Taking tumor necrosis factor (TNF) inhibitors may increase a person’s risk for developing inflammatory central nervous system (CNS) diseases by 36 percent compared to conventional treatments, according to a large study. Researchers found the risk was consistent, regardless of what autoimmune condition a person had or which anti-TNF treatment they were taking.
TNF inhibitors are widely used for reducing inflammation in autoimmune diseases, including axial spondyloarthritis. They’re a type of biologic that blocks tumor necrosis factor, a protein involved in inflammation. Diseases affecting the CNS — including multiple sclerosis (MS) and meningitis — are rare but serious potential side effects of TNF inhibitor therapy.
For the study, researchers analyzed more than 1 million people across 18 studies and identified a potential link between anti-TNF treatments and an increased risk for CNS-related conditions. They found people were at greatest risk for developing demyelinating conditions such as MS, in which the immune system attacks the protective myelin sheath around nerves, leading to nerve damage.
Healthcare providers sometimes prescribe TNF inhibitors — such as golimumab (Simponi) and infliximab (Remicade) — to treat moderate to severe axial spondyloarthritis when other treatments aren’t effective. Researchers have long suspected a link between these drugs and a higher risk for CNS diseases. Some of these drugs specifically list “demyelinating disorders” among their rare but serious potential side effects. This large study strengthens the evidence of an association.
While these medications may slightly increase the risk for CNS conditions, the overall likelihood of developing one remains low. All treatments have potential risks, which should be carefully weighed when developing a treatment plan. If you’re managing ankylosing spondylitis or nonradiographic axial spondyloarthritis, it’s crucial to discuss the risks and benefits of your therapy with your doctor and report any concerning symptoms promptly.
Learn more about advanced treatments for spondylitis, including TNF inhibitors.
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Why would this be a side effect? So we trade inflammation control of our tendons and ligaments for inflammation of our nerves? Is there a different protein that attacks our myelin sheaths? Confused.
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