Inhibition of complement in Guillain‐Barré syndrome: the <scp>ICA‐GBS</scp> study

Davidson, Amy; Halstead, Susan K.; Goodfellow, John; Chavada, Govind; Mallik, Arup; Overell, James; Lunn, Michael P.; McConnachie, Alex; Doorn, P. van; Willison, Hugh J.

doi:10.1111/jns.12194

Cited by 76 publications

(39 citation statements)

References 24 publications

(22 reference statements)

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“…In addition, development of new therapeutic options, such as complement inhibition, may be needed for patients with poor prognosis. This issue is now under investigation (Yamaguchi et al, ; Davidson et al, ) .…”

Section: Discussionmentioning

confidence: 99%

Markers for Guillain‐Barré syndrome with poor prognosis: a multi‐center study

Yamagishi

Suzuki

Sonoo

et al. 2017

J Peripheral Nervous Sys

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Guillain-Barré syndrome (GBS) is an acute monophasic neuropathy. Prognostic tools include the modified Erasmus GBS outcome score (mEGOS), Erasmus GBS respiratory insufficiency score (EGRIS), and the increase in serum IgG levels (ΔIgG) 2 weeks after intravenous immunoglobulin (IVIg) treatment. Given that proportions of GBS subtypes differ between Western countries and Japan, the usefulness of these tools in Japan or other countries remains unknown. We enrolled 177 Japanese patients with GBS from 15 university hospitals and retrospectively obtained mEGOS and EGRIS for all and ΔIgG status for 79 of them. High mEGOS scores on admission or on day 7 were significantly associated with poorer outcomes (unable to walk independently at 6 months). High EGRIS scores (≥5 points) were associated with an increased risk for mechanical ventilation. Patients with ΔIgG <1,108 mg/dl had significantly poorer outcomes. We suggest that mEGOS, EGRIS, and ΔIgG in GBS are clinically relevant in Japan.

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Section: Discussionmentioning

confidence: 99%

Markers for Guillain‐Barré syndrome with poor prognosis: a multi‐center study

Yamagishi

Suzuki

Sonoo

et al. 2017

J Peripheral Nervous Sys

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“…We excluded patients who had died or were lost to follow-up in the first 7 days from study entry, or who received a second IVIg course because of a reported treatment related fluctuation (TRF) observed by the local physician 13. We also excluded patients who participated in a randomised controlled study (Second Immunoglobulin Dose in GBS patients (SID-GBS) trial14 15 or Inhibition of Complement Activation in GBS (ICA-GBS) trial) 16…”

Section: Methodsmentioning

confidence: 99%

Original research: Second IVIg course in Guillain-Barré syndrome with poor prognosis: the non-randomised ISID study

Verboon

Berg

Cornblath

et al. 2019

J Neurol Neurosurg Psychiatry

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ObjectiveTo compare disease course in patients with Guillain-Barré syndrome (GBS) with a poor prognosis who were treated with one or with two intravenous immunoglobulin (IVIg) courses.MethodsFrom the International GBS Outcome Study, we selected patients whose modified Erasmus GBS Outcome Score at week 1 predicted a poor prognosis. We compared those treated with one IVIg course to those treated with two IVIg courses. The primary endpoint, the GBS disability scale at 4 weeks, was assessed with multivariable ordinal regression.ResultsOf 237 eligible patients, 199 patients received a single IVIg course. Twenty patients received an ‘early’ second IVIg course (1–2 weeks after start of the first IVIg course) and 18 patients a ‘late’ second IVIg course (2–4 weeks after start of IVIg). At baseline and 1 week, those receiving two IVIg courses were more disabled than those receiving one course. Compared with the one course group, the adjusted OR for a better GBS disability score at 4 weeks was 0.70 (95%CI 0.16 to 3.04) for the early group and 0.66 (95%CI 0.18 to 2.50) for the late group. The secondary endpoints were not in favour of a second IVIg course.ConclusionsThis observational study did not show better outcomes after a second IVIg course in GBS with poor prognosis. The study was limited by small numbers and baseline imbalances. Lack of improvement was likely an incentive to start a second IVIg course. A prospective randomised trial is needed to evaluate whether a second IVIg course improves outcome in GBS.

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“…Lastly, we need to translate increased understanding of pathogenesis to meaningful treatment or prevention. Immunotherapeutic trials of blocking the complement cascade (ie, eculizumab, 88,89 monoclonal antibodies binding to complement factor 5) are under way.…”

Section: Precautionsmentioning

confidence: 99%

Guillain-Barré Syndrome

Wijdicks

Klein

2017

Mayo Clinic Proceedings

177

146

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Guillain-Barré syndrome is an acute inflammatory immune-mediated polyradiculoneuropathy presenting typically with tingling, progressive weakness, and pain. Variants and formes frustes may complicate recognition. The best known variant is the sensory ataxic form of Miller Fisher syndrome, which also affects the oculomotor nerves and the brain stem. Divergent pathologic mechanisms lead to demyelinating, axonal, or mixed demyelinating-axonal damage. In the demyelinating form, yet to be identified antigens are inferred by complement activation, myelin destruction, and macrophage-activated cleanup. In the axonal and Miller Fisher variants, gangliosides (GM1, GD1a, GQ1b) are targeted by immunoglobulins and share antigenic epitopes with some bacterial and viral antigens. Campylobacter jejuni infection is associated with an axonal-onset variant; affected patients commonly experience more rapid deterioration. Many other antecedent infectious agents have been recognized including the most recently identified, Zika virus. Supportive care remains the mainstay of therapy. Plasma exchange or intravenous immunoglobin hastens recovery. Combination immunotherapy is not more effective, and the efficacy of prolonged immunotherapy is unproven. One in 3 patients will have deterioration severe enough to require prolonged intensive care monitoring or mechanical ventilation. Full recovery is often seen; most patients regain ambulation, even in severe cases, but disability remains in up to 10% and perhaps more. Numerous challenges remain including early identification and control of infectious triggers, improved access of modern neurointensive care worldwide, and translating our understanding of pathogenesis into meaningful preventive or assistive therapies. This review provides a historical perspective at the centenary of the first description of the syndrome, insights into its pathogenesis, triage, initial immunotherapy, and management in the intensive care unit.

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Inhibition of complement in Guillain‐Barré syndrome: the ICA‐GBS study

Cited by 76 publications

References 24 publications

Markers for Guillain‐Barré syndrome with poor prognosis: a multi‐center study

Markers for Guillain‐Barré syndrome with poor prognosis: a multi‐center study

Original research: Second IVIg course in Guillain-Barré syndrome with poor prognosis: the non-randomised ISID study

Guillain-Barré Syndrome

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