Fibromyalgia could stem from autoimmune problems

Many symptoms of fibromyalgia syndrome (FMS) are caused by antibodies that increase the activity of pain-sensing nerves, according to UK and European research.

This may mean that FMS is a disease of the immune system, rather than originating in the brain as currently thought, opening new options for treatment.

FMS is a chronic condition that causes pain and stiffness in muscles and bones across the body, which can worsen with activity or stress. The pain is often coupled with symptoms such as tenderness, fatigue, difficulty sleeping and problems with concentration and memory, severely impacting quality of life.

It affects approximately 2–5% of people worldwide, 80% of whom are women. It commonly develops between the ages of 25 and 55, though children are also affected. The symptoms can often be imperceptible from the outside, making it difficult for those living with it.

Research into FMS is lacking – we don’t completely understand the cause, it is difficult to diagnose, and there is no cure. Current research suggests that FMS originates in the way the brain processes pain signals, rather than in the muscles and bones themselves.

But this new study, led by David Andersson from King’s College London, injected mice with antibodies of people with FMS and found that the animals developed typical symptoms such as increased pain sensitivity (including sensitivity to cold and pressure), muscle weakness and reduced movements and grip strength. The symptoms continued for several weeks, until the antibodies were cleared from the mice’s systems and they recovered.

Mice injected with antibodies from people without FMS were not affected.

This suggests that antibodies play a key role in the disease, and points towards the potential effectiveness of currently available treatments, such as therapies reducing antibody levels in patients.

“Establishing that fibromyalgia is an autoimmune disorder will transform how we view the condition and should pave the way for more effective treatments for the millions of people affected,” says Andersson.

“Previous exploration of therapies has been hampered by our limited understanding of the illness. This should now change.”

Treatment for FMS is currently focused on gentle exercise and pain management, but the researchers argue that other therapeutic options should now be considered.

The study also involved Swedish researchers, including Camilla Svensson from the Karolinska Institute, who notes: “Antibodies from people with FMS living in two different countries, the UK and Sweden, gave similar results, which adds enormous strength to our findings.

“The next step will be to identify what factors the symptom-inducing antibodies bind to. This will help us not only in terms of developing novel treatment strategies for FMS, but also of blood-based tests for diagnosis, which are missing today.”

The paper is published in the Journal of Clinical Investigation.

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