The patient was discharged and demonstrated an ability to walk 10 days after steroid introduction; nivolumab and steroid therapy were continued. and lack of specific examinations. Therefore, a comprehensive approach, including assessments of autoantibodies and functional imaging, might be important for the diagnosis of neurologic irAEs. strong class=”kwd-title” Keywords: nivolumab, immune related adverse event, DAT, SPECT, anti-thyroid antibody, Hashimoto’s encephalopathy Introduction Nivolumab is usually a representative monoclonal antibody against programmed cell death protein 1 (PD-1). Although immune-checkpoint inhibitors (ICIs) are widely used for anti-cancer therapy, they can cause immune-related adverse events (irAEs). Representative irAEs are dermatosis and digestive symptoms, but neurological irAEs, such as myasthenia gravis (MG) and Guillain-Barr syndrome, have also been reported (1). We herein statement a patient with subacute progressive ataxia without parkinsonism except for tremor, combined with intractable nausea and dizziness; the patient was euthyroid and experienced anti-thyroid peroxidase (TPO) and anti-thyroglobulin (Tg) antibodies. Paraneoplastic neurological antibodies and evidence of brain metastasis were absent. I-2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (I-FP-CIT) dopamine transporter single-photon emission computed tomography (DAT-SPECT) and N-isopropyl-p-(123I)-iodoamphetamine SPECT (IMP-SPECT) revealed abnormal findings, which were consistent with the patient’s symptoms. Steroid treatment markedly improved the neurological symptoms. Given this clinical course, we speculated that the patient experienced a neurological irAE, much like Hashimoto’s encephalopathy, induced by nivolumab. Case Statement A 68-year-old man with gastric malignancy and multiple hepatic metastases began nivolumab treatment (3 mg/kg biweekly) because standard chemotherapy had been ineffective. After starting nivolumab, the tumor size decreased along with tumor marker levels. However, the patient experienced dizziness on movement and nausea after the sixth nivolumab injection. Nivolumab treatment was continued because PF-CBP1 of its malignancy suppression PF-CBP1 efficacy. The patient’s PF-CBP1 walking difficulty persisted, and involuntary tremor-like movement of both hands appeared, which gradually worsened. A neurologist was consulted, and PF-CBP1 two months after the initial neurological symptoms appeared, a neurologic examination recognized irregular left-dominant involuntary movement of both hands, comprising ataxia, postural tremor (Supplementary material), truncal ataxia, and dizziness on Rabbit Polyclonal to SLC25A12 movement. However, the patient did not experience unconsciousness, nystagmus, paralysis, rigidity, akinesis, or bathyhypesthesia. The findings of laboratory examinations are shown in Table. The patient was euthyroid but experienced elevated anti-TPO (130 IU/mL) and anti-Tg (479 IU/mL) antibody levels. There were no antibodies suggestive of paraneoplastic neurological syndrome (PNS), nor were there collagen disease markers, anti-GQ1b-IgG antibodies, anti-glutamic acid decarboxylase (GAD) antibodies, or anti-acetylcholine receptor (AChR) antibodies. The tumor marker levels improved to almost normal. Table. Laboratory Findings. folic acid6.4ng/mLAnti-Amphiphysin antibodynegative[Cerebrospinal fluid]Vitamin.B12654pg/mLAnti-CV2 antibodynegativeInitial pressure90mmH2OVitamin.E1.78mg/dLAnti-Ma2/Ta antibodynegativeProtein35mg/dLACE19.7IU/LAnti-Ri antibodynegativeSugar63mg/dLFe87g/dLAnti-Yo antibodynegativeCell count4/LFerritin24ng/mLAnti-Hu antibodynegativeNeutrophil0/LCu91g/dLAnti-recoverin antibodynegativeLymphocyte4/LCeruloplasmin19mg/dLAnti-SOX1 antibodynegativeIgG-index0.47ESR7mm/hAnti-titin antibodynegativeOCBsnegativeAnti-nuclear antibodynegativeAnti-zic4 antibodynegativeMBP 31.3pg/mLRF8U/LAnti-GAD65 antibodynegativeCEA 0.5ng/mLAnti-SS-A antibody 1.0U/LAnti-Tr antibodynegativeAnti-GAD antibody 0.5ng/mLAnti-SS-B antibody 1.0U/LCEA8.5ng/mLAnti-TPO antibody 9IU/mLPR3-ANCA 1.0U/LCA19-912U/mLAnti-Tg antibody 10IU/mLMPO-ANCA 1.0U/LsIL-2R545U/mLIgG1,031mg/dLAFP7ng/mLCytologynegativeIgA240mg/dLVZV-IgG EIA6.7IgM32mg/dLVZV-IgM EIA0.31CH5048.3CH50/mLHSV-IgG EIA75.3Free T32.7pg/mLHSV-IgM EIA0.39Free T40.9ng/dLEBV VCAI-IgG320timesTSH1.96IU/mLEBV VCAI-IgM 10timesAnti-TPO antibody130IU/mLEBV EBNA-IgG40timesAnti-Tg antibody479IU/mLCMV-IgG43UA/mLCortisol58.7g/dLCMV-IgMnegativeI.D.ACTH15.1pg/mLAnti-HBs antigennegativeAnti-GQ1b IgG antibodynegativeAnti-HCV antibodynegativeAnti-GAD antibodynegativeRPRnegativeAnti-AChR antibody 0.3nmol/LTPHAnegative Open in a separate window AChR: acetylcholine receptor, ACTH: adrenocorticotropic hormone, AFP: -fetoprotein, ANCA: antineutrophil cytoplasmic antibody, CA19-9: carbohydrate antigen 19-9, CEA: carcinoembryonic antigen, CMV: cytomegalovirus, EBV: Epstein-Barr virus, ESR: erythrocyte sedimentation rate, HBs: hepatitis B surface, HCV: hepatitis C virus, HSV: herpes simplex virus, GAD: glutamic acid decarboxylase, MBP: myelin basic protein, MPO: myeloperoxidase, OCBs: oligoclonal bands, PR3: proteinase3, RF: rheumatoid factor, RPR: quick plasma reagin, sIL-2R: soluble interleukin-2 receptor, Tg: thyroglobulin, TPHA: treponema pallidum hemagglutination assay, TPO: thyroid peroxidase, VZV: varicella zoster virus There were no amazing findings in the cerebrospinal fluid (CSF), nor on electroencephalography (EEG), nerve conduction studies, or somatosensory evoked potential examinations. Head gadolinium-enhanced PF-CBP1 magnetic resonance imaging did not show any amazing abnormalities, including cerebellar atrophy, stroke, and metastasis (Physique A and B); in contrast, IMP-SPECT revealed a cerebral blood flow (CBF) reduction in both occipital lobes and the cerebellar vermis (Physique C). Truncal ataxia was consistent with abnormal findings in the cerebellar vermis. Even though left-dominant tremor-like involuntary movement was difficult to explain.