Glucocorticoid-Induced Hyperglycemia in Patients With Cancer: Mechanisms, Clinical Implications, and Management Strategies.

OBJECTIVE

To review the pathophysiology, risk factors, clinical implications, monitoring strategies, and therapeutic approaches for glucocorticoid-induced hyperglycemia (GCIH), with a focus on patients with cancer.

METHODS

This narrative review integrates findings from clinical studies, expert guidelines, and recent advances in glucose monitoring and pharmacologic therapy, particularly in oncologic settings where glucocorticoid use is common.

RESULTS

GCIH is a frequent and often underrecognized complication, even in individuals without preexisting diabetes. In patients with cancer, GCIH is associated with increased risk of infections, chemotherapy delays, longer hospital stays, and higher mortality. Key mechanisms include enhanced insulin resistance, increased hepatic gluconeogenesis, and β-cell dysfunction. Afternoon and postprandial hyperglycemia are typical due to the pharmacodynamics of once-daily morning glucocorticoids. Self-monitoring of blood glucose (SMBG) and continuous glucose monitoring (CGM) are essential tools. HbA1c may assist in baseline assessment, but fructosamine better reflects short-term glycemic changes. Insulin is the treatment of choice for moderate to severe GCIH, with basal-bolus regimens, especially using NPH insulin aligned with glucocorticoid timing, providing effective control. Selected non-insulin agents may be considered in stable outpatients with mild hyperglycemia. However, standardized definitions, evidence-based algorithms, and randomized trials remain limited.

CONCLUSION

Optimal GCIH management requires proactive monitoring and individualized treatment strategies tailored to glucocorticoid type, dose, and clinical setting. Further research should aim to refine diagnostic criteria, validate therapeutic protocols, and assess emerging technologies such as automated insulin delivery systems and selective glucocorticoid receptor modulators.