Exciting New Publication On Fibromyalgia- New study shows Fibromyalgia likely the result of autoimmune problems
The King’s-led study, in collaboration with University of Liverpool and the Karolinska Institute,
New research 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.
The results show that fibromyalgia is a disease of the immune system, rather than the currently held view that it originates in the brain.
The study, published in the Journal of Clinical Investigation, demonstrates that the increased pain sensitivity, muscle weakness, reduced movement, and reduced number of small nerve-fibres in the skin that are typical of FMS, are all a consequence of patient antibodies.
These amazing findings have uncovered a whole new area of therapeutic options and should give real hope to fibromyalgia patients.
Passive Transfer of Fibromyalgia Symptoms from Patients to Mice
Dr Andreas Goebel,the PRI Director said, “When initiated this study in the UK, I expected that some fibromyalgia cases may be autoimmune. But David Anderssons team have discovered pain-causing antibodies in each recruited patient. The results offer amazing hope that invisible, devastating fibromyalgia symptoms become treatable.
The study, demonstrates that the increased pain sensitivity, muscle weakness, reduced movement, and reduced number of small nerve-fibres in the skin that are typical of FMS, are all a consequence of patient antibodies.
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 and a reduced grip strength. In contrast, mice that were injected with antibodies from healthy people were unaffected, demonstrating that patient antibodies cause, or at least are a major contributor to the disease. The results show that fibromyalgia is a disease of the immune system, rather than the currently held view that fibromyalgia originates in the brain.
Importantly, 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 available and are used to treat other autoantibody-mediated disorders.
You can access the publication here