New research has shown that fibromyalgia is most likely to be caused by autoimmune issues.
A study by researchers from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, in collaboration with the University of Liverpool and the Karolinska Institute, has shown that many of the symptoms in fibromyalgia syndrome (FMS) are caused by antibodies that increase the activity of pain-sensing nerves throughout the body.
FMS is a long-term condition that causes pain all over the body. As well as widespread pain, common symptoms of fibromyalgia include increased sensitivity to pain, extreme tiredness, headaches, and muscle stiffness.
Currently, the most common belief is that fibromyalgia originates in the brain, but the results from the study suggest that it is actually a disease of the immune system.
The findings have been published in the Journal of Clinical Investigation.
The researchers injected mice with antibodies from people living with FMS and observed that the mice rapidly developed an increased sensitivity to pressure and cold, as well as displaying reduced movement grip strength. In contrast, mice that were injected with antibodies from healthy people were unaffected, demonstrating that patient antibodies cause, or are at least a major contributor to, the disease.
Paving the way for new potential treatments
Additionally, the mice injected with fibromyalgia antibodies recovered after a few weeks, when antibodies had been cleared from their system. This finding strongly suggests that therapies which reduce antibody levels in patients are likely to be effective treatments. Such therapies are already available and are used to treat other disorders that are caused by autoantibodies.
Dr David Andersson, the study’s primary investigator from King’s IoPPN, said: “The implications of this study are profound. 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. Our work has uncovered a whole new area of therapeutic options and should give real hope to fibromyalgia patients.
“Previous exploration of therapies has been hampered by our limited understanding of the illness. This should now change. Treatment for FMS is focussed on gentle aerobic exercises, as well as drug and psychological therapies designed to manage pain, although these have proven ineffective in most patients and have left behind an enormous unmet clinical need.”
Dr Andreas Goebel, the study’s principle clinical investigator from the University of Liverpool, said: “When I initiated this study in the UK, I expected that some fibromyalgia cases may be autoimmune. But David’s team have discovered pain-causing antibodies in each recruited patient. The results offer amazing hope that the invisible, devastating symptoms of fibromyalgia will become treatable.”
Professor Camilla Svensson, the study’s primary investigator from Karolinska Institute, said: “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.”