Abstract
Immune checkpoint inhibitors have transformed the landscape of oncological therapy, but at the price of a new array of immune related adverse events. Among these is β-cell failure, leading to checkpoint inhibitor-related autoimmune diabetes (CIADM) which entails substantial long-term morbidity. As our understanding of this novel disease grows, parallels and differences between CIADM and classic type 1 diabetes (T1D) may provide insights into the development of diabetes and identify novel potential therapeutic strategies. In this review, we outline the knowledge across the disciplines of endocrinology, oncology and immunology regarding the pathogenesis of CIADM and identify possible management strategies.
Highlights
The demonstrated successes of immune checkpoint inhibitors (ICIs) have resulted in a paradigm shift in the management of many malignancies
ICI-associated autoimmune diabetes mellitus (CIADM, termed CPI-DM) is a novel form of autoimmune diabetes that arises as a rare complication of therapy, with an incidence between 0.21.4% [1,2,3,4,5,6]
We review the body of evidence across human and animal studies that add to our understanding of checkpoint inhibitor-related autoimmune diabetes (CIADM) pathogenesis and islet autoimmunity in general
Summary
The demonstrated successes of immune checkpoint inhibitors (ICIs) have resulted in a paradigm shift in the management of many malignancies. Readers should interpret with caution reported cases of CIADM patients to ensure the diagnosis was applied with definitive evidence of insulin deficiency or autoimmunity, rather than generic ICI-related hyperglycemia which may occur in the context of other therapies such as corticosteroids. Diagnosis of T1D requires demonstration of hyperglycaemia and is supported by evidence of autoimmunity and insulin deficiency, with 90% of patients being positive for islet autoantibodies at some point in their clinical course [40, 41].
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