Evidence map›Paper›PMID 42305552›Full record

ArticleFrontiers in immunology2026

Severe cerebellitis as a manifestation of infliximab-associated overlap of neurosarcoidosis and myelin oligodendrocyte glycoprotein antibody-associated disease - case report.

Gregor Hütter, Maximilian Winkelhausen, Lars Tönges, Ralf Gold, Simon Faissner

Abstract readCase Reports
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

5 authors.

Gregor HütterDepartment of Neurology, St. Josef-Hospital, Bochum, Germany.
Maximilian WinkelhausenDepartment of Neurology, St. Josef-Hospital, Bochum, Germany.
Lars TöngesDepartment of Neurology, St. Josef-Hospital, Bochum, Germany.
Ralf GoldDepartment of Neurology, St. Josef-Hospital, Bochum, Germany.
Simon FaissnerDepartment of Neurology, St. Josef-Hospital, Bochum, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Tumor necrosis factor-α (TNF-α) inhibitors such as infliximab are widely used in autoimmune disorders. Paradoxical inflammatory reactions including systemic sarcoidosis and neurosarcoidosis are increasingly recognized but remain rare. Case presentation: We report a 56-year-old male with ulcerative colitis under infliximab therapy presenting with acute dysarthria and gait instability. Neurological examination revealed truncal ataxia. Brain and spinal MRI were normal. Cerebrospinal fluid analysis showed lymphocytic pleocytosis, reduced glucose, increased lactate, and elevated protein with marked blood-brain barrier disruption. Sarcoidosis-associated markers (neopterin, ACE, IL-2 receptor) were elevated. Pulmonary CT and lymph node biopsy confirmed systemic sarcoidosis. Moreover, MOG-antibodies were detected in both serum and CSF. After initial empirical anti-infective therapy, high-dose corticosteroids were initiated, resulting in full recovery. Infliximab therapy was discontinued. Conclusion: This case demonstrates infliximab-associated overlapping autoimmunity with sarcoidosis, probable neurosarcoidosis and MOGAD presenting with acute cerebellitis. Clinicians should consider neurosarcoidosis and MOGAD in patients on TNF-α-inhibitors presenting with neurological deficits, even in the absence of radiological findings. Early discontinuation of the triggering agent and timely corticosteroid therapy are essential for favorable outcomes.

Indexed as

Central Nervous System DiseasesInfliximabMyelin Oligodendrocyte Glycoprotein Antibody-Associated DiseaseSarcoidosisColitis, UlcerativeHumansMaleMiddle AgedInfliximabautoimmune neurologycerebellitisinfliximabMOGADneurosarcoidosisTNF-α- inhibitor

Identifiers

PMID42305552
PMCPMC13265301

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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.