Cancer treatments have greatly evolved to offer better results with fewer adverse effects. A newer family, called Immune Checkpoint Inhibitors (ICPis), falls under this category. ICPis are a type of immunotherapy for various cancers such as multiple myeloma, non-small cell lung cancer, and Hodgkin’s lymphoma. In this blog, we will share some information on how these treatments work and why they may cause a patient to develop Rheumatoid Arthritis.
Our bodies have immune cells called T cells that constantly look for dangers like viruses and bacteria. Healthy cells have checkpoints on their surfaces to prevent T cells from attacking them. However, cancer cells can disguise themselves by copying these checkpoints, allowing them to spread unchecked. Checkpoint inhibitors work by exposing the cancer cells’ disguise, enabling T cells to recognize and attack them. This ramps up our immune system and may lead to autoimmune conditions like rheumatoid arthritis. In fact, studies have found that 1-7% of patients treated with ICPis develop this condition.
Treatment for rheumatoid arthritis caused by ICPis often starts with a steroid medication called prednisone to quickly manage symptoms. A recent study published in the Journal of Rheumatology found that traditional disease-modifying treatments (methotrexate, leflunomide, hydroxychloroquine, and sulfasalazine) successfully led to low disease activity for patients who developed rheumatoid arthritis caused by ICPis regardless of whether the ICPi treatment was discontinued.
Early reporting of joint symptoms and a quick start to treatment can greatly improve outcomes for those affected by this unexpected side effect of immune checkpoint inhibitors.
Joyce Ayad is a 4th year pharmacy student from the University of Waterloo, currently completing her final rotation at Charlton Health. She believes in providing patient-focused care, supported by her previous experience working with specialty drugs, the pharmaceutical industry, and more. Joyce is eager to become a licensed pharmacist this year.
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