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Published on: February 8, 2019
Vasculitis associated with tumor necrosis factor-α inhibitors
Olayemi Sokumbi1, David A Wetter, Ashima Makol
1Department of Dermatology, Mayo Clinic, Rochester, MN 55905, USA.
Vasculitis can develop with tumor necrosis factor-α (TNF-α) inhibitor use, primarily affecting the skin but also systemic organs. Discontinuation of TNF-α therapy and treatment led to improvement in most patients.
Area of Science:
- Rheumatology
- Immunology
- Dermatology
Background:
- Tumor necrosis factor-α (TNF-α) inhibitors are widely used for inflammatory conditions.
- Vasculitis is a rare but serious adverse event associated with TNF-α inhibitor therapy.
- Understanding the characteristics of TNF-α inhibitor-induced vasculitis is crucial for patient management.
Purpose of the Study:
- To characterize the clinical presentation, histopathology, and outcomes of vasculitis developing during TNF-α inhibitor therapy.
- To identify risk factors and patterns of vasculitis associated with specific TNF-α inhibitors.
Main Methods:
- Retrospective review of patients diagnosed with vasculitis induced by anti-TNF-α therapy at Mayo Clinic (1998-2011).
- Analysis of clinical data, histopathologic findings, treatment regimens, and patient outcomes.
Main Results:
- Eight patients (mean age 48.5, 75% female) developed vasculitis after a mean of 34.5 months of TNF-α inhibitor use.
- Rheumatoid arthritis (50%) and inflammatory bowel disease (50%) were common underlying conditions.
- Cutaneous small-vessel vasculitis (63%) was most frequent, presenting as palpable purpura; systemic involvement included peripheral nervous system (50%) and kidney (13%).
- Infliximab (63%) was the most common agent used.
Conclusions:
- TNF-α inhibitor-induced vasculitis can manifest as cutaneous small-vessel vasculitis or systemic vasculitis involving nerves and kidneys.
- Discontinuation of TNF-α therapy, along with prednisone and other agents, resulted in resolution of vasculitis in 7 of 8 patients.
- No recurrence was observed after discontinuation of TNF-α therapy.
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