A case of fulminant Type 1 diabetes following anti-PD1 immunotherapy in a genetically susceptible patient

Programmed cell death-1 protein (PD-1) is an immune checkpoint that has gained popularity in the treatment of several advanced cancers. Inhibiting this checkpoint is known to enhance immune response, but is also known to diminish immune tolerance and to increase autoimmune toxicity. We discuss a cas...

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Bibliographic Details
Published in:Immunotherapy 2017-06, Vol.9 (7), p.531-535
Main Authors: Araújo, Manuel, Ligeiro, Dário, Costa, Luís, Marques, Filipa, Trindade, Helder, Correia, José Manuel, Fonseca, Candida
Format: Article
Language:English
Subjects:
Adenocarcinoma
Antigens
Apoptosis
Autoimmune diseases
Cancer
Cell activation
Cell death
Consortia
Diabetes
Diabetes mellitus (insulin dependent)
Genotype & phenotype
Genotypes
Histocompatibility antigen HLA
Immune checkpoint
Immune response
Immunological tolerance
Immunology
Immunotherapy
Insulin
Ligands
Lung cancer
Lymphocytes T
Monoclonal antibodies
PD-1 protein
Peptides
Side effects
Targeted cancer therapy
Toxicity
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Summary:Programmed cell death-1 protein (PD-1) is an immune checkpoint that has gained popularity in the treatment of several advanced cancers. Inhibiting this checkpoint is known to enhance immune response, but is also known to diminish immune tolerance and to increase autoimmune toxicity. We discuss a case of rapid onset fulminant Type 1 diabetes induced by treatment with anti-programmed cell death-1 monoclonal antibody, nivolumab, in a patient with late-stage non-small-cell lung adenocarcinoma. The patient had no history of previous diabetes but did reveal a high-risk genotype for Type 1 diabetes development (DR3-DQ2; DR4-DQ8). This finding supports that acute Type 1 diabetes can be an important adverse effect of immunotherapies targeting T-cell activation regulation. Because of the severity of this adverse effect, physicians should be aware of it, and studies directed to the detection of new biomarkers for early risk stratification (e.g., HLA) should be sought.
ISSN:1750-743X
1750-7448
DOI:10.2217/imt-2017-0020