Síndrome de Guillain-Barré debido al virus del Zika durante el embarazo

López-Sánchez, Geraldine; Santos-Bolívar, Joel

doi:10.1016/j.medcli.2016.02.002

Cited by 18 publications

(15 citation statements)

References 5 publications

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“…All patients with GBS had laboratory-confirmed Zika virus infection except for 42 of 44 in Brazil and all those in El Salvador. The intervals between Zika virus infection and neurological symptoms delays of 3 to 12 d [108, 111, 112] are consistent with a postinfectious autoimmune mechanism [5]. In one ecological study in Bahia, Brazil, a lag of 5 to 9 wk between the epidemic peaks of cases with acute exanthematous illness and GBS was attributed to data collection issues [78].…”

Section: Resultsmentioning

confidence: 91%

“…We reviewed six items [54, 102, 111, 112, 114, 116] in four groups (S6 Table). Anti-ganglioside antibodies, whose presence supports the clinical diagnosis of GBS, were found in the serum of a third of patients in a case-control study in French Polynesia [112] and in one patient from Venezuela [111].…”

Section: Resultsmentioning

confidence: 99%

“…Anti-ganglioside antibodies, whose presence supports the clinical diagnosis of GBS, were found in the serum of a third of patients in a case-control study in French Polynesia [112] and in one patient from Venezuela [111]. The case-control study and two in silico studies also provide some evidence for molecular mimicry of Zika virus epitopes and host antigens [112].…”

Section: Resultsmentioning

confidence: 99%

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Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

et al. 2017

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BackgroundThe World Health Organization (WHO) stated in March 2016 that there was scientific consensus that the mosquito-borne Zika virus was a cause of the neurological disorder Guillain–Barré syndrome (GBS) and of microcephaly and other congenital brain abnormalities based on rapid evidence assessments. Decisions about causality require systematic assessment to guide public health actions. The objectives of this study were to update and reassess the evidence for causality through a rapid and systematic review about links between Zika virus infection and (a) congenital brain abnormalities, including microcephaly, in the foetuses and offspring of pregnant women and (b) GBS in any population, and to describe the process and outcomes of an expert assessment of the evidence about causality.Methods and FindingsThe study had three linked components. First, in February 2016, we developed a causality framework that defined questions about the relationship between Zika virus infection and each of the two clinical outcomes in ten dimensions: temporality, biological plausibility, strength of association, alternative explanations, cessation, dose–response relationship, animal experiments, analogy, specificity, and consistency. Second, we did a systematic review (protocol number CRD42016036693). We searched multiple online sources up to May 30, 2016 to find studies that directly addressed either outcome and any causality dimension, used methods to expedite study selection, data extraction, and quality assessment, and summarised evidence descriptively. Third, WHO convened a multidisciplinary panel of experts who assessed the review findings and reached consensus statements to update the WHO position on causality. We found 1,091 unique items up to May 30, 2016. For congenital brain abnormalities, including microcephaly, we included 72 items; for eight of ten causality dimensions (all except dose–response relationship and specificity), we found that more than half the relevant studies supported a causal association with Zika virus infection. For GBS, we included 36 items, of which more than half the relevant studies supported a causal association in seven of ten dimensions (all except dose–response relationship, specificity, and animal experimental evidence). Articles identified nonsystematically from May 30 to July 29, 2016 strengthened the review findings. The expert panel concluded that (a) the most likely explanation of available evidence from outbreaks of Zika virus infection and clusters of microcephaly is that Zika virus infection during pregnancy is a cause of congenital brain abnormalities including microcephaly, and (b) the most likely explanation of available evidence from outbreaks of Zika virus infection and GBS is that Zika virus infection is a trigger of GBS. The expert panel recognised that Zika virus alone may not be sufficient to cause either congenital brain abnormalities or GBS but agreed that the evidence was sufficient to recommend increased public health measures. Weaknesses are the limited assessment of ...

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Section: Resultsmentioning

confidence: 91%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

et al. 2017

View full text Add to dashboard Cite

show abstract

“…All patients with Guillain-Barré syndrome had laboratory confirmed Zika virus infection except for 42 of 43 in Brazil and all those in El Salvador. The intervals between Zika virus and neurological symptoms delays of three to 12 days [115, 118, 119] are consistent with a post-infectious autoimmune mechanism [5]. In one ecological study in Bahia, Brazil, the lag between the epidemic peaks of cases with acute exanthematous illness and Guillain-Barré syndrome was five to nine weeks; the authors concluded that the actual delay might be shorter because the surveillance data recorded the date of hospitalisation rather than the onset of symptoms [84].…”

Section: Resultsmentioning

confidence: 99%

“…We reviewed six items [61, 109, 118, 119, 121, 123] in four groups that addressed two of three questions about biologically plausible mechanisms by which Zika virus could act as a trigger of Guillain-Barré syndrome (S5a Table). Anti-ganglioside antibodies, whose presence supports the clinical diagnosis of Guillain-Barré syndrome, were found in the serum of a third of patients in a case-control study in French Polynesia [119] and in one patient from Venezuela [118]. The case-control study and two in silico studies also provide some evidence for molecular mimicry of Zika virus epitopes and host antigens [119].…”

Section: Resultsmentioning

confidence: 99%