Evidence map›Paper›PMID 42633032›Full record

ArticleMultiple sclerosis journal - experimental, translational and clinical

Effect of ocrelizumab on rates of retinal atrophy in relapsing multiple sclerosis.

Brenna McCormack, Anna Bacchetti, Ting-Yi Lin, Giulia S Moretti, Angeliki Filippatou, Georgios Gakis, Martin Maurice O'Donnell, Clare McGarvey Lambert, Nathanael J Lee, Kaitlyn Ecoff and 16 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Multiple sclerosis journal - experimental, translational and clinical. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

26 authors.

Brenna McCormackDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0009-0002-6678-7021
Anna BacchettiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0009-0000-9434-8531
Ting-Yi LinDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0001-9605-8095
Giulia S MorettiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0009-0001-1532-5284
Angeliki FilippatouDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0003-0419-233X
Georgios GakisDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-7339-4659
Martin Maurice O'DonnellDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0001-7846-6597
Clare McGarvey LambertDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-1194-0538
Nathanael J LeeDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-1772-1723
Kaitlyn EcoffDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Simidele DavisDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Gabriel Otero-DuranDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Ananya GulatiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Adam DidouchevskiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Ernest LieversDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Nicole PellegriniDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Omar EzzedinDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Jeffrey LambeDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hussein MoussaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Kathryn FitzgeraldDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0003-3137-0322
Scott D NewsomeDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-5284-4681
Ellen M MowryDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0003-0623-5188
Elias S SotirchosDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-8812-1637
Peter A CalabresiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-7776-6472
Bardia NourbakhshDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-6617-2003
Shiv SaidhaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0001-6387-0714

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Ganglion cell + inner plexiform layer (GCIPL) atrophy reflects global neurodegeneration and disability in multiple sclerosis (MS). The effect of ocrelizumab, an anti-CD20 monoclonal antibody and highly-effective disease modifying therapy (DMT), on rates of GCIPL atrophy in people with MS remains understudied. Objectives: To assess if ocrelizumab attenuates retinal atrophy rates, particularly GCIPL atrophy, and change in clinical measures in people with relapsing MS (PwRMS), and how this compares to natalizumab (another highly-effective DMT), as well as the related anti-CD20 therapy rituximab. Methods: PwRMS receiving ocrelizumab, natalizumab, or rituximab, untreated people with progressive MS (PwPMS), and healthy controls underwent Cirrus HD-OCT, 100% and 2.5%-contrast letter acuity (LA) assessments longitudinally. MS participants underwent Expanded Disability Status Scale (EDSS) assessments. Statistical analyses used linear mixed-effects regression models adjusting for age, sex, race, disease duration, optic neuritis history, and interval between DMT initiation and OCT monitoring; accounting for within-subject, inter-eye correlations. Results: In ocrelizumab-treated PwRMS, GCIPL atrophy rate was -0.15 µm/year (SE = 0.03, p < 0.001, n = 88 [168 eyes]), similar to GCIPL atrophy in natalizumab- or rituximab-treated PwRMS, and healthy controls, although slower than in untreated PwPMS (-0.35 µm/year, SE = 0.04, p < 0.001, n = 40 [78 eyes]). EDSS and LA scores remained stable in ocrelizumab-treated PwRMS, and similar to natalizumab- or rituximab-treated PwRMS. Conclusion: GCIPL atrophy is attenuated and clinical function relatively stable in PwRMS treated with ocrelizumab.

Indexed as

biomarkersdisease modifying therapiesMultiple sclerosisocrelizumaboptical coherence tomography

Identifiers

PMID42633032
PMCPMC13498846

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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.