Evidence map›Paper›PMID 35264149›Full record

ArticleBMC neurology2022

Failure of alemtuzumab therapy in three patients with MOG antibody associated disease.

Sinali O Seneviratne, Mark Marriott, Sudarshini Ramanathan, Wei Yeh, Fabienne Brilot-Turville, Helmut Butzkueven, Mastura Monif

Open access · goldAbstract readCase Reports
In one paragraph

Article in BMC neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Movement Disorders in MOGAD: A Systematic Review.Medicina (Kaunas, Lithuania) · 2026
    Pooled it
  2. Article
  3. Article
  4. MOG Antibody Disease: Nuances in Presentation, Diagnosis, and Management.Current neurology and neuroscience reports · 2024
    Review
  5. MOG antibody-associated optic neuritis.Eye (London, England) · 2024
    Review
  6. Article
  7. Quality of life is impaired in myelin oligodendrocyte glycoprotein antibody associated disease.Multiple sclerosis journal - experimental, translational and clinical
    Article
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

7 authors at 3 institutions in 1 country.

Sinali O SeneviratneCurtin University, Kent Street, Bentley, Perth, WA, 6102, Australia.
Mark MarriottDepartment of Neurology, Royal Melbourne Hospital, 300 Grattan Street, Parkville VIC 3050, Australia.
Sudarshini RamanathanTranslational Neuroimmunology Group, Kids Neuroscience Centre, The Kids Research Institute at the Children's Hospital, Westmead, NSW, Australia.
Wei YehDepartment of Neurology, Alfred Hospital, 55 Commercial Rd, Melbourne, VIC, 3004, Australia.
Fabienne Brilot-TurvilleTranslational Neuroimmunology Group, Kids Neuroscience Centre, The Kids Research Institute at the Children's Hospital, Westmead, NSW, Australia.
Helmut ButzkuevenDepartment of Neurology, Alfred Hospital, 55 Commercial Rd, Melbourne, VIC, 3004, Australia.
Mastura MonifDepartment of Neurology, Royal Melbourne Hospital, 300 Grattan Street, Parkville VIC 3050, Australia. mastura.monif@monash.edu.ORCID http://orcid.org/0000-0001-6404-9768
The Royal Melbourne Hospital · AUThe Alfred Hospital · AUThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyelin Oligodendrocyte Glycoprotein antibody-associated disease (MOGAD) is most classically associated in both children and adults with phenotypes including bilateral and recurrent optic neuritis (ON) and transverse myelitis (TM), with the absence of brain lesions characteristic of multiple sclerosis (MS). ADEM phenotype is the most common presentation of MOGAD in children. However, the presence of clinical phenotypes including unilateral ON and short TM in some patients with MOGAD may lead to their misdiagnosis as MS. Thus, clinically and radiologically, MOGAD can mimic MS and clinical vigilance is required for accurate diagnostic workup. CASE PRESENTATION: We present three cases initially diagnosed as MS and then treated with alemtuzumab. Unexpectedly, all three patients did quite poorly on this medication, with a decline in their clinical status with worsening of expanded disability status scale (EDSS) and an increasing lesion load on magnetic resonance imaging of the brain. Subsequently, all three cases were found to have anti-MOG antibody in their serum.

conclusionsThese cases highlight that if a patient suspected to have MS does not respond to conventional treatments such as alemtuzumab, a search for alternative diagnoses such as MOG antibody disease may be warranted.

Indexed as

Myelitis, TransverseOptic NeuritisAlemtuzumabAutoantibodiesHumansMyelin-Oligodendrocyte GlycoproteinAlemtuzumabAutoantibodiesMyelin-Oligodendrocyte GlycoproteinAutoimmuneDemyelinationEncephalomyelitisMOG antibodyMultiple sclerosis

Identifiers

PMID35264149
PMCPMC8905766
OpenAlexW4220657560

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.