Treatment of immune checkpoint inhibitor-induced inflammatory arthritis

Susanna Jeurling, Laura C. Cappelli

Research output: Contribution to journalReview articlepeer-review

Abstract

Purpose of reviewThis review summarizes the current evidence on treatment strategies for inflammatory arthritis because of cancer treatment with immune checkpoint inhibitors (ICI), prognosis of ICI-induced arthritis, and management of patients with preexisting inflammatory arthritis receiving ICI therapy.Recent findingsInflammatory arthritis is the most common rheumatic immune-related adverse event observed in patients receiving ICI therapy. Most patients can successfully be treated with low doses of corticosteroids or conventional synthetic disease modifying anti-rheumatic drugs (DMARDs). A small minority will develop severe symptoms requiring biologic therapy including TNF inhibitors and IL-6 receptor inhibitors. Many cases of inflammatory arthritis will resolve with cessation of ICI therapy. Some patients will develop persistent arthritis despite discontinuation. Patients with preexisting inflammatory arthritis (e.g. rheumatoid arthritis) commonly flare on ICI therapy, but can usually be managed with corticosteroids.SummaryInflammatory arthritis following ICI therapy for cancer is relatively common and the practicing rheumatologist should be able to recognize and manage it in conjunction with Oncology. The majority of patients respond to corticosteroids, but some will need treatment with conventional synthetic or biologic DMARDs. Additional studies should investigate the effects of immunosuppression on tumor response and the use of ICI therapy in patients with preexisting autoimmune disease.

Original languageEnglish (US)
Pages (from-to)315-320
Number of pages6
JournalCurrent opinion in rheumatology
Volume32
Issue number3
DOIs
StatePublished - May 1 2020

Keywords

  • cancer
  • immune checkpoint inhibitor
  • inflammatory arthritis

ASJC Scopus subject areas

  • Rheumatology

Fingerprint Dive into the research topics of 'Treatment of immune checkpoint inhibitor-induced inflammatory arthritis'. Together they form a unique fingerprint.

Cite this