Hyperglycemia and diabetes are increasingly recognized in patients undergoing cancer therapy, resulting from both shared risk factors and treatment-related metabolic disturbances. Approximately 20% of patients with cancer have diabetes, and both pre-existing and new-onset hyperglycemia are associated with poorer survival, increased recurrence, and reduced treatment efficacy. Several anticancer therapies contribute to hyperglycemia through diverse mechanisms. Glucocorticoids commonly induce postprandial hyperglycemia by increasing hepatic glucose production, promoting insulin resistance, and impairing β-cell function. Conventional chemotherapy can provoke transient or persistent hyperglycemia and exacerbate diabetes-related complications, particularly in patients with pre-existing diabetes. Targeted therapies, including tyrosine kinase inhibitors and mTOR inhibitors such as everolimus, are associated with significant rates of hyperglycemia by impairing insulin secretion and increasing insulin resistance. Somatostatin analogues, especially second-generation agents, may reduce insulin secretion and worsen glucose tolerance. Immune checkpoint inhibitors can rarely induce insulin-dependent diabetes through immune-mediated β-cell destruction. Given the clinical impact of treatment-induced hyperglycemia on prognosis, treatment continuity, and quality of life, systematic glucose monitoring and individualized management are essential throughout cancer care. A multidisciplinary approach involving oncologists and endocrinologists is critical for optimizing metabolic control and improving overall outcomes.
A Ram Hong (Tue,) studied this question.