Endocrine Abstracts

JOINT2533

Introduction: Cushing’s syndrome (CS) is a rare endocrinopathy characterized by prolonged hypercortisolism, which can arise from several etiologies. Due to its heterogeneous clinical presentation and overlap with other conditions, the diagnosis of CS is often delayed, sometimes for years after the initial onset of symptoms.

Case report: A 56-year-old woman with a medical history of type 2 diabetes (T2D), hypertension (HTN), dyslipidemia, and osteopenia presents for follow-up in our outpatient clinic, referred by her primary care physician. Her treatment plan included metformin and dapagliflozin for T2D, irbesartan and amlodipine for HTN, atorvastatin for dyslipidemia, and vitamin D for osteopenia. Her primary complaints included generalized weakness and difficulty losing weight despite following a low-carbohydrate diet. Additionally, she reported gradual weight gain over the past four years, particularly in the abdominal region. Her BMI had increased from 29.1 kg/m² to 34.2 kg/m², and her waist circumference measured 109 cm. At the time of assessment, her blood pressure was 145/95 mmHg, and her glycated hemoglobin (HbA1c) was 8.6%. Consequently, hydrochlorothiazide and semaglutide were added to her regimen to address her blood pressure and glycemic control. After three months, the patient’s HbA1c increased slightly to 8.8%, and her blood pressure was 141/88 mmHg. A complete blood count and metabolic panel were ordered, along with fasting and postprandial blood glucose tests. While the patient’s fasting blood glucose ranged from 115 to 132 mg/dl, her postprandial glucose levels were notably elevated, reaching up to 280 mg/dl, particularly after lunch and dinner. Considering these findings, the patient underwent morning cortisol and ACTH testing, which revealed low ACTH and elevated cortisol levels. A low-dose dexamethasone suppression test showed no significant decrease in cortisol levels (4.78 µg/dl). An abdominal computed tomography (CT) scan was then conducted, identifying a 2.4 cm left adrenal nodule, consistent with an adrenal adenoma, while the right adrenal gland appeared normal. The patient was referred to an endocrine surgeon, and a minimally invasive adrenalectomy was scheduled three months later. Throughout this period, her blood glucose and blood pressure were carefully managed. Postoperative histopathology confirmed the presence of an adrenal adenoma, with no evidence of malignancy.

Conclusion: This case underscores the importance of considering hypercortisolism as a differential diagnosis in patients with T2D who struggle with achieving optimal blood glucose control. Clinicians should remain vigilant in identifying such conditions, as they can complicate the management of diabetes and other comorbidities, undermining treatment effectiveness and patient outcomes.