Evidence map›Paper›PMID 39651331›Full record

ArticleMultiple sclerosis journal - experimental, translational and clinical

CNS B cell infiltration in tumefactive anti-myelin oligodendrocyte glycoprotein antibody-associated disease.

Ryotaro Ikeguchi, Natsuki Kanda, Masaki Kobayashi, Kenta Masui, Masayuki Nitta, Tatsuro Misu, Yoshihiro Muragaki, Takakazu Kawamata, Noriyuki Shibata, Kazuo Kitagawa and 1 more

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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. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

11 authors.

Ryotaro IkeguchiDepartment of Neurology, Tokyo Women's Medical University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-1197-1705
Natsuki KandaDepartment of Neurology, Tokyo Women's Medical University, Tokyo, Japan.
Masaki KobayashiDepartment of Neurology, Tokyo Women's Medical University, Tokyo, Japan.
Kenta MasuiDepartment of Pathology, Tokyo Women's Medical University, Tokyo, Japan.
Masayuki NittaDepertment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.
Tatsuro MisuDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yoshihiro MuragakiDepertment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.
Takakazu KawamataDepertment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.
Noriyuki ShibataDepartment of Pathology, Tokyo Women's Medical University, Tokyo, Japan.
Kazuo KitagawaDepartment of Neurology, Tokyo Women's Medical University, Tokyo, Japan.
Yuko ShimizuDepartment of Neurology, Tokyo Women's Medical University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-1903-1400

Funding

Wellcome Trust FC001030
6 · The paper itself

Abstract

Background: Few studies have examined B cells among patients with anti-myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD), including brain pathology. Objective: To describe cases of tumefactive MOGAD with B-cell dominant central nervous system (CNS) infiltration. Methods: In this study, we reviewed three cases with clinical and brain histopathological features with tumefactive MOGAD. Results: Forty-nine cases of tumefactive brain lesions (TBL) between January 2003 and December 2023 were included; of these, seven had MOGAD. Three underwent a brain biopsy. B-cell dominant CNS infiltration was observed in two cases. In two cases with B-cell dominant CNS infiltration, symptoms included fever, headache, nausea, somnolence, and focal neurological deficits. Cerebrospinal fluid examination revealed both mild pleocytosis and negative oligoclonal IgG bands. Magnetic resonance imaging of the brain revealed large abnormal lesions extending from the basal ganglia to the parietotemporal lobe in both cases. These cases showed a good response to steroids; however, one case relapsed. Brain pathology showed demyelination and perivascular lymphocytic infiltration. One showed small vessel vasculitis. Deposition of the activated complement component was absent or rarely observed. Loss of MOG was observed in two cases. Conclusion: MOGAD could exhibit B-cell dominant CNS infiltration and small vessel vasculitis. MOGAD should be considered in differential diagnosis of TBL.

Indexed as

Anti-myelin oligodendrocyte glycoprotein antibody-associated diseaseB cellbrain histopathologybrain tumormyelin oligodendrocyte glycoproteintumefactive brain lesion

Identifiers

PMID39651331
PMCPMC11622319

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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.