SAT-204 - Florid Psychosis and Brain Volume Loss Unmasking Adrenal Cushing Syndrome in A 12 Year Old Girl

Background
Cushing syndrome (CS) in children classically presents with rapid weight gain and growth deceleration. Psychiatric symptoms such as mood change or depression are well described, but frank psychosis is rare, particularly in pediatrics. To our knowledge, this preadolescent girl represents the youngest reported case of CS presenting with florid psychosis.

Clinical Presentation
A 12- year- old girl presented to the ED with abrupt onset severe psychosis and altered mental status characterized by paranoid delusions, visual hallucinations, disorganized behavior, agitation, and catatonia. Over 18 months, she gained 35 lb, with height decreasing from the 75th% at age 10 years to the 25th%. In response to weight related bullying, she restricted caloric intake to ≤1000 kcal/day with excessive exercise, resulting in 31 lb (19%) weight loss over 6 months. She was admitted for inpatient management of acute psychosis. Physical examination revealed a BMI at the 96th%, central obesity, rounded facies with dorsocervical fat pad, abdominal striae, and acanthosis nigricans. Initial evaluation for autoimmune encephalitis included brain MRI, which demonstrated diffuse cerebral volume loss compared with prior imaging. Given the history of rapid weight gain, growth deceleration, and characteristic physical findings, CS was suspected. Biochemical evaluation showed an elevated morning serum cortisol of 22.4 μg/dL with loss of diurnal variation (midnight cortisol 24.6 μg/dL). Twenty-four hour urinary free cortisol was markedly elevated at 1,369 μg/g creatinine. Serum ACTH was suppressed ( < 5 pg/mL), and cortisol failed to suppress following low and high dose dexamethasone. Abdominal CT revealed a 2.9 × 2.4 cm left adrenal mass consistent with an adrenocortical adenoma, confirming ACTH-independent CS. She underwent left adrenalectomy with peri-operative stress dose hydrocortisone, tapered to physiologic dose. Neuropsychiatric symptoms gradually improved with antipsychotic medication, psychotherapy, and electroconvulsive therapy.

Discussion
Hypercortisolism affects limbic and prefrontal brain regions, disrupting stress response circuits and causing mood disturbance, cognitive impairment, and, rarely, frank psychosis. When psychosis is the dominant presenting feature, CS may be mistaken for a primary psychiatric disorder, delaying endocrine diagnosis. This case underscores that weight loss through caloric restriction and exercise does not exclude hypercortisolism. Diffuse cerebral volume loss on brain MRI—reported in adults and limited pediatric cases—provided a critical diagnostic clue, reflecting glucocorticoid-mediated neurotoxicity. Early recognition of CS in children presenting with new onset psychosis is essential to reduce cardiometabolic risk and potentially irreversible neurologic sequelae.

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