Resolution of Metabolic Disorders and Overweight in a Patient with ACTH-independent Cushing's Syndrome after Unilateral Adrenalectomy

Abstract

Excessive production of cortisol by abnormal adrenocortical tissue causes clinical manifestations of Cushing' s syndrome and is associated with metabolic abnormalities including abdominal obesity, hyperglycemia, dyslipidemia, and hypertension, which increase the risk for type 2 diabetes mellitus as well as vascular morbidity and mortality. Removing the cause of hypercortisolism is initially required to resolve metabolic disorders in patients with adrenal Cushing' s syndrome. A 38-year-old woman with diabetes mellitus and hypertension, which were not well controlled by medications, complained of abdominal obesity, rounded face, thin limbs, and bruising. Based on clinical manifestations and laboratory findings, she was diagnosed with Cushing' s syndrome due to unilateral cortisol-producing adrenal adenoma. After left adrenalectomy, the patient' s blood glucose improved to a satisfactory level, and she rapidly discontinued insulin and oral glucose-lowering agent therapy. Her body mass index decreased to the normal range, and her other metabolic symptoms, dyslipidemia and hypertension, also improved significantly. She has maintained resolution of metabolic disorders and overweight for eight years since surgery without recurrence of Cushing' s syndrome.

Neonatal nicotine exposure changes insulin status in fat depots: sex-related differences

“…The high levels of both ACTH and corticosterone in nicotineexposed males per se help to explain obesity because it is known that excess cortisol, as in patients with Cushing's disease, leads to abdominal obesity. 61,62 Also, increased tissue sensitivity to GC (conversion and action) has pro-adipogenic and lipogenic actions. 63 Here, the protein content of 11βHSD1 and GC receptor was not altered in either sex or fat depots.…”