Abstract


Introduction
Pembrolizumab is a novel monoclonal antibody against programmed cell death protein-1 (PD-1) which is used in the treatment of metastatic melanoma. Several endocrine related autoimmune adverse events have been reported with the use of Pembrolizumab such as thyroiditis, and hypophysitis (1). Autoimmune T1 DM is relatively less commonly reported but can present more dramatically with more permanent effect. We report a case of T1 DM which developed after initiation of Pembrolizumab in a patient with metastatic uveal melanoma.
Case Presentation: view more

Introduction
Pembrolizumab is a novel monoclonal antibody against programmed cell death protein-1 (PD-1) which is used in the treatment of metastatic melanoma. Several endocrine related autoimmune adverse events have been reported with the use of Pembrolizumab such as thyroiditis, and hypophysitis (1). Autoimmune T1 DM is relatively less commonly reported but can present more dramatically with more permanent effect. We report a case of T1 DM which developed after initiation of Pembrolizumab in a patient with metastatic uveal melanoma.
Case Presentation:
The patient was a 48 year old man with a history of stage IV metastatic uveal melanoma to the stomach, lung and left adrenal gland, treated previously with immune-modulators such as ipilimumab, and trametinib. As his cancer progressed on these treatments, he was initiated on pembrolizumab therapy. His hemoglobin A1c when on ipilimumab and trametinib was 5.4% and 5.7% respectively. During the sixth cycle of treatment with pembrolizumab, he developed polyuria and polydipsia with blood glucose in the 500s and elevation of hemoglobin A1c to 8.9%. He was initiated on Glipizide and Metformin and referred to endocrinology. On endocrine evaluation, patient was found to have insulin level of <2.0 mIU/mL, c-peptide 0.6 ng/mL with a random plasma glucose of 318 mg/dL. He had an elevated anti-GAD65 antibody level at 0.07 nmol/L, with positive serum ketones and without anion gap acidosis. The patient was initiated on insulin therapy for treatment of new onset Type 1 Diabetes. His symptoms resolved completely and with multiple dose insulin he was able to maintain good glycemic control.
Discussion:
We believe that the underlying autoimmunity was unmasked by the institution of immune therapy. A decreased expression of PD-1 gene has been observed in CD4+ T cells of patients with autoimmune T1 DM in recent studies (2). PD-1 blockade in non-obese mice has been shown to produce T1 DM (3). In the context of the increasing indications of anti-PD1 therapy in different cancers, blood glucose screening may have a role in preventing life threatening complications like diabetic ketoacidosis. More studies are needed in human models to study the role of PD-1 blockade and deficiency in the pathogenesis of T1 DM.

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