Fibromyalgia: an autoimmune disease?

During all the time that has elapsed since the start of the pandemic, research into fibromyalgia has not stopped and there are two aspects that have come to light in recent months that, in my opinion, are highly relevant.

I have to say that they do not have an immediate application for patients, but they are going to open new avenues of knowledge to better understand what is happening in this disease and in other similar ones.

The first of these is work carried out in the laboratory in which blood has been drawn from patients with fibromyalgia and the immunoglobulins, that is, the antibodies, have been purified. Next, an experimental model of fibromyalgia made up of mice – which has already been tested previously and we know that it serves to see how the experimental drugs that will later be applied to humans work – have been injected with these human antibodies. In a short space of time, the mice develop a clinical picture similar to fibromyalgia, with hypersensitivity to pain, apathy, fatigue, sleep disturbances and a general situation that could be defined as a depressive syndrome.

That is, there has been a transfer of the disease from humans to mice through the antibodies present in fibromyalgia patients, which strongly suggests that there is something in the blood of fibromyalgia patients capable of causing the disease.

The second line of research has been provided by the so-called persistent COVID (long COVID). This is a clinical picture that appears after COVID has passed, and its main symptoms consist of fatigue, joint pain, shortness of breath, sleep disturbances, anxiety, cognitive disorders, smell disturbances and poor mood.

As can be seen, it is a symptomatology very similar to that of fibromyalgia and it was initially thought that these patients had developed it in the context of the acute stress of COVID. We have studied this chart in depth and have reached somewhat different and quite enlightening conclusions.

In the first place, persistent COVID is also developed by patients with fibromyalgia and also by patients with other rheumatic diseases, so it is not a condition that appears more frequently among patients with fibromyalgia, as might be expected due to the greater sensitivity that these patients have in situations of stress.

Second, the symptoms are practically the same, although it is true that with greater intensity in patients with fibromyalgia. It is known that comorbidity between fibromyalgia and other diseases intensifies the symptoms of diseases associated with fibromyalgia and in this study we have found the same dynamic.

Third, in fibromyalgia patients who subsequently developed persistent COVID, there was no worsening of fibromyalgia, but the same severity remained. This suggests that the symptoms of both diseases may follow independent pathways.

It is known that coronavirus infection is capable of causing a large immune response with the appearance of multiple antibodies against different proteins in the body. We also know that some of these antibodies play a pathogenic role in certain rare autoimmune diseases, so it is reasonable to think that the symptoms of persistent COVID could have an autoimmune origin.

Since the symptoms of persistent COVID are similar to those of fibromyalgia, we can conclude that persistent COVID and fibromyalgia, although they are two different diseases, could share similar pathogenic mechanisms.

As can be seen, the two studies described in this article walk in the same direction and open a new horizon in the investigation of fibromyalgia and related syndromes. However, we must be cautious waiting for new findings to confirm these interesting discoveries.

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