What are the risks and benefits of TNF-? antagonists for the treatment of ankylosing spondylitis (AS) and undifferentiated spondyloarthropathy (USpA)?

Updated: Sep 03, 2019
  • Author: Lawrence H Brent, MD; Chief Editor: Herbert S Diamond, MD  more...
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There is some concern regarding an increased risk of malignancy in patients receiving TNF-α antagonists. The most attention has been focused on lymphoma and nonmelanotic skin cancers in patients with rheumatoid arthritis, although this has been difficult to document in such patients and has not been described in patients with AS. In rare cases, cytopenias have been associated with TNF-α antagonists.

Patients with rheumatoid arthritis who have recently started TNF-α antagonists may be at increased risk for new-onset congestive heart failure even in the absence of any obvious risk factors for the disease. These agents should not be initiated in patients with uncompensated congestive heart failure.

Patients should be screened for latent tuberculosis, hepatitis B, and HIV infection before beginning TNF-α antagonist therapy. [120] Although these agents should not be used in patients with active hepatitis B infection, they appear to be safe in patients with chronic hepatitis C infections. Rarely, autoimmune syndromes (eg, a lupuslike illness) have been noted in patients receiving TNF-α antagonists. More commonly, a positive antinuclear antibody (ANA) test result may occur during treatment without clinical disease.

Demyelinating syndromes have rarely been documented in patients receiving TNF-α antagonists, though no direct link has been proved. These agents should not be used in patients with multiple sclerosis or other demyelinating diseases. New-onset psoriatic skin lesions have been documented after initiation of TNF-α antagonists.

In a prospective study of 334 patients with AS, response to treatment with TNF-α inhibitors was associated with a 50% reduction in the risk of radiographic progression of AS. However, nearly 4 years of treatment were necessary for the benefit to become apparent. Moreover, in patients who first began TNF-inhibitor treatment 10 or more years after disease onset, AS progression was twice as likely as it was in patients who started treatment earlier. [121, 122]

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