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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

EV1091

Steroid-induced mania during treatment of secondary adrenal insufficiency following immune checkpoint inhibitor toxicity

STEROID-INDUCED MANIA DURING SECONDARY ADRENAL INSUFFICIENCY TREATMENT AFTER IMMUNE CHECKPOINT INHIBITOR TOXICITY

Stress-dose hydrocortisone administered for secondary adrenal insufficiency following immune checkpoint inhibitor toxicity triggered acute mania, while antipsychotic treatment was complicated by QTc prolongation.

This case is presented to illustrate the treatment dilemma of steroid-induced mania in a patient with immune checkpoint inhibitor (ICI) toxicity, secondary adrenal insufficiency, and QTc-related treatment limitations. A 62-year-old woman with metastatic mucosal melanoma had received ipilimumab and nivolumab, followed by prolonged high-dose prednisone and mycophenolate for immune-mediated hepatitis and myocarditis; the prednisone course lasted approximately 14 months, with a maximum dose of 200 mg/day, tapered to 5 mg/day before the patient discontinued it approximately two weeks before admission. She presented with fatigue, generalized pain, postprandial vomiting, and poor oral intake and was found to have starvation ketosis, hypomagnesemia, hypoalbuminemia, and secondary adrenal insufficiency; initial laboratory results showed Mg 1.1 mg/dL, albumin 3.3 g/dL, morning cortisol 0.1 µg/dL, and ACTH < 1.5 pg/mL, and the treatment plan was to administer 100 mg of intravenous hydrocortisone followed by a transition to physiological replacement. Within hours of starting hydrocortisone, she developed elevated mood, irritability, distractibility, and insomnia; overnight, pressured speech, grandiosity, tangential thinking, paranoia, impaired attention, psychotic symptoms, and loss of insight emerged. A psycho-oncology assessment led to a diagnosis of medication-induced bipolar and related disorder, with a manic episode; delirium and a mood disorder due to adrenal insufficiency were considered in the differential diagnosis. Among the risk factors reported by Akid and colleagues, high-dose and prolonged corticosteroid exposure, female sex, hypoalbuminemia, older age, severe medical illness, sleep disruption, polypharmacy, and QTc risk were present; a psychiatric history was partially present (depression and anxiety, but no bipolar disorder or family history). The baseline QTc was 341 ms and rose to a maximum of 548 ms during treatment with olanzapine, intravenous ondansetron, and escitalopram; after these medications were discontinued and treatment was switched to oral aripiprazole 5 mg daily, the QTc decreased toward baseline. The case illustrates the paradox of corticosteroid use in psycho-oncology: although steroids were necessary to manage ICI-related immune toxicity and secondary adrenal insufficiency, re-exposure triggered mania, and although antipsychotic treatment improved the manic symptoms, QTc prolongation necessitated a medication change.

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