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; Mai Mino; Satoru Takase; Hiroaki Okazaki; Robert A. Hegele; Michael Ploug; Xuchen Hu; Jun Wada; Stephen G. Young; Anne P. Beigneux

doi:10.1016/j.jacl.2018.10.004

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, Mai Mino, Satoru Takase, Hiroaki Okazaki, Robert A. Hegele, Michael Ploug, Xuchen Hu, Jun Wada, Stephen G. Young^*, Anne P. Beigneux

^*Corresponding author af dette arbejde

5 Citationer (Scopus)

Abstract

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.

Originalsprog	Engelsk
Tidsskrift	Journal of Clinical Lipidology
Vol/bind	13
Udgave nummer	1
Sider (fra-til)	62-69
Antal sider	8
ISSN	1933-2874
DOI	https://doi.org/10.1016/j.jacl.2018.10.004
Status	Udgivet - 1 jan. 2019

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10.1016/j.jacl.2018.10.004

Citationsformater

Eguchi, J., Miyashita, K., Fukamachi, I., Nakajima, K., Murakami, M., Kawahara, Y., Yamashita, T., Ohta, Y., Abe, K., Nakatsuka, A., Mino, M., Takase, S., Okazaki, H., Hegele, R. A., Ploug, M., Hu, X., Wada, J., Young, S. G., & Beigneux, A. P. (2019). GPIHBP1 autoantibody syndrome during interferon β1a treatment. Journal of Clinical Lipidology, 13(1), 62-69. https://doi.org/10.1016/j.jacl.2018.10.004

Eguchi, J, Miyashita, K, Fukamachi, I, Nakajima, K, Murakami, M, Kawahara, Y, Yamashita, T, Ohta, Y, Abe, K, Nakatsuka, A, Mino, M, Takase, S, Okazaki, H, Hegele, RA, Ploug, M, Hu, X, Wada, J, Young, SG & Beigneux, AP 2019, 'GPIHBP1 autoantibody syndrome during interferon β1a treatment', Journal of Clinical Lipidology, bind 13, nr. 1, s. 62-69. https://doi.org/10.1016/j.jacl.2018.10.004

@article{a0bd22231b6649cc88c87b2ee2ed26bc,

title = "GPIHBP1 autoantibody syndrome during interferon β1a treatment",

abstract = "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.",

keywords = "Autoantibodies, Chylomicronemia, GPIHBP1, Hypertriglyceridemia, Interferon β1a",

author = "Jun Eguchi and Kazuya Miyashita and Isamu Fukamachi and Katsuyuki Nakajima and Masami Murakami and Yuko Kawahara and Toru Yamashita and Yasuyuki Ohta and Koji Abe and Atsuko Nakatsuka and Mai Mino and Satoru Takase and Hiroaki Okazaki and Hegele, {Robert A.} and Michael Ploug and Xuchen Hu and Jun Wada and Young, {Stephen G.} and Beigneux, {Anne P.}",

year = "2019",

month = jan,

day = "1",

doi = "10.1016/j.jacl.2018.10.004",

language = "English",

volume = "13",

pages = "62--69",

journal = "Journal of Clinical Lipidology",

issn = "1933-2874",

publisher = "Elsevier",

number = "1",

}

TY - JOUR

T1 - GPIHBP1 autoantibody syndrome during interferon β1a treatment

AU - Eguchi, Jun

AU - Miyashita, Kazuya

AU - Fukamachi, Isamu

AU - Nakajima, Katsuyuki

AU - Murakami, Masami

AU - Kawahara, Yuko

AU - Yamashita, Toru

AU - Ohta, Yasuyuki

AU - Abe, Koji

AU - Nakatsuka, Atsuko

AU - Mino, Mai

AU - Takase, Satoru

AU - Okazaki, Hiroaki

AU - Hegele, Robert A.

AU - Ploug, Michael

AU - Hu, Xuchen

AU - Wada, Jun

AU - Young, Stephen G.

AU - Beigneux, Anne P.

PY - 2019/1/1

Y1 - 2019/1/1

N2 - 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.

AB - 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.

KW - Autoantibodies

KW - Chylomicronemia

KW - GPIHBP1

KW - Hypertriglyceridemia

KW - Interferon β1a

U2 - 10.1016/j.jacl.2018.10.004

DO - 10.1016/j.jacl.2018.10.004

M3 - Journal article

C2 - 30514621

AN - SCOPUS:85057438145

SN - 1933-2874

VL - 13

SP - 62

EP - 69

JO - Journal of Clinical Lipidology

JF - Journal of Clinical Lipidology

IS - 1

ER -

GPIHBP1 autoantibody syndrome during interferon β1a treatment

Abstract

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