alexa A Case of Nivolumab-Induced Fulminant Type 1 Diabetes with Steroids and Glucagon-Like Peptide 1 Administration during the Early Onset
ISSN: 2165-7920

Journal of Clinical Case Reports
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Case Report

A Case of Nivolumab-Induced Fulminant Type 1 Diabetes with Steroids and Glucagon-Like Peptide 1 Administration during the Early Onset

Ayako Fukui1, Keiji Sugiyama2,3, Tsutomu Yamada1*, Machiko Tajitsu1, Xia Cao1, Junko Nagai1, Yuko Yambe1, Kyoko Imamura2, Kazuki Nozawa2, Chiyoe Kitagawa2and Takashi Murase1

1Department of Endocrinology and Diabetes, National Hospital Organization, Nagoya Medical Center, Nagoya, Japan

2Department of Clinical Oncology, National Hospital Organization, Nagoya Medical Center, Nagoya, Japan

3Department of Clinical Oncology, 3Aichi Cancer Center, Nagoya, Japan

*Corresponding Author:
Tsutomu Yamada
Department of Endocrinology and Diabetes,
National Hospital Organization
Nagoya Medical Center, Nagoya, Japan
Tel: +81-52- 951-1111
Fax: +81-52-951-0664
E-mail: [email protected]

Received Date: October 27, 2016; Accepted Date: November 16, 2016; Published Date: November 22, 2016

Citation: Fukui A, Sugiyama K, Yamada T, Tajitsu M, Cao X, et al. (2016) A Case of Nivolumab-Induced Fulminant Type 1 Diabetes with Steroids and Glucagon- Like Peptide 1 Administration during the Early Onset. J Clin Case Rep 6:883. doi: 10.4172/2165-7920.1000883

Copyright: © 2016 Fukui A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: Nivolumab is a humanized IgG4 anti-programmed cell death protein-1 (PD-1) antibody. In recent years, type 1 diabetes associated with anti-PD-1 immunotherapy has been reported.

Case report: We report a 62-year-old woman with primary choroidal melanoma who developed fulminant type 1 diabetes after anti-PD-1 immunotherapy (nivolumab). She had elevated levels of blood glucose and total blood ketone body. Her hemoglobin A1c level was at the upper limit of normal, and she had decreased endogenous insulin secretion. Anti-glutamic acid decarboxylase and anti-islet antigen 2 antibody tests were negative. Endogenous insulin was still being secreted at the time of diagnosis; therefore, we administered steroids and glucagon-like peptide-1 (GLP-1). However, insulin secretion did not recover. Approximately 10 months after onset, her diabetes was under control with intensive insulin therapy and voglibose treatment.

Discussion: The mechanism of diabetes caused by nivolumab is unclear, but it may involve the excessive autoimmune response associated with PD-1 inhibition. GLP-1 has a protective effect on the pancreas by promoting differentiation and proliferation of pancreatic β cells and suppressing pancreatic β cell apoptosis. We attempted to treat with steroids and GLP-1 before depletion of endogenous insulin to suppress the hyperimmunization and protect the pancreatic β cells. Insulin secretion did not recover. However, no reports have described using these therapies to treat diabetes associated with immune checkpoint inhibitors during early onset to date. We consider this case is the meaningful report as a negative data.

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