Endocrine Abstracts

JOINT2321

Introduction: Differentiating between secondary diabetes caused by Cushing’s syndrome (CS) and preexisting type 2 diabetes (T2D) remains a clinical challenge. While cortisol excess is known to induce hyperglycemia, it is unclear whether diabetes in CS patients resolves entirely after remission or if some patients continue to exhibit features of T2D. This study investigates the nature of diabetes in patients following CS treatment.

Methods: A cohort of 22 patients diagnosed with CSwas followed after treatment to assess glycemic outcomes. Patients were classified based on their diabetes status at baseline (diabetic vs. non-diabetic), and post-treatment evaluations included fasting blood glucose (FBG), glycated hemoglobin (HbA1c), homeostatic model assessment of insulin resistance (HOMA-IR), and beta-cell function (HOMA-B). Statistical analyses were performed to compare pre- and post-treatment glycemic parameters.

Results: Following remission, the majority of patients experienced significant improvements in glycemic control, with a 23% reduction in fasting blood glucose (P=0.001) and a 0.9% decrease in HbA1c (P = 0.008). Among the 10 patients diagnosed with diabetes before CS treatment, six (60%) achieved normoglycemia post-remission, while four (40%) remained diabetic despite cortisol suppression. Patients with persistent diabetesexhibited metabolic features consistent with type 2 diabetes, including higher baseline insulin resistance (HOMA-IR: 3.7 ± 0.8 vs. 2.1 ± 0.6, P = 0.01)and lower beta-cell function (HOMA-B: 52.4 ± 12.7 vs. 78.9 ± 15.3, P = 0.03)compared to those who achieved normoglycemia. Furthermore, this group had significantly higher baseline BMI (31.2 ± 3.8 vs. 27.6 ± 2.9 kg/m², P = 0.02)and a greater prevalence of metabolic syndrome components. Interestingly, a subset of patients without prior diabetes (n =12) developed impaired glucose metabolism post-remission.

Discussion: These findings highlight the heterogeneous nature of diabetes in CS patients. While hyperglycemia in some individuals appears to be directly driven by cortisol excess and resolves post-treatment, others exhibit metabolic profiles characteristic of underlying type 2 diabetes. Persistent diabetes in CS patients may be attributed to preexisting insulin resistance, obesity, or irreversible pancreatic beta-cell dysfunction, rather than secondary diabetes alone.

Conclusion: Although most patients experience an improvement in glycemic control following Cushing’s syndrome remission, a subset remains diabetic, exhibiting features suggestive of type 2 diabetes rather than pure secondary diabetes. These results emphasize the need for long-term metabolic monitoringin CS patients, particularly those with risk factors for insulin resistance. Further studies are required to determine whether targeted interventions, such as weight management and insulin-sensitizing therapies, could improve long-term glycemic outcomes.