88), and facial palsy 51% (95%CI 44-58). Median time between infectious and neurological symptoms was 5-12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables. The clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959). Background The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS. Methods We searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated. Results Thirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15–47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93–99), diminished/absent reflexes 96% (95%CI 88–100), sensory symptoms 82% (95%CI 76–88), and facial palsy 51% (95%CI 44–58). Median time between infectious and neurological symptoms was 5–12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables. Conclusions The clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959). The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS.BACKGROUNDThe Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS.We searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated.METHODSWe searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated.Thirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15-47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93-99), diminished/absent reflexes 96% (95%CI 88-100), sensory symptoms 82% (95%CI 76-88), and facial palsy 51% (95%CI 44-58). Median time between infectious and neurological symptoms was 5-12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables.RESULTSThirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15-47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93-99), diminished/absent reflexes 96% (95%CI 88-100), sensory symptoms 82% (95%CI 76-88), and facial palsy 51% (95%CI 44-58). Median time between infectious and neurological symptoms was 5-12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables.The clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959).CONCLUSIONSThe clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959). BackgroundThe Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS.MethodsWe searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated.ResultsThirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15-47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93-99), diminished/absent reflexes 96% (95%CI 88-100), sensory symptoms 82% (95%CI 76-88), and facial palsy 51% (95%CI 44-58). Median time between infectious and neurological symptoms was 5-12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables.ConclusionsThe clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959). |
| Author | Cunha, Sergio Leonhard, Sonja E. Bresani-Salvi, Cristiane C. Lyra Batista, Joanna D. Brito Ferreira, Maria Lucia Jacobs, Bart C. P. Militão de Albuquerque, Maria de Fatima |
| AuthorAffiliation | 7 NESC Department, Oswaldo Cruz Foundation, Ministry of Health, Recife, Brazil Australian Red Cross Lifelood, AUSTRALIA 1 Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands 3 Medical Sciences College, Federal University of Fronteira Sul, Chapecó, Brazil 6 Department of Neurology, Hospital da Restauração, Recife, Brazil 2 Laboratory of Virology and Experimental Therapy, Oswaldo Cruz Foundation, Ministry of Health, Recife, Brazil 4 Department of Preventive Medicine, Federal University of Pernambuco, Recife, Brazil 5 Department of Immunology, Erasmus University Medical Center, Rotterdam, The Netherlands |
| AuthorAffiliation_xml | – name: 7 NESC Department, Oswaldo Cruz Foundation, Ministry of Health, Recife, Brazil – name: 5 Department of Immunology, Erasmus University Medical Center, Rotterdam, The Netherlands – name: 1 Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands – name: 4 Department of Preventive Medicine, Federal University of Pernambuco, Recife, Brazil – name: 6 Department of Neurology, Hospital da Restauração, Recife, Brazil – name: Australian Red Cross Lifelood, AUSTRALIA – name: 2 Laboratory of Virology and Experimental Therapy, Oswaldo Cruz Foundation, Ministry of Health, Recife, Brazil – name: 3 Medical Sciences College, Federal University of Fronteira Sul, Chapecó, Brazil |
| Author_xml | – sequence: 1 givenname: Sonja E. orcidid: 0000-0003-4832-6926 surname: Leonhard fullname: Leonhard, Sonja E. – sequence: 2 givenname: Cristiane C. surname: Bresani-Salvi fullname: Bresani-Salvi, Cristiane C. – sequence: 3 givenname: Joanna D. surname: Lyra Batista fullname: Lyra Batista, Joanna D. – sequence: 4 givenname: Sergio surname: Cunha fullname: Cunha, Sergio – sequence: 5 givenname: Bart C. surname: Jacobs fullname: Jacobs, Bart C. – sequence: 6 givenname: Maria Lucia surname: Brito Ferreira fullname: Brito Ferreira, Maria Lucia – sequence: 7 givenname: Maria de Fatima surname: P. Militão de Albuquerque fullname: P. Militão de Albuquerque, Maria de Fatima |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32339199$$D View this record in MEDLINE/PubMed |
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| Copyright | 2020 Leonhard et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2020 Leonhard et al 2020 Leonhard et al |
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| DOI | 10.1371/journal.pntd.0008264 |
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| Notes | new_version ObjectType-Article-2 SourceType-Scholarly Journals-1 content type line 14 ObjectType-Feature-3 ObjectType-Evidence Based Healthcare-1 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 ObjectType-Undefined-3 SEL, CCBS, MLBF, JLB, SC and MFPMA declare no competing interests. BCJ has received funding from Annexon Biosciences, Baxter, CSL Behring, Hansa Biopharma and Grifols. |
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| Snippet | The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific... Background The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a... Guillain-Barré syndrome (GBS) is a rare but severe neurological disease, characterized by an acute onset flaccid paralysis. GBS is thought to be caused by an... BackgroundThe Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a... Background The Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a... |
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| SubjectTerms | Bias Biology and life sciences Campylobacter Case reports Cohorts Cytomegalovirus Demographics Demyelination DNA Electrical impedance Electrophysiology Epidemiology Guillain-Barre syndrome Heterogeneity Infections Infectious diseases Laboratories Literature reviews Medicine and Health Sciences Meta-analysis Neurology Nucleotide sequence Paralysis Pathogens PCR Phenotypes Protocols Reflexes Research and Analysis Methods Sensorimotor system Signs and symptoms Symptoms Systematic review Tropical diseases Variables Vector-borne diseases Viruses Zika virus |
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| Title | Guillain-Barré syndrome related to Zika virus infection: A systematic review and meta-analysis of the clinical and electrophysiological phenotype |
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