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GPIHBP1 autoantibody syndrome during interferon β1a treatment

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Intermittent chylomicronemia caused by intermittent GPIHBP1 autoantibodies

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. An enzyme-linked immunosorbent assay for measuring GPIHBP1 levels in human plasma or serum

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Effect of tofacitinib on lipid levels and lipid-related parameters in patients with moderate to severe psoriasis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. GPIHBP1 autoantibodies in a patient with unexplained chylomicronemia

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. ANGPTL4 inactivates lipoprotein lipase by catalyzing the irreversible unfolding of LPL's hydrolase domain

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Intermittent chylomicronemia caused by intermittent GPIHBP1 autoantibodies

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Unfolding of monomeric lipoprotein lipase by ANGPTL4: Insight into the regulation of plasma triglyceride metabolism

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Crystal Structures of Human C4.4A Reveal the Unique Association of Ly6/uPAR/α-neurotoxin Domain

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  • Jun Eguchi
  • Kazuya Miyashita
  • Isamu Fukamachi
  • Katsuyuki Nakajima
  • Masami Murakami
  • Yuko Kawahara
  • Toru Yamashita
  • Yasuyuki Ohta
  • Koji Abe
  • Atsuko Nakatsuka
  • Mai Mino
  • Satoru Takase
  • Hiroaki Okazaki
  • Robert A Hegele
  • Michael Ploug
  • Xuchen Hu
  • Jun Wada
  • Stephen G Young
  • Anne P Beigneux
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BACKGROUND: Autoantibodies 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.

OBJECTIVE: A 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.

METHODS: We 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.

RESULTS: During 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.

CONCLUSION: The 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.

OriginalsprogEngelsk
TidsskriftJournal of Clinical Lipidology
Vol/bind13
Udgave nummer1
Sider (fra-til)62-69
Antal sider8
ISSN1933-2874
DOI
StatusUdgivet - 2019

ID: 55804175