Evidence map›Paper›PMID 27776522›Full record

ArticleJournal of neuroinflammation2016

Inositol 1,4,5-trisphosphate receptor type 1 autoantibodies in paraneoplastic and non-paraneoplastic peripheral neuropathy.

Sven Jarius, Marius Ringelstein, Jürgen Haas, Irina I Serysheva, Lars Komorowski, Kai Fechner, Klaus-Peter Wandinger, Philipp Albrecht, Harald Hefter, Andreas Moser and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Neuropsychiatric Disorders Due to Limbic Encephalitis: Immunologic Aspect.International journal of molecular sciences · 2020
    Review
  9. ITPR1 autoimmunity: Frequency, neurologic phenotype, and cancer association.Neurology(R) neuroimmunology & neuroinflammation · 2018
    Article
  10. Review
  11. An overview of pathways encoding nociception.Clinical and experimental rheumatology
    Review
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

14 authors at 6 institutions in 2 countries.

Sven JariusMolecular Neuroimmunology Group, Department of Neurology, University Hospital Heidelberg, Otto Meyerhof Center, Im Neuenheimer Feld 350, 69120, Heidelberg, Germany. sven.jarius@med.uni-heidelberg.de.
Marius RingelsteinDepartment of Neurology, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225, Düsseldorf, Germany.
Jürgen HaasMolecular Neuroimmunology Group, Department of Neurology, University Hospital Heidelberg, Otto Meyerhof Center, Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
Irina I SeryshevaDepartment of Biochemistry and Molecular Biology, The University of Texas Medical School at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
Lars KomorowskiInstitute of Experimental Immunology, affiliated to Euroimmun AG, Seekamp 31, 23560, Lübeck, Germany.
Kai FechnerInstitute of Experimental Immunology, affiliated to Euroimmun AG, Seekamp 31, 23560, Lübeck, Germany.
Klaus-Peter WandingerDepartment of Neurology, University of Schleswig Holstein, Ratzeburger Allee 160, 23538, Lübeck, Germany.
Philipp AlbrechtDepartment of Neurology, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225, Düsseldorf, Germany.
Harald HefterDepartment of Neurology, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225, Düsseldorf, Germany.
Andreas MoserDepartment of Neurology, University of Schleswig Holstein, Ratzeburger Allee 160, 23538, Lübeck, Germany.
Eva Neuen-JacobDepartment of Neuropathology, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225, Düsseldorf, Germany.
Hans-Peter HartungDepartment of Neurology, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225, Düsseldorf, Germany.
Brigitte WildemannMolecular Neuroimmunology Group, Department of Neurology, University Hospital Heidelberg, Otto Meyerhof Center, Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
Orhan AktasDepartment of Neurology, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225, Düsseldorf, Germany. orhan.aktas@uni-duesseldorf.de.
Heinrich Heine University Düsseldorf · DEEuroimmun Medizinische Labordiagnostika (Germany) · DEUniversity Hospital Heidelberg · DEUniversity of Lübeck · DEHeidelberg University · DEThe University of Texas Health Science Center at Houston · US

Funding

Structure-Function Studies Of IP3R ChannelsR01GM072804 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SERYSHEVA, IRINA I · 2005 to 2023
$4.8M
NIGMS NIH HHS R01 GM072804
6 · The paper itself

Abstract

backgroundRecently, we described a novel autoantibody, anti-Sj/ITPR1-IgG, that targets the inositol 1,4,5-trisphosphate receptor type 1 (ITPR1) in patients with cerebellar ataxia. However, ITPR1 is expressed not only by Purkinje cells but also in the anterior horn of the spinal cord, in the substantia gelatinosa and in the motor, sensory (including the dorsal root ganglia) and autonomic peripheral nervous system, suggesting that the clinical spectrum associated with autoimmunity to ITPR1 may be broader than initially thought. Here we report on serum autoantibodies to ITPR1 (up to 1:15,000) in three patients with (radiculo)polyneuropathy, which in two cases was associated with cancer (ITPR1-expressing adenocarcinoma of the lung, multiple myeloma), suggesting a paraneoplastic aetiology.

methodsSerological and other immunological studies, and retrospective analysis of patient records.

resultsThe clinical findings comprised motor, sensory (including severe pain) and autonomic symptoms. While one patient presented with subacute symptoms mimicking Guillain-Barré syndrome (GBS), the symptoms progressed slowly in two other patients. Electrophysiology revealed delayed F waves; a decrease in motor and sensory action potentials and conduction velocities; delayed motor latencies; signs of denervation, indicating sensorimotor radiculopolyneuropathy of the mixed type; and no conduction blocks. ITPR1-IgG belonged to the complement-activating IgG1 subclass in the severely affected patient but exclusively to the IgG2 subclass in the two more mildly affected patients. Cerebrospinal fluid ITPR1-IgG was found to be of predominantly extrathecal origin. A

conclusionsOur findings expand the spectrum of clinical syndromes associated with ITPR1-IgG and suggest that autoimmunity to ITPR1 may underlie peripheral nervous system diseases (including GBS) in some patients and may be of paraneoplastic origin in a subset of cases.

Indexed as

AdenocarcinomaAdultAgedAnimalsAutoantibodiesCell ProliferationCytokinesFemaleHumansInositol 1,4,5-Trisphosphate ReceptorsLeukocytes, MononuclearLung NeoplasmsMacaca mulattaMaleMiddle AgedPeripheral Nervous System DiseasesAutoantibodiesCytokinesInositol 1,4,5-Trisphosphate ReceptorsITPR1 protein, humanAcute sensorimotor polyradiculopathyAdenocarcinoma of the lungAnti-neuronal autoantibodiesAutoimmune cerebellar ataxiaAutonomic neuropathyCranial nerve palsyFacial nerve paralysisGuillain-Barré syndrome (GBS)Inositol 1,4,5-trisphosphate type 1 receptor antibodiesLung cancerMultiple myelomaNeuritisNeuropathologyPainParaneoplastic neurological syndromePolyneuropathy

Identifiers

PMID27776522
PMCPMC5078930
OpenAlexW2533204707

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.