Non-tuberculous mycobacterial shoulder arthritis with acute exacerbation soon after initiation of immune checkpoint inhibitor: A case report

• Published in: Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy 2024-12, p.102596, Article 102596
• Main Authors: Inada, Shugo, Omori, Keitaro, Nomura, Toshihito, Kitagawa, Hiroki, Shigemoto, Norifumi, Hattori, Noboru, Ohge, Hiroki
• Format: Article
• Language: English
• Subjects: extrapulmonary non-tuberculous mycobacterial infections; immune checkpoint inhibitor; immune-related adverse event; Mycobacterium intracellulare; non-tuberculous mycobacterium
• ISSN: 1341-321X; 1437-7780; 1437-7780
• DOI: 10.1016/j.jiac.2024.102596

Immune checkpoint inhibitors (ICIs) have been approved for treating various cancers; however, they can cause immune-related adverse events. Generally, ICIs are not associated with an increased risk of infection, however, several reports demonstrated infections caused by nontuberculous mycobacterium (NTM) during ICI therapy. Here, we report a case of NTM shoulder arthritis with acute exacerbation immediately after ICI initiation. A 75-year-old man was diagnosed with left shoulder arthritis caused by Mycobacterium intracellulare eight months before receiving ICI treatment and was treated with clarithromycin and ethambutol. However, the mild redness, swelling, heat, and shoulder pain persisted. The patient was diagnosed with hepatocellular carcinoma and atezolizumab and bevacizumab treatment was initiated; one day after the initiation of therapy, the patient presented with a fever and worsened shoulder symptoms. Considering the suspected worsening of NTM arthritis, sitafloxacin was additionally administered, and surgical debridement was performed. M. intracellulare was isolated through culturing shoulder synovial tissue; immunohistochemical staining analysis revealed programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) expression in granulation tissue cells. After the arthritis symptoms decreased, atezolizumab plus bevacizumab was resumed and continued with no recurrence of arthritis. The NTM exacerbation on the day after ICI administration suggests the potential involvement of the PD-1/PD-L1 pathway in the pathogenesis of NTM; moreover, adverse inflammatory reactions to NTM were possibly triggered through the blockade of this pathway.