New-onset agitation and grandiose ideas in a patient started on high-dose steroids

A 45-year-old woman with systemic lupus erythematosus (SLE) was admitted to the rheumatology ward with a disease flare, comprising a facial rash, polyarthritis, and fever. Her regular medication was hydroxychloroquine 200 mg twice daily, which she had taken for three years. On admission, she was started on prednisolone 60 mg once daily for the flare, and ibuprofen 400 mg three times daily for joint pain. She had no history of psychiatric illness and had not taken systemic corticosteroids in the preceding twelve months.

The first six days of admission were unremarkable: her fever settled, joint pain improved, and the rash began to fade. On day 7, the nursing staff noted that she was restless and had not slept for two nights. On review, she was agitated, talkative, and expressed grandiose ideas, insisting that she had found a cure for lupus. She was oriented in time and place, but her insight was limited. There were no hallucinations or mood-congruent delusions. Her vital signs were stable, temperature 36.8°C, blood pressure 128/76 mmHg, and she was apyrexial. Neurological examination was normal, with no focal deficits or meningism.

Blood tests on day 7 showed haemoglobin 10.2 g/dL, white cell count 9.1 × 10⁹/L, CRP 45 mg/L (down from 80 on admission), creatinine 62 µmol/L, ALT 28 IU/L, and normal electrolytes. Complement C3 and C4 were slightly reduced, and anti-dsDNA antibodies were elevated, consistent with active SLE. A urine dipstick for illicit drugs was negative. Blood cultures and urine cultures were sterile. MRI of the brain was reported as normal, and an EEG showed no epileptiform activity. Lumbar puncture was considered, but not performed given the absence of focal signs and the low suspicion of neuropsychiatric lupus.

The clinical team considered whether her new psychiatric symptoms could be due to neuropsychiatric lupus, but the absence of focal neurological signs, the normal MRI and EEG, and the fact that her inflammatory markers were improving made this less likely. The temporal relationship with the introduction of prednisolone, seven days before symptom onset, and the abrupt onset of symptoms after a period of improvement, suggested a drug-related cause. Over the next three days, the prednisolone dose was tapered to 10 mg daily. Her agitation and insomnia resolved within 48 hours, and the grandiose ideas diminished over five days. She remained on hydroxychloroquine and ibuprofen throughout. A deliberate rechallenge with prednisolone was not performed, but she was subsequently maintained on a lower dose of 7.5 mg daily without recurrence of symptoms. The episode prolonged her hospital stay by an additional week. A psychiatric opinion confirmed the diagnosis of an acute, reversible psychosis, and she was managed with supportive care and a small dose of a short-acting anxiolytic for a few days.

This case highlights the need to consider drug-related causes for behavioural changes in patients with inflammatory diseases, especially when multiple agents are used. The patient's age, the high dose of prednisolone, and the absence of a prior psychiatric history are notable factors.