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Endocrine Abstracts (2025) 110 EP128 | DOI: 10.1530/endoabs.110.EP128

1Hospital of Charles Nicolle, Tunis, Tunisia


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Introduction: While remission of Cushing’s syndrome (CS) generally leads to improved glycemic control, some patients continue to experience persistent diabetes. Identifying factors influencing this persistence is crucial for optimizing long-term metabolic management.

Methods: A cohort of 22 patientsin remission from CS was assessed for glycemic outcomes. Patients were classified into two groups based on the persistence of diabetes post-remission. Several factors were analyzed, including age, BMI, disease duration, baseline cortisol levels, and pre-remission insulin dependence. Glycemic parameters were compared before and after remission.

Results: Among the 22 patients, 10 (45.5%) had persistent diabetes post-remission.There were no significant differences in age (persistent vs. non-persistent: 48.2 ± 10.4 vs. 45.7 ± 9.1 years, P = 0.42), BMI (29.6 ± 4.8 vs. 28.9 ± 4.2 kg/m2, P = 0.58), or disease duration (5.7 ± 2.1 vs. 5.2 ± 1.9 years, P = 0.61).However, baseline cortisol levels were significantly higher in patients with persistent diabetes (522.3 ± 87.6 vs. 398.4 ± 74.1 nmol/l, P = 0.02). Additionally, pre-remission insulin therapy was more frequent in patients with persistent diabetes (70% vs. 30%, P = 0.04), suggesting a possible association with beta-cell dysfunction.

Discussion: The absence of correlation with traditional metabolic risk factors (age, BMI, disease duration) suggests that hyperglycemia persistence post-CS remission is mainly driven by the severity of hypercortisolism at diagnosis and its impact on pancreatic function. The significant association with higher baseline cortisol levels highlights the role of prolonged glucocorticoid exposure in beta-cell dysfunction and insulin resistance, potentially leading to irreversible metabolic changes. Patients requiring insulin before remission appear to be at higher risk, supporting the hypothesis of pre-existing pancreatic damage exacerbated by chronic cortisol excess. Further studies are needed to explore long-term glucose metabolism recovery and predictive markers for diabetes resolution.

Conclusion: Although remission of CS improves glucose metabolism, persistent diabetes is associated with higher baseline cortisol levels and pre-remission insulin dependence, suggesting a potential irreversible impact on beta-cell function. Long-term follow-up and early metabolic interventions may help improve outcomes in these patients.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

European Society of Endocrinology 
European Society for Paediatric Endocrinology 

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