Evidence map›Paper›PMID 30514621›Full record

ArticleJournal of clinical lipidology

GPIHBP1 autoantibody syndrome during interferon β1a treatment.

Jun Eguchi, Kazuya Miyashita, Isamu Fukamachi, Katsuyuki Nakajima, Masami Murakami, Yuko Kawahara, Toru Yamashita, Yasuyuki Ohta, Koji Abe, Atsuko Nakatsuka and 9 more

Open access · greenAbstract readCase Reports
In one paragraph

Article in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. An overview of persistent chylomicronemia: much more than meets the eye.Current opinion in endocrinology, diabetes, and obesity · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. A protein of capillary endothelial cells, GPIHBP1, is crucial for plasma triglyceride metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Chylomicronemia from GPIHBP1 autoantibodies.Journal of lipid research · 2020
    Review
  14. Review
  15. Article
  16. 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

19 authors at 7 institutions in 4 countries.

Jun EguchiDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Kazuya MiyashitaImmuno-Biological Laboratories (IBL) Co., Ltd., Fujioka, Gunma, Japan; Department of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Japan.
Isamu FukamachiImmuno-Biological Laboratories (IBL) Co., Ltd., Fujioka, Gunma, Japan.
Katsuyuki NakajimaDepartment of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Japan.
Masami MurakamiDepartment of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Japan.
Yuko KawaharaDepartment of Neurology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Toru YamashitaDepartment of Neurology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Yasuyuki OhtaDepartment of Neurology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Koji AbeDepartment of Neurology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Atsuko NakatsukaDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Mai MinoDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Satoru TakaseDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hiroaki OkazakiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Robert A HegeleDepartment of Medicine and Robarts Research Institute, Western University, London, Ontario, Canada.
Michael PlougFinsen Laboratory, Rigshospitalet, Copenhagen N, Denmark; Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen N, Denmark.
Xuchen HuDepartments of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Jun WadaDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan. Electronic address: junwada@okayama-u.ac.jp.
Stephen G YoungDepartments of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Departments of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. Electronic address: sgyoung@mednet.ucla.edu.
Anne P BeigneuxDepartments of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. Electronic address: abeigneux@mednet.ucla.edu.
Okayama University · JPGunma University · JPUniversity of California, Los Angeles · USThe University of Tokyo · JPMedical & Biological Laboratories (Japan) · JPUniversity of Copenhagen · DKWestern University · CA

Funding

UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
The Lipin Protein Family and Triglyceride Metabolism P01HL090553 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2008 to 2018
$23.3M
Understanding the Influence of Lipid Homeostasis on T cell FunctionP01HL146358 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TONTONOZ, PETER J · 2019 to 2023
$11.7M
Refining Physiologic Mechanisms for Intravascular Triglyceride MetabolismR01HL087228 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEIGNEUX, ANNE, FONG, LOREN GI · 2007 to 2024
$7.8M
Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
Investigating Mechanisms for Lipid Transport in Health and DiseaseR35HL139725 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2018 to 2024
$6.1M
New Avenues in GPIHBP1 ResearchR01HL094732 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEIGNEUX, ANNE · 2009 to 2012
$1.8M
Defining mechanisms for lipid transport across capillary endothelial cellsR01HL125335 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2015 to 2017
$1.2M
NHLBI NIH HHS P01 HL090553NHLBI NIH HHS P01 HL146358NHLBI NIH HHS R01 HL087228NHLBI NIH HHS R01 HL094732NHLBI NIH HHS R01 HL125335NHLBI NIH HHS R35 HL139725NHLBI NIH HHS T32 HL069766
6 · The paper itself

Abstract

backgroundAutoantibodies against glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) cause chylomicronemia by blocking the ability of GPIHBP1 to bind lipoprotein lipase (LPL) and transport the enzyme to its site of action in the capillary lumen.

objectiveA patient with multiple sclerosis developed chylomicronemia during interferon (IFN) β1a therapy. The chylomicronemia resolved when the IFN β1a therapy was discontinued. Here, we sought to determine whether the drug-induced chylomicronemia was caused by GPIHBP1 autoantibodies.

methodsWe tested plasma samples collected during and after IFN β1a therapy for GPIHBP1 autoantibodies (by western blotting and with enzyme-linked immunosorbent assays). We also tested whether the patient's plasma blocked the binding of LPL to GPIHBP1 on GPIHBP1-expressing cells.

resultsDuring IFN β1a therapy, the plasma contained GPIHBP1 autoantibodies, and those autoantibodies blocked GPIHBP1's ability to bind LPL. Thus, the chylomicronemia was because of the GPIHBP1 autoantibody syndrome. Consistent with that diagnosis, the plasma levels of GPIHBP1 and LPL were very low. After IFN β1a therapy was stopped, the plasma triglyceride levels returned to normal, and GPIHBP1 autoantibodies were undetectable.

conclusionThe appearance of GPIHBP1 autoantibodies during IFN β1a therapy caused chylomicronemia. The GPIHBP1 autoantibodies disappeared when the IFN β1a therapy was stopped, and the plasma triglyceride levels fell within the normal range.

Indexed as

AdultAutoantibodiesAutoimmune DiseasesCells, CulturedDrug-Related Side Effects and Adverse ReactionsFemaleHumansHyperlipoproteinemia Type IInterferon-betaMultiple SclerosisProtein BindingReceptors, LipoproteinSyndromeTriglyceridesWithholding TreatmentAutoantibodiesGPIHBP1 protein, humanInterferon-betaReceptors, LipoproteinTriglyceridesAutoantibodiesChylomicronemiaGPIHBP1HypertriglyceridemiaInterferon β1a

Identifiers

PMID30514621
PMCPMC6379125
OpenAlexW2896745557

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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.