Symptoms of this still poorly understood disease are believed to be caused by antibodies that increase the activity of pain-sensing nerves throughout the body, a study reveals.
- Contrary to what the medical profession had previously suggested, fibromyalgia does not originate solely in the brain.
- This new research conducted on mice shows that antibodies present in the body of people with this disease may be the cause of symptoms such as pain and muscle weakness.
- This discovery opens the way to a new therapeutic avenue.
Affecting 2 to 4% of the adult population and in particular women, fibromyalgia is a chronic disease that can lead to chronic diffuse, joint and muscle pain, extreme fatigue, difficulty sleeping and depressive symptoms. Recognized by the World Health Organization in 1992, fibromyalgia is a disease with a complex diagnosis, and therefore often poorly treated or even ignored by the medical profession.
A new study, conducted by the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, in collaboration with the University of Liverpool and the Karolinska Institute in Sweden, may help to better understand the origins of this disease. According to its authors, who publish their findings in the Journal of Clinical Investigationfibromyalgia is a disease of the immune system and therefore does not, as previously thought, originate in the brain.
Antibodies responsible for symptoms
The researchers worked from a mouse model, and indeed found that symptoms of fibromyalgia, including increased pain sensitivity, muscle weakness, reduced movement and fewer small nerve fibers in the skin are consequences of a patient’s antibody reaction.
The researchers injected mice with antibodies from people living with fibromyalgia and observed that the mice quickly developed increased sensitivity to pressure and cold, as well as reduced grip strength for movement. In comparison, mice in the control group that received antibodies from healthy people were unaffected. This would therefore prove that the antibodies of the patients are at the origin of the disease, or at least largely contribute to it.
Hope for an effective treatment
The scientists also found that mice given antibodies from fibromyalgia patients recovered after a few weeks, when the antibodies were cleared from their system. This finding therefore suggests that therapies that reduce antibody levels in patients are likely to be effective treatments. A discovery that is all the more hopeful since such therapies are already available and regularly used to treat other disorders caused by autoantibodies.
“The implications of this study are profound. Establishing that fibromyalgia is an autoimmune disorder will transform the way we view the disease and should pave the way for more effective treatments for the millions of people affected. Our work has highlighted a whole new area of treatment options and should give real hope to fibromyalgia patients.”says Dr. David Andersson, principal investigator of the study at King’s College.
“Previous exploration of therapies has been hampered by our limited understanding of the disease. This should now change. Treatment of FMS focuses on gentle aerobic exercise, as well as drug and psychological therapies to manage pain, although proved ineffective in most patients and left behind huge unmet clinical needs”he concludes.
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