Evidence map›Paper›PMID 28233109›Full record

ReviewClinical rheumatology2017

Is secukinumab a safe alternative treatment for ankylosing spondylitis with Guillain Barré syndrome after anti-TNF-α treatment? Case report and literature review.

Savvas Psarelis, Andreas P D Hajineocli, Eleni Hadjicosta, Hugh St A Elliott, Paul Johnson

Abstract readCase ReportsReview
PubMed Publisher
In one paragraph

Review in Clinical rheumatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Savvas PsarelisSt George's, University of London Medical Programme, Delivered in Cyprus by the University of Nicosia Medical School, Nicosia, Cyprus. serres23@yahoo.gr.
Andreas P D HajineocliSt George's, University of London Medical Programme, Delivered in Cyprus by the University of Nicosia Medical School, Nicosia, Cyprus.
Eleni HadjicostaSt George's, University of London Medical Programme, Delivered in Cyprus by the University of Nicosia Medical School, Nicosia, Cyprus.
Hugh St A ElliottSt George's, University of London Medical Programme, Delivered in Cyprus by the University of Nicosia Medical School, Nicosia, Cyprus.
Paul JohnsonSt George's, University of London Medical Programme, Delivered in Cyprus by the University of Nicosia Medical School, Nicosia, Cyprus.
University of Nicosia · CY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this report, we aim to add to the existing body of evidence regarding a link between anti- tumor necrosis factor alpha (anti-TNF-α) treatment and demyelination leading to neurological disorders, specifically Guillain Barré syndrome (GBS), and treatment with an interleukin-17A (IL17A) antagonist as a safe alternative for ankylosing spondylitis (AS). A literature review was carried out of current research concerning anti-TNF-α and induced GBS. Only papers published in English were reviewed and only peer-reviewed journals searched. Papers published up to September 2016 were included. Animal studies were excluded. Data bases searched for publications online included: Pub Med, Google Scholar, The Cochrane Library, and Web of Science. Searched terms include "anti-TNF" and "Guillain Barré", "IL17 Ankylosing Spondylitis", "Secukinumab" and "TNF-α", "adalimumab", "infliximab", and "etanercept". All combinations and outcomes were used, and from these searches, a provisional reference list was constructed. The short-listed articles were read and their reference lists were reviewed. The electromyogram done for the patient showed demyelination, the MRI of the brain showed no pathologies, and the MRI of the spine was consistent with ankylosing spondylitis without myelopathy. The lumbar puncture results showed albuminocytological dissociation that was consistent with GBS. TNF has a proinflammatory action, and various immunoregulatory actions that, together, seem to promote the development of peripheral neuropathies syndromes in the organism. However, there is no clear mechanism of why or how anti-TNF-α treatment can induce a demyelinating event in a patient. In the case presented, it was found that the patient developed GBS due to treatment with etanercept, an anti-TNF agent. The treatment was stopped immediately. Two years later, he was switched to secukinumab and has been well controlled for the last 8 months with no neurological findings.

Indexed as

Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedEtanerceptGuillain-Barre SyndromeHumansImmunoglobulins, IntravenousImmunologic FactorsImmunosuppressive AgentsInterleukin-17MaleMiddle AgedSpondylitis, AnkylosingTumor Necrosis Factor-alphaAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedEtanerceptImmunoglobulins, IntravenousImmunologic FactorsImmunosuppressive AgentsInterleukin-17secukinumabTumor Necrosis Factor-alphaAnkylosing Spondylitis (Rheumatic Disease)Anti-TNF-αGuillain Barré syndromeSecukinumab

Identifiers

PMID28233109
OpenAlexW2590045192

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.