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Dear Editor, Immune checkpoint inhibitors have been spotlighted as a recent crucial therapy in many kinds of solid cancers. Atezolizumab is an immune checkpoint inhibitor that increases antitumor T-cell activity through binding to programmed death-ligand 1 that suppresses effector T cells.1 The potentiation of T-cell activity by atezolizumab may induce an uncontrolled immune response that can lead to a wide range of adverse events.2 One of the rare adverse reactions of atezolizumab is meningitis or encephalitis. Here we report a severe case of autoimmune encephalitis that developed after administering atezolizumab to a patient with bladder cancer. A 49-year-old male was admitted to our hospital for status epilepticus and encephalitis of unknown origin. He was diagnosed with urothelial carcinoma of the bladder, and received the first cycle of 1,200-mg atezolizumab (Fig. 1). After administering atezolizumab he suffered general weakness and eventually showed stuporous mentality and three generalized tonic-clonic seizures upon admission. Brain MRI showed diffuse leptomeningeal enhancement. A cerebrospinal fluid (CSF) examination showed an opening pressure of 23 cm H2O and that a sample of 50 white blood cells comprised 8 polymorphonuclear cells, 1 lymphocyte, and 41 cells of other types. Leptomeningeal seeding was first suspected considering his past medical history and the dominant CSF profile of the other cells. However, no malignant cells were found in CSF cytology. Antibiotics were administered since we could not fully exclude bacterial meningitis. However, the CSF profile had worsened at follow-up. We were concerned about the possibility that atezolizumab might have caused autoimmune encephalitis, and so steroid pulse therapy (1 g of methylprednisolone daily) was administered. This did not produce any improvement, and so intravenous immunoglobulin (IVIG) therapy was started. The patient initially improved clinically and follow-up MRI showed the resolution of leptomeningeal enhancement. All findings in the CSF study were negative: paraneoplastic antibodies (anti-Hu, anti-Ri, and anti-Yo antibodies), bacterial culture, fungus culture, tuberculous PCR, and viral PCR including herpes simplex virus 1 and 2, Epstein-Barr virus, varicella zoster virus, cytomegalovirus, and John Cunningham virus. The patient experienced drowsiness about 1 month after the first IVIG therapy, so a second round of IVIG therapy was applied. However, this did not produce any further clinical improvement. There was no epileptiform discharge in electroencephalography, and the findings of a follow-up CSF study were completely normal with no malignant cells in cytology (Fig. 1). The patient had suffered persistent fever and his CRP level had seldom dropped below 20 mg/dL despite receiving antibiotics. The median onset delay for immune-related colitis in patients with urothelial carcinoma who receive atezolizumab was 1.7 months.3 The present patient was suspected as having immune-related colitis because of continuous disAhwon Kim Bhumsuk Keam Hyeon Cheun Soon-Tae Lee Hyung Seok Gook Moon-Ku Han

Immune-Checkpoint-Inhibitor-Induced Severe Autoimmune Encephalitis Treated by Steroid and Intravenous Immunoglobulin