Amanda Leiter1, Emily Carroll2, Danielle Brooks3, Jennifer Ben Shimol4, Elliot Eisenberg5, Juan P Wisnivesky6, Matthew D Galsky7, Emily J Gallagher8. 1. Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States. Electronic address: Amanda.Leiter@mssm.edu. 2. Division of Rheumatology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 3. Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 4. Department of Rheumatology, Edith Wolfson Medical Center, Holon, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 5. Division of Pulmonology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 6. Division of General Internal Medicine, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 7. Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 8. Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Abstract
AIMS: Immune-mediated beta cell destruction is known to cause hyperglycemia in patients receiving immune checkpoint inhibitor (ICI) cancer therapy. However, it is uncommon, and little is known about the full spectrum of hyperglycemia in patients receiving ICIs. We aimed to characterize the prevalence and factors associated with hyperglycemia in patients treated with ICIs. METHODS: We retrospectively analyzed patients receiving ICIs at an NCI-designated Cancer Center. We assessed the proportion of patients with new onset hyperglycemia (random glucose >11.1 mmol/L) after starting ICIs and used logistic regression to determine hyperglycemia predictors in patients without known diabetes. RESULTS: Of 411 patients, 385 had post-ICI glucose data. 105 (27%) had hyperglycemia. Of this group, 29 (28%) had new onset hyperglycemia, 19 of whom had glucocorticoid-associated hyperglycemia. The remaining 10 had unexplained hyperglycemia and none had known autoimmune diabetes. Among patients without known diabetes, race/ethnicity, obesity, and pre-ICI hyperglycemia were significantly associated with hyperglycemia after starting ICIs. CONCLUSIONS: We found that new hyperglycemia in patients receiving ICIs was most commonly related to glucocorticoids. A small patient subset had new unexplained hyperglycemia, suggesting ICIs might have a role in promoting hyperglycemia. Recognizing factors associated with hyperglycemia in this population is crucial for appropriate management.
AIMS: Immune-mediated beta cell destruction is known to cause hyperglycemia in patients receiving immune checkpoint inhibitor (ICI) cancer therapy. However, it is uncommon, and little is known about the full spectrum of hyperglycemia in patients receiving ICIs. We aimed to characterize the prevalence and factors associated with hyperglycemia in patients treated with ICIs. METHODS: We retrospectively analyzed patients receiving ICIs at an NCI-designated Cancer Center. We assessed the proportion of patients with new onset hyperglycemia (random glucose >11.1 mmol/L) after starting ICIs and used logistic regression to determine hyperglycemia predictors in patients without known diabetes. RESULTS: Of 411 patients, 385 had post-ICI glucose data. 105 (27%) had hyperglycemia. Of this group, 29 (28%) had new onset hyperglycemia, 19 of whom had glucocorticoid-associated hyperglycemia. The remaining 10 had unexplained hyperglycemia and none had known autoimmune diabetes. Among patients without known diabetes, race/ethnicity, obesity, and pre-ICI hyperglycemia were significantly associated with hyperglycemia after starting ICIs. CONCLUSIONS: We found that new hyperglycemia in patients receiving ICIs was most commonly related to glucocorticoids. A small patient subset had new unexplained hyperglycemia, suggesting ICIs might have a role in promoting hyperglycemia. Recognizing factors associated with hyperglycemia in this population is crucial for appropriate management.
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