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Osaki M, Tachikawa R, Ohira J, et al. Anti-transcriptional intermediary factor 1-γ antibody-positive dermatomyositis induced by nivolumab for lung adenocarcinoma: A case report. Invest New Drugs. 2020;39(1):251-255doi: 10.1007/s10637-020-00974-7.
Osaki, M., Tachikawa, R., Ohira, J., Hara, S., & Tomii, K. (2021). Anti-transcriptional intermediary factor 1-γ antibody-positive dermatomyositis induced by nivolumab for lung adenocarcinoma: A case report. Investigational new drugs, 39(1), 251-255. https://doi.org/10.1007/s10637-020-00974-7
Osaki, Megumu, et al. "Anti-transcriptional intermediary factor 1-γ antibody-positive dermatomyositis induced by nivolumab for lung adenocarcinoma: A case report." Investigational new drugs vol. 39,1 (2021): 251-255. doi: https://doi.org/10.1007/s10637-020-00974-7
Osaki M, Tachikawa R, Ohira J, Hara S, Tomii K. Anti-transcriptional intermediary factor 1-γ antibody-positive dermatomyositis induced by nivolumab for lung adenocarcinoma: A case report. Invest New Drugs. 2021 Feb;39(1):251-255. doi: 10.1007/s10637-020-00974-7. Epub 2020 Jul 10. PMID: 32651759.
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Invest New Drugs. 2021 Feb;39(1):251-255. doi: 10.1007/s10637-020-00974-7. Epub 2020 Jul 10.

Anti-transcriptional intermediary factor 1-γ antibody-positive dermatomyositis induced by nivolumab for lung adenocarcinoma: A case report.

Investigational new drugs

Megumu Osaki, Ryo Tachikawa, Junichiro Ohira, Shigeo Hara, Keisuke Tomii

Affiliations

  1. Department of Respiratory Medicine, Kobe City Medical Center General Hospital, 2-1-1, Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan. [email protected].
  2. Department of Respiratory Medicine, Kobe City Medical Center General Hospital, 2-1-1, Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
  3. Department of Neurology, Kobe City Medical Center General Hospital, Kobe, Hyogo, Japan.
  4. Department of Pathological Diagnostics, Kobe City Medical Center General Hospital, Kobe, Hyogo, Japan.

PMID: 32651759 DOI: 10.1007/s10637-020-00974-7

Abstract

Immune checkpoint inhibitors can induce immune-related adverse events (irAEs) in different organs. Dermatomyositis is a rare form of systemic irAE. Although dermatomyositis-specific antibodies, especially anti-transcriptional intermediary factor 1-γ (anti-TIF1-γ) antibodies, have been detected in a few cases of immune checkpoint inhibitor-associated dermatomyositis, their titers before immunotherapy have not been examined. We hereby report the first irAE case of dermatomyositis accompanied by seroconversion of anti-TIF1-γ antibody following nivolumab treatment for advanced lung adenocarcinoma. A 64-year-old Japanese male with an advanced lung adenocarcinoma (cT4N2M1a stage IVA) received nivolumab as third-line therapy. Skin rashes appeared two days later, and were treated with a topical steroid as just drug eruptions. 7 weeks later, he was emergently admitted because of high serum creatine kinase level. Clinical examination showed deteriorated rashes along with slightly weakened proximal muscles. Muscle biopsy revealed myopathic changes consistent with dermatomyositis. Anti-TIF1-γ antibody was positive, which was found to be within normal range before nivolumab administration. He was diagnosed with dermatomyositis and treated with systemic corticosteroids, tacrolimus, and intravenous immunoglobulin. However, these drugs showed limited effectiveness against the progression of muscle weakness. He died of respiratory failure due to lung cancer and muscle weakness progression 6 months after the admission. In conclusion, our case demonstrates that the development of dermatomyositis was causally related to immune activation by nivolumab. Given the potential exacerbation of autoimmune paraneoplastic disorders in cancer patients receiving immunotherapy, clinicians should be aware of early manifestations of systemic irAEs that require prompt diagnosis and intervention.

Keywords: Dermatomyositis-specific autoantibody; Immune checkpoint inhibitor; Immune-related adverse event; Non-squamous non-small-cell lung carcinoma; Paraneoplastic syndrome; Programmed cell death protein 1

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